Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS 2 > BMS236 Building Nervous Systems > Flashcards

BMS236 Building Nervous Systems Flashcards

1
Q

What ways are the PNS classified?

A 
How they connect to CNS
- Cranial and spinal nerves 
Direction of propagation 
- Afferent
- Efferent
Motorneurone's target effectors
- Somatic and autonomic (sympathetic and parasympathetic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What has research shown us about fish brains?

A

There is a tube that carries nerves from distal parts of body to a central point
- Unconscious and mechanical brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What has research shown us about reptilian brains?

A

Nerves sorted into specialised modules e.g.. light sensitive = vision
- Mechanical and unconscious brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What has research shown us about mammalian brains?

A
  • Hypothalamus - reaction to stimuli
  • Thalamus - vision smell and hearing to be used together
  • Limbic system - emotions but unconscious
  • Amygdala and hippocampus - crude memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What has research shown us about human brains?

A
  • Enlargement of areas associated with thinking, planning and communicating
  • Larger cortex pushing cerebellum to current position
  • Skull bones pushed outwards forming flat forehead
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are Brodmann’s areas of the brain?

A

Systematic map of brain based upon cell types

  • Broca’s area (44)
  • Wernike’s area (22)
  • Motor cortex (4)
  • Visual cortex (14)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are Broca’s and Wernike’s areas of the brain?

A
  • Broca’s - Produces speech by controlling muscles to speak

- Wernicke’s - has grammatical rules for language

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is anatomical modularity?

A

Connecting modules that work together to complete tasks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are some parts of the brain hard wired to become allocated t a specific task?

A

Evolution has made it essential that humans have vision, the ability to move precisely and speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why can humans do things that have no evolutionary advantage e.g. play music?

A
  • Maybe to attract opposite sex and pass on genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does a musicians brain differ?

A

increased size

  • caused by neurones sprouting new connections to allow for complex movements involved in musical performance
  • Shows plasticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is brain plasticity?

A

Ability to produce new and destroy old connections between neurones in response to physical demands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is the brain so powerful?

A

Brain has 10^11 neurones and each has 1000-10000 synapses meaning 10^14 connections in human brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do sponges show signs of an early nervous system?

A

Water flow needs to be regulated by myocytes which are specialised muscle like cells which respond to stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the characteristics of primordial nervous systems?

A
  • Appearance of neurones
  • First neurones probably sensorimotor cells
  • Began to differentiate down a nerve pathway instead of a skin pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the characteristics of a hydra nervous system?

A

Derivation of different types of neurones from ectoderm

  • Motor neurones which receive inputs from the sensory neurones
  • Interneurons - lie between sensory and motor neurones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is a worms nervous system more complex than in hydra?

A
  • Gangliation
  • Cephalization - formation of brain - worms have difference in anterior/prosterior
  • Bilateral symmetry
  • Fasiculation - nerves beginning to bundle
  • entire nervous system was internal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give an example of how the segmented worms nervous system evolved?

A
  • Fusion of longitudinal nerve cords

- Brain evolved to regulate feeding - sense food and ability to grab it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give an example of how the C. Elegans nervous system has evolved?

A
  • Nervous system mapped
    • Ventral dorsal ad lateral nerve cords
  • Most neurons derived from one cell
  • Neurones share lineage with hypodermis (skin) - evidence that a decision is made whether to become skin or nervous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give an example of how the drosophila nervous system has evolved?

A
  • Optic lobes
  • Beginning of proper brains
  • Formation of neuroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give an example of how vertebrates nervous system has evolved?

A
  • have a common body plan
  • early nervous system is similar across all families
  • Nervous system forms from ectoderm that would otherwise be skin
  • Nervous system is dorsal instead of ventral - somewhere in evolution head turned around so ventral things became dorsal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give the common features of xenopus (vertebrate) and insects nervous systems

A
  • Neurogenic region next to ectoderm
  • Neurogenic region migrates downwards
  • Gastrulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give the different features of xenopus (vertebrate) and insects nervous systems

A
  • Neural cells do not delaminate

- Neural cells stay as a layer called the neuroepithelium (neural plate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is cell differentiation?

A

Process by which cells become different from each other and acquire specialised properties
Governed by gene expression which can be changed in response to morphogens or transcription factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is BMP?

A

A protein that will cause a cascade that will cause the differentiation of cells into skin ectoderm
- It has been conserved through time and evolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is chordin?

A

An antagonist to BMP (inhibits BMP signalling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does the neurogenic region arise?

A

BMP signalling is inhibited by chordin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the homologue of BMP and Chordin in insects?

A 
BMP = dpp
Chordin = sog

So sog inhibits DPP causing the cells to become the neurogenic region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where in the cell does the neurogenic region develop?

A

Chordin and BMP diffuse from opposite ends so where they meet is where the neural tube develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the pathway for ectoderm differentiating into epidermis?

A
  • BMP binds to BMP receptor and a secondary signal (Smad) is phosphorylated
  • Smad can then up regulate transcription factors like Msx1, GATA1 which leads to epidermal differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the pathway for ectoderm differentiating into neural tissue?

A
  • BMP inhibited
  • No Smad phosphorylated so different transcription factors are up regulated (xlpou2, soxd)
  • Neural differentiation pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is neurulation?

A

When the neural plate rolls up to form the neural tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the Spemann organiser?

A

A specialised part of the mesoderm that expresses transcriptional factors (Gsc) expressing antagonists of BMP eg. chordin which diffuse into the ectoderm and bind with BMP
- Forming neural plate in ectoderm neighbouring the organiser

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What decides the location of the organiser in the mesoderm?

A

Low levels of the nodal protein leads to ventral mesoderm

High levels gives the organiser

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What happens to the organiser cells in the mesoderm?

A
  • Differentiate into anterior endoderm, prechordal mesoderm and notochord
  • It involutes, intercalates and undergoes convergent extension
  • Forms the midline of the neural plate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Give some experimental evidence for neural induction?

A
  • A donor organiser was grafted from a donor onto a host newt
  • found that a ‘twinned’ embryo developed with a secondary neural axis
  • Secondary neural tube was host derived showing it was induced from the ectoderm in response to signals from the organiser
  • The prechordal mesoderm ad notochord where donor derived showing they’re formed from the organiser
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How were BMP inhibitors discovered?

A

Extracted all mRNA from organiser cells and reverse transcribed them to cDNA. This was tested to look for a protein that would mimic the organisers ability to induce a secondary neural plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give experimental evidence for the fate of the organiser (Henson’s node)

A

Cut out the node and culture

It develops into a long rod shape which is the notochord and at the anterior end the prechordal mesoderm develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the activation transformation model?

A

The idea that neural inducing molecules such as BMP inhibitors (Chordin) and ant antagonists only remain in the prechordal mesoderm (part of organiser that is involuted first) not all of it. the later part of the node expresses Wnt, FGF and retanoic acid which posterialises anterior tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When establishing an A P regional identity what is present on the anterior side?

A

BMP and Wnt antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

When establishing an A P regional identity what is present on the posterior side?

A

Want, FGF and retanoic acid - promise posteriorisation and growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the key concept when establishing a regional pattern?

A

having 2 antagonist molecules at each end of a forming structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the two models for the use of concentration gradients by morphogens?

A
  • Alan turing reaction diffusion model

- Lewis Wolpert’s French flag model

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the French flag model?

A

The idea that different levels of a morphogen concentration leads to a different cell fate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is a morphogen?

A

A diffusible molecule that causes a particular response from a cell depending on its concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are hox genes?

A
  • Control segmentation and specify A P

- Massively conserved through time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What controls the patterns of hox?

A

Retanoic acid gradient

  • high concs lead to neck
  • low concs to tail
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the neural plate border?

A

A specialised border that develops at the neural - ectoderm boundary (edge of the neural plate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the border cells required for?

A
  • Neural cress formation

- Roof plate formation and dorsal neural tube differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is responsible for the formation of the peripheral nervous system?

A

The neural crest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is the neural crest formed?

A
  • Border is established between neural plate and surface ectoderm which expresses transcription factors such as msx - induce at intermediates levels of BMP signalling
  • Wnts, FGFs act together with msx1 - these transcription factors characterise neural plate border cell
  • Wnt signals act together wot NPB transcription factors to up regulate more transcription factors (c-Myc, Id, Snail) that characterise neural crest cells
  • Neural crest cell transplantation factors up regulate a further set of genes that promote epithelial mesenchymal cell transition.
  • Neural crest cells delaminate from the border and migrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What causes the early border cells to be established?

A

Intermediate levels of BMP signalling triggering transcription factors (msx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What transcription factors are known to give cells ‘stem like” behaviours: proliferation and multipotency and what are there roles?

A

( c - MYC, Id, Sox9)
Role in formation of neural crest cells
They activate genes that control proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why are neural crest cells referred to as the ‘4th germ layer’?

A

Because it gives rise to high number of different types of cell

  • Peripheral nervous sytem
  • Facial cartilage
  • Schwann cells
  • dentine of teeth
  • Enteric nervous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How are neural crest cells fate determined?

A
  • Partially by how genes
  • time of generation of neural crest cells
  • Migratory pathway - encounter different signals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Do all neural plate border cells form neural crest cells?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What happens to neural plate border cells that don’t develop into neural crest cells?

A

A few are retained at the border and form roof plate cells - it is not clear why some cells are retained are and others aren’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Why are roof plate cells important?

A

Important in the final step of neurulation and in dorsal neural tube patterning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How do roof plate cells lead to neural tube progenitors to acquire dorsal identities?

A
  • Roof plate cells up regulated BMPs and Wnts
  • Secreted and diffuse into dorsal tube
  • Indice expression of transcription factors (Pax6, Pac7, Pax3, Lim1) that cause neural tube progenitors to acquire dorsal identities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is it thought that BMP’s induce a different dorsal cell type?

A
  • It was thought that they act as morphogens

- But recent work shows that roof plates may express many different BMP’s which induce a particular dorsal cell type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What cell types differentiate dorsally?

A

Roof plate cells, neural crest cells, different classes of dorsal sensory relay interneurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What cell type secrete a morphogen inducing a ventral fate?

A

Norochord

Floor plate cells located at the ventral midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How was the role of floor plate cells tested?

A
  • Ectopically implanting a donor notochord which induced an ectopic floor plate and saw it induced ventral neurones such as motor neurones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What causes the formation of the floor plate?

A

The notochord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What gene is responsible for the production of the protein that is secreted from the floor plate?

A

Hedgehog gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What mRNA is expressed in the notochord and floor plate?

A

shh mRNA

- Only gets upregulated when notochord formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Why does shh act as a morphogen?

A

Made and secreted from floor plate diffuses into neighbouring cells and establishes a concentration gradient resulting in ventralisation due to the induction of expression of transcription factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What happens if shh soaked beads are implanted into a cell?

A

Secondary neural plate and notochord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does Shh act as positivity feedback mechanism?

A

A high concentration of shh protein induces floor plate which unregulated shh gene leading to more shh protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the role of shh in the developing nervous system?

A

shh acts at early stage to confer a DV pattern of transcription factor on progenitor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the morphogens that pattern the DV axis?

A

The opposing gradients of BMP and shh - act antagonistically to each other
shh does not act at the same early stages of BMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the key stages in ventralisation?

A
  • Notochord secretes shh
  • shh diffuses through spinal cord - conc gradient (morphogen)
  • It induces different patterns of transcription factors
  • High concs of shh cause floor plate cells to develop which occupy ventral midline of neural tube - activates shh
  • shh mRNA in both notochord and floor plate
  • shh diffuses into neighbouring cells causing ventral fate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Why has the investigation into dorsal and ventralisation helped in drug discovery?

A

Knowing how processes work and how the nervous system forms allows us to push embryonic stem cells towards a defined fate which can be used in new drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are radial glia?

A

Neural stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How are radial glia formed?

A
  • During early development, some cells continue to span the width of the neural tube
  • Their nuclei migrate back/fourth at different stages in mitotic cycle
  • These are radial glia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do radial glial cells become a proliferating progenitors daughter cell?

A

Neural stem cells maintain a luminal contact and over time cell bodies come to occupy ventricular zone (ependymal zone)

  • depending on the plane of diffusion they can give rise to two radial glia and proliferating daughter progenitor
  • Proliferating progenitors move into the adjacent mantle zone and differentiated cells moves away into the outer marginal zone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What happens in a proneural and a neurogenic mutant?

A

Wild type drosophila
- Have cells that have proneural genes so are able to come neurones
Proneural mutant
- No cells become neurones
Neurogenic mutant (notch-/-)
- But in a neurogenic mutant more neurones are formed
Shows Notch required to prevent a cell becoming a neurone - acts locally on immediately to adjacent cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is lateral inhibition?

A

Involves transmission of an inhibitory signal between a pair or cluster of cells to prevent cells that receive the signal from adopting a specific fate
When the central cell in the pro neural cluster inhibits the surrounding cells and stops from becoming neuroblast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How does the neurectoderm become a neuroblast and epidermis cells through lateral inhibition?

A
  • Cells express both Notch and Delta equally
  • One cell starts to express more delta
  • Other cells increase in notch in order to receive the amount of delta
  • The increase in notch causes the inhibition of delta in those cells
  • The difference in notch and delta increases leading to a neuroblast (with high delta) and epidermis (with high notch)
    => Lateral inhibition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Are all cells in a proneural cluster capable of becoming a neuroblast?

A

Yes the proneural glosser is an equivalence group

Notch -/- or Delta -/- causes all cells to become neuroblast - must be competent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is a proneural cluster?

A

Groups of cells in the neurectoderm

One cell in the cluster will become a neuroblast and the others will become epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What happens to progenitors that don’t differentiate?

A

They have a certain shape
Exist as radial glia (neural stem cells)
Provide a pool of undifferentiated cells that are used to build yo the nervous system over time in embryogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the highest level in the motor system hierarchy?

A

Primary motor cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the middle level in the motor system hierarchy?

A

Brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the lowest level in the motor system hierarchy?

A

Spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the role of the highest level in the motor system hierarchy?

A

Projects directly to spinal cord via corticospinal tract

Regulates the motor tracts that originate in brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the role of the middle level in the motor system hierarchy?

A

Lateral descending system controls distal limbs is important for goal directed movements of hand and arms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the role of the lowest level in the motor system hierarchy?

A

Contains neuronal circuits that mediate reflexes autonomous such as walking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What does monosynaptic mean?

A

One sensory neurone and one motor neurone

- Simplest reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What does polysynaptic mean?

A

Many neurones and interneurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What happens if you artificially stimulate the Motor cortex, brainstem or spinal cord?

A

No big movements at most twitches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the overall role of the basal ganglia and cerebellum in motor control?

A
  • Monitor commands going down to muscles to make sure they are appropriate for the situation the person is in
  • If commands are inappropriate then they calculate correction signals which they send back up to motor cortex for approval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the role of the basal ganglia in motor control?

A

Acts as a feedback loop and sends info back to primary motor cortex
- Helps initiate and terminate movements and establish a normal level of muscle tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the role of the cerebellum in motor control?

A

Mainly feedback to motor cortex but can also send its error correcting signals straight down to the brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

When was the motor cortex discovered?

A

1870

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What happens when you stimulate the frontal lobe?

A

Movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How was the primary motor cortex discovered?

A

Different areas of the brain were electrically stimulated and ‘Brodmann’s area’ found to be the area that elected the most movement with the lowest intensity
- Primary motor cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Which parts of the body have the largest representation of control and why?

A

Hands fingers face - for fine movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the role of the upper motor neurones?

A

Carry motor commands down through the brain, brainstem and to the spinal cord
Involved in planning initiating and directing movements
Output to lower motor neurones via interneurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Where do upper motor neurones originate from?

A

Ancient motor centres of the brain stem

  • Vestibular nuclei
  • Superior colliculus
  • Recticular formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are the two types of upper motor neurone pathways?

A

Direct and indirect motor pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the direct motor pathway?

A

Input to lower motor neurones from axons extending directly from cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the indirect motor cortex?

A

Input to lower motor neurones from basal ganglia, cerebellum and cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the final common pathway?

A

Leads to muscle contraction from lower motor neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Where are the basal ganglia found?

A

Causate, putamen, substantia nigra, sub thalamic nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is Gilles de la Tourettes syndrome?

A

Causes twitching, face movements, uncontrolled swearing (rare) and unable to terminate movements
- Caused by problem with basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How does the cerebellum connect to the cortex?

A

via the thalamus and brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is required for muscle control?

A

Excitation of muscle by alpha - motor neurones
Continuous info from each muscle at each isntant
- Muscle length
- Muscle tension and rate of change of muscle tension development
- Lots of info relayed from these receptors to spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is the role of muscle spindles?

A

Send muscle length information to the spinal cord and cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are intrafusial and extrafusial fibres?

A

Intrafusial are inside the spindle and extrafusial are outside the spindle
Don’t actually contribute to muscle tension
Purely sensory role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are afferent fibres in the muscle spindles?

A

Wraps around equator of dynamic bag, static bag fibres and long and short chain fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the role of the gamma efferent motor neurons?

A

innervate bag fibres and short chain fibres innervate bag fibres and short chain fibres in order to change they length and mechanical properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Which terminal endings are wrapped around intrafusail muscle fibres?

A

Group Ia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is the role of group Ia terminal endings in muscle control?

A

Wrapped around the equator of both bag and nuclear chain intrafusial fibres
Pulling apart these cooked initiates an action potential on the axon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the different functions in group I and II terminal endings?

A

I - dynamic stretches - sensory endings relay information on the ‘dynamic’ phase of muscle stretch
ie. as stretch is occurring
II - Static stretches - sensory endings relay information on the static phase of muscle stretch
ie. its final length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Muscle spindles are only useful under tension, how is tension maintained?

A
  • Extrafusal fibres shorten around the spindles - loses tension
  • gamma motor neurones are coactivated with alpha motor neurones to ensure that the spindle shortens with the extrafusal fibres in order to maintain tension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Why does the brain need to fine tune its muscles?

A

Because there are 635 muscle - it would cause a sensory overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

How does the brain fine tune its muscle?

A
  • Serotonin increases gamma motor neurone activity ( action potential firing) - this causes intrafusal fibres can be slightly stiffer - stiffer materials transmit stretches with a greater fidelity
  • Noradrenaline decreases gamma motor neurone activity - causing intrafusal fibres to be more elastic and floppy - elastic materials don’t transmit stretches well
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the tendon jerk reflex?

A
  • Muscle stretched by hammer blow to its tendon
  • Primary sensory endings are activated and sends action potentials along the limb to the spinal cord
  • Muscle contracts in opposition to the stretch and the limb jerks as a consequence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is jendrassiks manoeuvre?

A

(putting hands together and pull)

  • causes excitation in upper segments of spinal cord
  • Excitation spills over to rest of spinal cord - causes leg twitch to increase as more motor units are involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the tonic vibration reflex?

A
  • Group II afferents fire at about 50Hz when arm is straight
  • Group III afferent fire at about 20Hz when fully flexed
  • Vibrator applied to tendon drives the group II afferents in muscle so they discharge at 100Hz
  • This makes the arm shorten as the brain must think it is really seethed as 50Hz is straight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is the stretch reflex?

A

Polysynaptic reflex

  • Spindle Ia makes excitatory connections on homonymous muscle (muscle the spindle is in) and are synergistic muscles (those that help the main muscle contraction)
  • Ia’s also act through inhibitory interneurones that innervate antagonistic muscles
  • When muscle is stretched the Ia firing rate increases
  • This cause contraction f the homonymous muscle and relaxation of antagonistic muscle
  • Reflex counteracts the stretch enhancing the springiness of the muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Where is the proprioreceptive info processed?

A

Spinal cord and somatosensory cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the central pathway in the somatosensory system known as?

A

Medial - lemniscal system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the steps in the dorsal medial lemniscal system?

A
  1. Central processes of dorsal root ganglia cells
    synapse on neurones in gracile and cuneate nuclei
    in lower medulla
  2. Axons from these nuclei ascend in medial
    lemniscus and synapse on neurones in ventral
    posterior lateral nucleus of thalamus
  3. Neurones of lateral nucleus send axons to
    primary somatosensory cortex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Where are the somatosensory cortices found?

A

Primary (s1)
The anterior parietal lobe and the posterior parietal cortex
Secondary (s11)
Deep within lateral sulcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What would happen if there was a lesion in somatosensory cortices?

A

Proprioceptive defects (ability to discriminate size, texture and shape)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the morphology of neurones designed to detect?

A

Food
Predators
Mates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is meant by the optic nerve being ‘information bottleneck’?

A

The optic nerve cat transmit all the information that is received by the retina as there is a limit to the thickness of it. So the retina also has to decide what is transmitted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is the main function o the retina?

A

Image acquisition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are the two main visual pathways?

A 
Ventral stream 
- V1 cortex to inferior temporal cortex
- Processes object identity
Dorsal stream 
- V1 cortex to posterior parietal
- Spatial location
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the role of the pupil in the eye?

A

Regulate the amount of light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the role of the lens in the eye?

A

Focuses image on fovea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the fovea?

A

Fovea is part of the retina with the highest visual acuity

- Rest of the retina has Lowe acuity and contains primarily rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What are muller cells?

A

Cells in the retina that light has to travel through before getting to the photoreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are horizontal and amacrine cells?

A

Interneurons between the layers of the retina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are the three layers of the retina?

A
  • Photoreceptors (rods and 3 types of cones)
  • Bipolar cells
  • Ganglion cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is the function of amacrine cells?

A

Inhibitory - inhibit bipolar cells and feed forward to ganglion cells - mostly gabaergic or gycinergic
Most diverse type of cell in retina (25 types) - showing importance of their function
Also have gap junctions between bipolar and ganglion cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is the function of the horizontal cells?

A

Inhibit photoreceptors nd feed forward to bipolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What kind of light do rod and cone cells receive?

A

Rod - dim

Cone - active and bright - colour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What is a difference instructor between rod and cone cells?

A

rod - more disc and molecules because they need to be stimulated by smaller amounts of light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

How does phototransduction occur?

A

In darkness
- Na+ and K+ channels open so the membrane is depolarised
- Activated by cGMP in the cytoplasm - keeping them open
In light
- ligand gated g coupled receptor is activated and the G protein breaks down into alpha and gamma subunits - activates phosphodiesterase - decreases cGMP in cytoplasm causing the Na+ K+ channel to close - hyper polarisation of photoreceptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is a ribbon synapse?

A

In retina

Constantly release glutamate - happens in darkness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Difference between on and off bipolar cells?

A

On cells - depolarise who light goes on them

Off cells - hyper polarise when light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Why do off bipolar cells hyper polarise in light?

A

Photoreceptors hyperpolarise in response to light so less glutamate and less activation of off bipolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Why do on bipolar cells depolarise in response to light?

A

They don’t express ionotropic glutamate receptors (channel) like off cells
They express metabotropic glutamate receptors which are g coupled receptors
When metabotropic receptors are activated cGMP drops down in cytoplasm closing Na+ K+ channel - Hyper polarisation
If less glutamate, less activation of metabotropic channels then depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What is the difference between ionotropic and metabotropic glutamate receptors?

A

Ionotropic
- Are channels
Metabotropic
- G coupled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is a receptive field in the retina?

A

An area of the retina which when illuminated activate a visual neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is centre - surrounded organisation of the receptive field?

A

Stimulation of the centre of bipolar cells leads to depolarisation and the stimulation of the periphery is of opposite polarity (hyper polarises)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Why does stimulation of the centre and periphery of bipolar cells lead to responses of opposite polarities?

A

When stimulate centre of receptive field, that photoreceptor hyper polarises. It is directly synapsed with the bipolar cell so that also hyper polarises
When stimulate the periphery, those photoreceptors hyper polarise but they are synapses with horizontal cells - these hyper polarise which steps the hypopolarisating of photoreceptor which depolarises bipolar cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

How does the centre surround organisation of the ganglion cells differ to that of bipolar cells?

A

Illumination of the whole receptive field does not activate ganglion cells it appears that ganglion cells are designed to respond to differences in illumination that occur within the receptive field

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What are the two classes of ganglion cells?

A

Paracellular - 80%

Magnocellular - 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Summerise the differences between paracellular and magnocellular ganglion cells?

A 
Paracellular 
- Smaller with smaller dendrites
- More densely packs 
- detect fine spatial details better
- smaller receptive fields
- Sustained response
- Detects form/colour
Magnocellular 
- Motion detection 
- High conduction velocity 
- More sensitive to light
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

How does the specific neuronal connectivity of the adult organism arise?

A

Two extreme hypothesis:
Weiss (1928) - Resonance theory - stochastic and diffuse neuronal outgrowth occurs to all targets followed by elimination of non functional connections
Sperry (1939) - Chemoaffinity hypothesis - Directed and specific outgrowth occurs through axons following “individual identification tags” carried by the “cells and fibers” of the embryo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What experiments evidence is there to prove Sperrys theories?

A

Sperry first did experiments in newts and then moved to frogs

  • he cut the optic nerve and removed the temporal retina (allow just nasal axons to grow back)
  • The axons grew back directly to the right place meaning sperry was right
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

How do we know that Weiss’s theory is incorrect by looking at embryos?

A

If Weiss were right, would expect to see random patterns of axons in embryos.
In fact see that patterns of axon outgrowth are highly organised, reproducible and stereotyped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Give some experimental evidence for axon guidance I chicks?

A
  • Early stage embryo
  • Cut and replace segment of neural tube before motor axons grow out
  • Despite displacement, motor axons still found way to their correct target
  • Suggests axon guidance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What are guidance cues?

A

Factors in the cells environment that axons use to find their correct target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What is Cajal’s growth cone?

A

The growing tip of the axon which Cajal proposed sensed cues in the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Why were insects used to identify locations of guidance cues?

A
  • Relatively simple nervous systems
  • Embryos easy to observe and manipulate
  • In the large insects, individual cells could be ablated using lasers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Why are grasshoppers in particular good to use as a model organism when investigating guidance cues?

A

Detailed analysis resulted I the identification of almost every neuron in the embryonic nerve cord allowing a map of axon predictions to be made

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

How was the theory that guidance cues could be found on axons tested?

A
  • Cells were ablated that were thought to be carrying potential cues
  • this caused the axon to stop at the axon where it would usually turn as the cue was not present
  • Shows evidence for growth cone and that axons can be directed in response to other axons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What is the labelled pathway hypothesis?

A
  • Axons can selectively fasciculate with other axons
  • Axon surface carry labels or cues
  • Different growth cones express different sets of receptors for such cues
  • Early axons (pioneers) form an axon scaffold on which later axons extend
  • Established axon surfaces as one potential source of guidance cues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Give evidence for axon scaffold in vertebrate

A
  • Ghosh and Shatz (1993)
    Visual cortex - Ablated sybplate neurones from one area and innervation of lateral geniculate nucleus failed in that area
  • Evidence for scaffold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

How do the pioneer axons find their way?

A

Growth cones appear to react at specific points
- For example, in the grasshopper embryo limb, the pioneer Ti1 (tibial1) growth cone makes a specific turn at the limb boundary, and then again as it approaches a specific cell, Cx1.
-Ablation of Cx1 causes the Ti1 growth cone to stall at the other side of the limb boundary.
- Neither Cx1 nor the limb boundary cells are distinguished by any obvious morphological features.
Cx1 and the other cells are sometimes referred to as ‘stepping stones’ or ‘guidepost cells’
Implies that there must be molecular differences in the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What are the three domains of the growth cone?

A

Central - Microtubules
Transitional - f actin
Peripheral - both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are lamella in growth cones?

A

In peripheral domain

  • The actin bundles are cross linked int a net
  • Highly motile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What are filopodia in growth cones?

A

In peripheral domain

  • The actin bundles are polarised to form larger bundles
  • Highly motile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What are f actin treadmills in a resting growth cone?

A

Tubulin is dragged sporadically into the filopodia

Happens much more dramatically when the growth cone comes into contact with an attractive cue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What happens when a growth cone comes into contact with an attractive cue?

A

They reorganise

  • F actin treadmilling slows and f actin accumulates
  • This stabilises the filopodium and drags microtubules into the back of the filopodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

How does actin treadmilling control filopodial extension?

A

When encountered a promoting cue

  • Molecular clutch is engaged and reward actin treadmilling slows - results in forward movement of the filopodium
  • Actomyosin based actin tubules link pulls microtubules into the wake of extending filopodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is required for forward movement of the filopodium?

A

Attachment of the growth cone to a substrate is not enough to drive forward movement, need stimulus of cue to rearrange cytoskeleton.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

How was it discovered that growth cones can be repelled as well as attracted?

A

Mixtures of neurone in culture were found to fasciculate only with their own kind
watching real growth cones showed that they were repulsed by each others axons and that contact led to their collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

How does the collapse of a growth cone occur?

A

Destabilises f actin - the opposite effect of an attractive cue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What experiment was shown to cause collapse of the growth cone?

A

Treatment whir EphB1 protein

  • Normally would have full growth cone collapse
  • Would have localised collapse of filopodia contributing to growth cone reorganisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What are semaphorins?

A

A family of inhibitory guidance cues

- Cause growth cones to turn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

How were semaphorins discovered?

A

Biochemical purification of the factor from the retina responsible for causing the collapse of sensory axons

178
Q

What firms can semaphorins come in?

A

Membrane bound

Secreted

179
Q

What are the four forces?

A

Contact attraction
Contact repulsion
Chemoattraction
Chemorepulsion

180
Q

What are permissive substrates?

A

Components that axons can attach and grow from

181
Q

What is the relationship between strength of adhesion and the amount of axon growth?

A

No simple relationship

e.g. collagen is better than laminin for adhesion but laminin is better than collagen for outgrowth

182
Q

Explain how laminin is permissive but not instructive

A

Laminin, a growth-promoting extracellular matrix protein, is localised in the optic nerve
Blockade of the receptors for laminin slows down the growth of retinal axons, but does not change their direction
Gradients of laminin in vitro do not direct axon growth.

183
Q

What are permissive and non permissive substrates also known as?

A

Permissive substrates - Contact attractants
Non permissive factors - contact repellents
Axon growth is a balance between permissive and non permissive factors

184
Q

What is the role of ephrins in axons guidance?

A

Non permissive factors used in early patterning and to guide axons - detected by receptor called ephs

185
Q

What is the role of ephrins in the mammalian embryo?

A

Ephs and ephrins cause repulsion between cells
Early on, this helps to compartmentalise the embryo into discrete domains
- used t keep axons out of specific places

186
Q

What is netrin?

A

A secreted protein similar to laminin which can associate with the extracellular matrix (in floor plate)
- Can turn commissural axons

187
Q

What happens to a axons once they have encountered targets?

A

They reprogram

- Lose responsiveness to netrins once crossed midline

188
Q

Why are lipophilic dyes useful when investigating axons?

A
  • Hydrophobic end
  • Can use them to trace axons, lineage and membrane trafficking
  • Dil is an example
189
Q

Give an example of how axons lose sensitivity to netrins during development?

A

Experiment
- On one side of the rodent hindbrain an ectopic floor plate is added so the commissural axons on that side sill have to cross it before the endogenous floor plate but other side doesn’t it
In the hindbrain
- axons exposed to ectopic floor plate before reaching midline turned
- Axons exposed to ectopic floor plate after crossing midline did not respond

190
Q

How do commissural axons respond to repellants after crossing the floor plate?

A

They become sensitive to them

  • Semaphotins and porteins called slit in the floor plate which repel them
  • Also expressed in spinal cord - creating a channel for axons to grow though
191
Q

How do growth cone sensitivities get reprogrammed?

A

As in the vertebrate floor plate, insect midline glial cells express diffusible attractants (netrins) and cell surface repellants (slits).
Levels of these determine

192
Q

How do levels of slit receptor determine whether axons can cross the midline?

A

Roundabout gene, Robo, encodes a receptor for the inhibitory protein Slit. Robo protein is expressed at high levels on axons that don’t cross the midline. Commissural axons initially express low levels but high levels after they cross.

193
Q

What gene is responsible for the inhibitory protein slit?

A

Roundabout gene, Robo

194
Q

What happens in Robo mutants and Comm mutants?

A

In Robo mutants (no Robo protein made), Slit is no longer detected, so all axons go back and forth across the midline forming Roundabouts of axons
When Comm protein is missing (Comm mutant), Robo protein is expressed at hi levels in those cells that would normally cross the midline, and which now extend their axons longitudinally

195
Q

What is Comm?

A

Comm is expressed only in those neurons that normally cross the midline and is switched off after they cross.

196
Q

Is Robo or Comm dominant?

A

If Comm’s expression is forced in all neurons, Robo protein is lost everywhere resulting in a phenotype just like the Robo mutant. ie Comm controls Robo

197
Q

How does Comm protein control Robo?

A

Comm encodes a “trafficking” protein that prevents Robo protein from reaching the cell surface so that the growth cone cannot receive Slit inhibitory signals before X-ing

198
Q

Are comm and Robo expressed in vertebrates?

A

There is no comm homolog
Robo homolog
- Robo1 - expressed before and after crossing midline
- Rig1 - expressed only in pre crossing fibres and appears to block Robo1 signalling until the midline is crossed

199
Q

What is controlling fasciculation?

A

How axons stay and get off the axons scaffold

  • Involves homophillic binding by cell adhesion molecules
  • e.g.. Fasciclin II
200
Q

What are homophillic interactions?

A

Homophilic (like binds to like) interactions can bind two cell surfaces together

201
Q

What do Fas II mutants show?

A

May defasciculated axons

202
Q

What does over expression of Fas II cause?

A

Novel fasciculations

203
Q

How cm axons get off the axon scaffold?

A

Interfere with adhesion by proteins that block
e.g. BEAT
Regulates FasII

204
Q

How do axons select their targets?

A
  • Discrete targets

- Topographic maps

205
Q

Give an experiment used to show axons look for discrete targets

A

In Grasshopper and Drosophila, ablation of specific target muscles (by ablation of muscle precursor cells) leads to failure of relevant motor axons to leave main motor trunk at appropriate branch points
Suggests that axons are “looking” for specific “labels” on their targets

206
Q

What happens if there is a loss of netrin in muscles?

A

the axons wander and do not make synapses (even though the muscle is there)

207
Q

What happens if there is ectopic netrin in muscles?

A

leads to axons innervating the wrong muscles

208
Q

What is Fas3?

A

The adhesion molecule Fas3 is expressed in specific muscles and in the motor axons that normally innervate them

209
Q

What happens when here is ectopic expression of Fas3?

A

leads Fas3-expressing axons to innervate new targets

210
Q

What was Sperrys theory regarding maintaining topology?

A

Neighbouring neurons send axons to neighbouring sites in their target to maintain the topology (order) in the target
Two possibilities how:
- Each axon has a unique label complementary to a unique label in the target
- That a co-ordinate system, encoded by gradients of signalling molecules, stamps a “latitude and longitude” onto cells of the target. This would be read by complementary gradients of receptors expressed in the retinal ganglion cells.

211
Q

Why do we need colour?

A

Helps in object recognition

212
Q

What are three types of cones?

A

Red
Green
Blue
Activate different types of bipolar cells

213
Q

Where are green and blue cones located and why?

A

Green - top
Blue - bottom
Light from the top (blue sky) activates bottom of the retina and light from bottom (green grass) activates the top

214
Q

What is the function of the superior colliculus?

A

Regulation of saccadic movements
Receives inputs from ganglion cells, auditory
system, somatosensory system
Integrates information from different sensory modalities

215
Q

What is a retinotopic map?

A

organisation whereby neighboring cells in the retina feed information to neighboring places in their target structures (LGN, SC, cortex)

216
Q

What type of organisation do command neurones have?

A

Retinotopic organisation

217
Q

What is the role of the lateral geniculate nucleus?

A

LGN preprocesses the visual information

218
Q

Give characteristics of lateral geniculate nucleus

A

6 layers
Monocular input
Layers alternate input from each eye
P and M ganglion cells remain segregated
Organised retinotopically
Ganglion cell axons make 1:1 connections with LGN projection neurons

219
Q

What are the receptive fields of LGN like?

A

Receptive fields of LGN neurons are similar to the receptive fields of retinal ganglion cells

220
Q

What Is the role of local interneurons in the LGN?

A

Important to process retina information

221
Q

Outline an experiment into the understanding of object recognition

A

Subject looks at an image of a particular object.
Few neurons in higher cortical areas fire
Stimulation of the same neurons causes perception of the same object

222
Q

What does object recognition allow us to do?

A

Recognise objects in an orientation not seen before
Recognise no matter what size
Effortless recognition of previously unseen objects

223
Q

What is the hierarchical model of object recognition?

A

Detection of edges –> Detection of combination of edges and contours –> Detection of object parts —> Detection of objects from one point of view —> View invariant object detection –> categorisation
Each level is reached as the complexity of the stimulus increases

224
Q

What is the reality of brain processing for object recognition?

A

Increase in complexity of responses of neurons along the ventral stream
Increase in the receptive field size of neurons along the ventral

225
Q

What are the two key features of the cortical structure?

A
  • Layering

- Columns (ocular dominance, orientation, direction and blobs)

226
Q

How do the different layers in the cortex receive inputs?

A

Different layers receive inputs from different parts of the brain
Interneurons process this information - input between layers in the same cortex

227
Q

What are the three types of columns in the cortex?

A

Ocular dominance column
Orientation (direction) columns
Blobs (colour)

228
Q

Give a study into ocular dominance columns

A

Inject radioactive glucose in cortex and stimulate one eye with light
Shows that each column receives inputs from either ipsilateral or contralateral eye

229
Q

What is a hypercolumn?

A

When all three types of columns come together

230
Q

What are the three types of cells in the cortex?

A

Simple
Complex
Hypercomplex

231
Q

Who was responsible for the discovering the cells in the cortex?

A

Hubel snd Weissel

232
Q

Outline the response on simple cells to Hubel and Weissels experiment

A

When shined a light on centre of the receptive field - cells respond
Surrounding cells - respond on the dark - showing it has an inhibitory surround
- Change orientation of the bar and no response
- They concluded that ganglion cells were in a line down the middle

233
Q

Outline the response on complex cells to Hubel and Weissels experiment

A

Differs from simple cell because responds to bar of light anywhere in the receptive field
Changes the orientation of the bar - cell doesn’t respond

234
Q

Outline the response on hypercomplex to Hubel and Weissels experiment

A

Repsonds to bar of light anywhere in receptive field
If part of the bar is not over the receptive field then no response
If change the orientation of the part of the bar not over the receptive field then spikes again

235
Q

Receptive fields downstream from V1 are complex so difficult to study, what methods are used?

A

Guessing

Computational models

236
Q

How are computational models used to study receptive fields?

A 
Record from a visual neuron
Apply thousands of images
Identify those that evoked spikes
Average them
or
Build a computational model that predicts responses to all of the images
237
Q

How is guessing used to study receptive fields?

A

Generate many images with defined geometrical properties (size, orientation, curvature, spatial frequency etc.)
Define orientation-, curvature-, frequency sensitivity
or
Make an educated guess of what should visual neuron respond to

238
Q

What does probing the receptive fields in V2 show?

A

That cells in V2 cortex reposted to more complex stimuli then V1 - gets more complex

239
Q

Give an experiment where face sensitive neurones in the temporal lobe are investigated?

A

Full face - cells respond
Partial face - not as many cells raspond
When characteristic features of a face are removed (e.g.. eyes, mouth, face shape) neurones don’t respond
- Neurones dont respond steadily - start to adapt

240
Q

What is the Jennifer anniston neurone?

A

A specific neurone is fired when saw pictures of Jennifer anniston
- Could be at any scale and orientation - same response
Didn’t with other neurones

241
Q

What are the main methods used to study vision?

A

Psychophysical methods and illusions
Lesions and other ways to silence neurons or parts of the brain
Anatomical studies and morphology (to study connections between neurons)
fMRI, electrophysiological recordings and imaging
Modeling and theoretical simulations

242
Q

What model organisms do you use to study vision and what are the pros/cons of using them?

A

Humans - ethics, can get verbal feedback
Primates - ethics, similar model to humans
Lower mammals (cats, rodents) - Key organisation of the brain is the same
Lower vertebrates (zebrafish) - Brain different to humans, transparent embryo
Invertebrates (Drosophila) - not good to compare to humans

243
Q

What is an example of the psychophysical experiment to study vision?

A

Investigate adaptation

  • Illusions with colour
  • Three pictures - George Bush and Barak Oboma
244
Q

How do you investigate where vision is processed in the brain?

A
  • Lesions - removing part of the brain and look at the damage or new behaviour
  • Whole brain imaging techniques -
  • Multi-electrode recordings in different brain areas
245
Q

What types of lesions can be used to study vision?

A

Directed (animal models) - can’t get feedback from them

After strokes and other neurodegenerative diseases

246
Q

What is fMRI?

A

Functional magnetic resonance imaging

247
Q

How is fMRI used to study the brain?

A

Active neurones use a lot of oxygen and glucose - you can then see which parts of the brain uses these using functional magnetic resonance imaging

  • Get a human subject and look at the images of the brain when looking at moving lights and stationary lights
  • Can see cortex is much more active in movement showing its importance in perceiving motion
248
Q

What methods in morphological studies can be used to study vision?

A

Fluorescence proteins
- Drive the expression of proteins in specific neurone subtypes so difference can be highlighted
Viruses
- Label one cell and pre synaptic neurones - can look at the circuitry - as the viruses will pass through the synapse as well

249
Q

What is an advantage of using electrophysiological recordings to study vision?

A

Can be used in vivo

- Meaning it will have a sensory input as slices that have been cut out will have lost its innervation

250
Q

Electrophysiological recordings can be used to study what kind of specimens?

A

In vivo
Slices
Cultured neurones (only for molecular mechanisms)

251
Q

Give an example of a modern morphological study?

A

Enhancer traps

252
Q

How do you validate an experiment?

A

Record activity of cell and neurones

Image the activity of a large population of neurones simultaneously

253
Q

How do you validate experimentally by recording?

A

Patch clamp method

254
Q

How do you validate experimentally by imaging?

A

GCaMP3

  • Reports changes in neuronal calcium activity and therefore neuronal activity
  • Brightness occurs when Intracellular Ca2+ is high
  • By observing changes in brightness you can there foe feel when the neurone is active and how much is active
255
Q

What are the advantages of validating experimentally by imaging?

A

Recording the activity of many neurons
Can record simultaneously the input and the output of a particular neuron (circuit reconstruction)
One can easily target particular neuronal types(e.g. Glu-ergic and GABA-ergic)

256
Q

What are the disadvantages of validating experimentally by imaging?

A

Cant image as fast as electrophysiology

- Cant detect high frequency spikes

257
Q

What is channelrhodopsin?

A
  • Opens when yellow light
  • Na+ enters
  • Depolarisation of neurone occurs - spikes
258
Q

What is halorhodopsin?

A
  • Cl- channel
  • Hyperpolarises with yellow light - doesn’t spike
  • Depolarised with blue light - spikes
259
Q

What is retinitis pigementosa?

A

Most abundant cause of blindness

  • No treatments
  • Caused by death of photoreceptors
260
Q

How can you attempt to treat retinitis pigementosa and what are the problems?

A

Try to use an artificial retina

  • But what part of the brain needs to be active as there are no photoreceptors
  • What method would you use to activate it
261
Q

Which parts of the brain would you stimulate to try and treat retinitis pigemtosa?

A 
Retina (mostly for retinitis pigmentosa)
Visual cortex (when the optic nerve didn’t develop or is destroyed)
262
Q

Why is it important to activate as early (anatomically) as possible in the visual pathway when treating retinitis pigmentosa?

A

Retina performs complex computations
Different ganglion cells have different functions and project to different brain areas
Stimulation of retinal ganglion cells with simple stimuli is useless (e.g. motion sensitive RGC is active only when there is motion)

263
Q

How could the you activate the retina cells in a patient with retinitis pigmentosa?

A
  • Electrical stimulation

- Channel rhodopsin and halorhodopsin

264
Q

What is the problem with activating an artificial retina?

A

Accessing bipolar cells or photoreceptors is difficult because ganglion layer is above so only accessible by electrode

265
Q

What are neurotrophins?

A

A family of growth factors in the nervous system

266
Q

Give an experiment conducted by Viktor Hamburger into neurotrophins?

A

Remove or add limb buds in chick embryo

- More/less innervation so more/less dorsal root ganglion neurones surviving

267
Q

What is meant by having limbs having trophic effect?

A

Implies that limbs being innervated is giving an advantage for the organisms survival

268
Q

What is the difference between tropism and trophism?

A

Trophism - relating to food or nutrition

Tropism - Meaning turning

269
Q

What experiment into neurotrophins was conducted by Bueker in 1948?

A

He reasoned that fast growing muscle like cells might secrete survival factors (limb buds are fast growing)

  • He therefore implanted sarcomas (tumours) into embryos
  • It caused an increase in the size of dorsal root ganglion
  • Provoked selective survival of non placodal sensory and sympathetic neurones
270
Q

What followed Beukers experiment into neurotropins?

A

Demonstrated presence of diffusible growth factor

  • Purified from snakes venom and mouse submaxillary gland
  • Found antibodies to the purified growth factor that could block dorsal root ganglion growth in vivo and in vitro
271
Q

What is the structure of the nerve growth factor (NGF)?

A 
Activated from submaxillary gland
Has subunits 
- alpha, beta, gamma
Beta subunit
- Dimer 
- Active component 
- alpha and gamma subunits only found in submax - storage
272
Q

Give an experiment demonstrating how NGF’s work?

A

In a partition chamber

  • DRG in centre - nerves grow out into outside chambers if NGF present in any chamber
  • If NGF only present in centre compartment then no outgrow
  • If NGF taken away from the axons that have outgrown then they die
273
Q

Give evidence for NGFs being tropic and trophic?

A

Responsible for survival of axons - when taken away from experiment they die
Can also guide axons in vitro

274
Q

What receptors for NGF’s are there?

A 
TrkA 
- high affinity 
- it is a classic RTK (kinase)
- they dimerise and phosphorylate 
- affects differentiation and growth
P75 - NTR 
- low affinity 
- Promote cell death
275
Q

Why is it difficult to identify another NGF in the nervous system?

A

Because there are low levels of them in the nervous system

276
Q

What is the role of p75 in NGF’s?

A

Control whether or not cell death is occurring

277
Q

Do all neurone types exhibit the same level of dependancy on neurotrophins?

A

No

  • Placodal sensory ganglia e.g. nodose prefer BDNF over NT-3
  • Crest- derived DRGs have subpopulations that respond to NGF, BDNF or NT3
  • Sympathetics respond to NGF or NT3 but not BDNF
278
Q

Is neurone dependancy on neurotrophins affected by time?

A

Yes neurones may have no dependancy

279
Q

What is the role of NT3 in early development?

A

NT3 can support many neurone types early in development eg. on the way to targets
Arrival at the target often coincides with new expression of neurotropin by target

280
Q

What do trigeminal neurones need during their development?

A

need BDNF and NT3 early
then NGF
then NGF or MSP

281
Q

In animals that don’t have neurotophins, what do they have instead?

A 
Dropsophilla and c.elegans 
- Other families
Glia - derived neurotrophic factors
e.g. GDNF supports midbrain dopaminergic neurons
- Cytokines
e.g. ciliary neurotrophic factor CNTF
hepatocyte GF
macrophage-stimulating protein (MSP)
- Testosterone effects on motorneuron pools accounting for sex differences
282
Q

Give an example of how neurotrophins effect dendritic morphology and connectivity?

A

Motor neurones innervating the triceps and pectoral muscles develop monosynaptic connections directly with PNS, whereas motor neurones innervating the cutaneous maximus (CM) and latissimus dorsi (LD) receive polysynaptic input from interneurons (IN).
Controlled by a neurotrophin secreted from CM and LD, which turns on the transcription factor (TF) Pea3 in the MNs.

283
Q

What percentage of neurones are lost during development?

A

50%

284
Q

Where does death occur in the developing nervous system?

A

Everywhere in the nervous system

285
Q

Why can death occur even though tissue size is increasing?

A

Because neurones are refining

- Relationship between the size of the target and how many neurones are required

286
Q

Give some examples of cell death in the developing nervous system

A 
Somatosensory barrels
- whiskers on rodents
- In CNS cortex - refined
Auditory system
- refined
- doesn't follow the correlation of size and neurones required - shows that other inputs are involved
287
Q

How does cell death in the developing nervous system occur?

A

Apoptosis - programmed cell death

288
Q

How do we know that apoptosis is an active process?

A

It is inhibited by actinomycin D or cycloheximide

289
Q

How are cells which have undergone apoptosis cleaned up?

A

Macrophages

290
Q

What is the intrinsic pathway (within a cell) for apoptosis?

A

DNA damage and p53 activation (tumour suppressor) —> Activation of mitochondria/ cytochrome c —-> activates initiator caspase 9 —> Effector cascade 3 —-> Apoptosis

291
Q

What is the extrinsic pathway for apoptosis?

A

Death ligands —> activates death receptors —> activated initiator caspase 8 —> Effector cascade 3 —-> Apoptosis

292
Q

What can pro and anti apoptotic signals do?

A

Enter the apoptosis pathway and activate apoptosis

Balance of the signals determine whether a cell lives or dies

293
Q

Give an example an experiment into pro and anti apoptotic signals

A

C.elegans

  • Knockout of Ced3 and Ced4
  • Cells lived that weren’t suppose to
  • Showing these pro apoptotic signals are required for cell death
294
Q

What is the mammalian homologue for the anti apoptotic gene ced 9?

A

bcl-2

295
Q

What was the idea of what promotes neurones survival?

A

That the target secretes a neurotrophic factor rewind for the presynaptic neurone to survive

296
Q

How did NGF deprivation prove evidence for neurotrophins involvement in neurone survival in the developing nervous system?

A

Nerve growth factor (NGF - a type of neurotrophin)

  • Deprived from sympathetic ganglion neurone in vitro
  • SGNs have p75NTR, TRKA receptors
  • Blocking NGF triggered apoptosis as the receptor for NGF is TRKA which is present
  • Also shown in knockout mice in vivo
297
Q

How can the withdrawal of NGF be rescued?

A

Adding anti-p75NTR blockers
- p75NTR is the other receptor present on the sympathetic nerve ganglion so even though TRKA isn’t activated by NGF, the other receptor stops the trigger of apoptosis

298
Q

What is the role of neurotrophins in deciding an axons survival?

A

They provide pro and anti apoptotic signals

- An individual neurone needs both the correct neurotrophins and the absence of the wrong neurotrophins to survive

299
Q

What are the roles of proneurotrophins in the control of cell death?

A

Pro NGF strongly activates p75NTR receptor which leads to apoptosis
- Levels of enzymes that cleave proneurotrophins are important - growth cones can release these enzymes

300
Q

How is brain derived neurotrophic factor (BDNF) released?

A

ProBDNF is synthesis

  • binds to carboxypeptide E
  • Leads to secretion - triggered by depolarisation or ligand binding
  • Cleaved to make proper form and release to axons
301
Q

How are the axons in a neuromuscular junction refined?

A

Want to end with one axon innervating one muscle fibre but start with much more

  • muscle fibre produces proBDNF which acts as a repellant
  • the ‘winner’ axon converts proBDNF into BDNF allowing it to survive
  • the ‘loser’ axon does not convert it - triggers retraction - if no other neuromuscular junction then apoptosis is triggered
302
Q

How is synapse formation competitive?

A

Not all neurones make synapses - outcompeted

Synapse formation can dictate neuronal or target surivial

303
Q

What is need to make a functional synapse?

A

Correct receptor being expressed
Synapse at the correct location
Correct part of the membrane to differentiate unto synapse
Receptors to make the target the tissue
The correct number of synapses made this can vary from 1 to 10000 per neuron

304
Q

Outline synaptogensis at a neuromuscular junction

A

Motor axon differentiates to motor nerve terminal at contact point
Contact point is dictated by gap junctions made by Schwann cells - redistricts where the junction can occur
Muscle forms the post - synaptic apparatus

305
Q

What morphological changes occur in synaptogensis in the spherical bushy cell (SBC)?

A
  • Small vesicles at presynaptic membrane
  • Narrow cleft between pre and post synaptic membranes - fill with special proteins
  • Post synaptic membrane apparels thickened
306
Q

What are the problems with the experiment conducting testing the morphological changes in synaptogensis in the spherical bushy cell (SBC)?

A

It was in vivo - so cant see what happens at the very early stages

307
Q

What morphological changes occur when a growth cone twins into a pre synapse?

A
  • Filopodia retraction - tight junction formation
  • Membrane and cell gycloproteins are added
  • Presynaptic vesicles, dense ECM and receptors accumulate at the cleft
308
Q

When does synaptogensis occur?

A

When axons reach targets - highly variable

309
Q

Give an example of when synaptogensis occurs?

A

Cat visual cortex

- Synapse density increased for one month after birth

310
Q

What dictates where synaptic sites are?

A

Site availability may be restricted
- Astrocytes may cover cell body but dendrites are free
Post synaptic cells may have pre-prepared sites

311
Q

How do synapse stick together?

A

Adhesion proteins

- Immunoglobulin domains that stick them together

312
Q

How does receptor clustering occur in synaptogensis?

A

e.g.
Initially ACh receptors are present at moderate levels on myotubule surface
Innervated by AChRs cluster in post synaptic membrane
The clustering involves both redistribution of AChR proteins and localised synaptic synthesis of AChRs
Aggregation of neurotransmitter receptors is the principle feature of synaptogensis

313
Q

What other receptors cluster during in synaptogensis?

A

Glycine, GABA, Glutamate

314
Q

Give an experiment studying what evokes clustering of receptors in synaptogensis

A

Denatured and destroyed muscle to break neuromuscular junctions

  • MMuscles regenerate and clustering occurs again
  • Must be something in the basal lamina causing this
  • The proteoglycan Agrin was discovered
315
Q

What protein is responsible for receptor clustering in synaptogensis?

A

Agrin

316
Q

Where is Agrin made?

A

Made in nerves and moves to basal lamia

317
Q

What is the mechanism of action for Agrin?

A

Z+ agrin is released from the axon - has a high affinity for MuSK (a kinase)

  • Agrin binds to MuSK protein and signals Raspyn
  • Raspy clusters which have Ach receptors - end up with lots of Act receptors clustered
318
Q

What occurs in MuSK knockout mice?

A

They are insensitive to agrin

319
Q

How does the shape of the post synaptic apparatus change after maturation?

A

Junction changes from a simple oval plaque to a pretzel like set of branches

320
Q

How does the topography of the post synaptic apparatus change after maturation?

A

Junctional membrane changes from a flat sheet to invaginated surface with gutters and folds - receptors cluster at the top

321
Q

How does the extracellular membrane of the post synaptic apparatus change after maturation?

A

Changes to basal lamina over the ACh rich

membrane and cytoskeleton under it

322
Q

How does the channel function of the post synaptic apparatus change after maturation?

A

Composition of AchR subunit changes

323
Q

How does the molecular partitioning of the post synaptic apparatus change after maturation?

A

Ion and ligand gated channels segregate into discrete alternating domains

324
Q

How does presynaptic division occur?

A

The growth cone has the receptors and the cell the ligands
- Growth cone - frizzled receptors
- Granule cells - express Wnt7a
Contact recruits vesicles and synaptic proteins to form presynaptic site

325
Q

Explain climbing fibre loss as an example of refinement

A

Initially interact with lots of cells which is refined
Ina. mature cerebellum there is 1 climbing fibre per purine cell
In development, typically up to 4 climbing fibres per day

326
Q

How does refinement occur in synaptogensis?

A

Synapse refinement is required to ensure the right number of synapses and that they are focused
Connection focusing
- Immature inputs are not segregated
- eg. Reorganise so cortex receives info from different parts
Transmitter choice
- Choice may be due to environment
- Not all hard wired in

327
Q

How do excitatory synapses use activity to build a synapse?

A

Acquisition of presynaptic release machinery and postsynaptic NMDA receptors
If no additional input, they remain silent because they lack sufficient AMPA receptors
Activity recruits AMPA to activate synaptic activity

328
Q

What are the types of memory?

A

Declarative (facts/events) and non declarative (unconsciously)
Long and short term

329
Q

What neurotransmitters are present in presynaptic neurone for memory?

A

Excitatory - glutamate - leads to depolarisation

Inhibitory - GABA - hyperpolarisation

330
Q

How can the sensitivity of the a synapse involved in memory be regulated?

A
  • Regulated of voltage gated Ca2+ channel - activation released neurotransmitters
  • Position of Ca2+ channels - closer it is to the vesicle containing neurotransmitters, the less depolarisation required for its release
331
Q

What is the role of syntax, SNAP25 and synaptobrevin in memory in simple organisms?

A

They interact with each other and drive the synaptic vesicle to its release - releasing neurotransmitters

332
Q

What is the role of synaptotagmin in memory synapses?

A

Calcium sensor

  • without it the channel wouldn’t be calcium dependant
  • Some require different concentration of calcium to activate it - change its sensitivity
333
Q

What are the three types of vesicles in the presynaptic bouton?

A

Readily releasable poll - close to the membrane
Proximal pool - substitute readily
Reserve pool - resting pool

334
Q

How can the types of vesicles available in the presynaptic vesicle lead to a type of plasticity?

A

The speed of release for readily releasable is quick but speed of conversion of proximal pool to readily releasable is slower - there will be a tie when no vesicles are ready to be released - lose sensitivity

335
Q

What are the three types of glutamate receptors involved in post synaptic density in memory synapses?

A

NMDA receptor
AMPAR - Non NMDA receptor
mGlut receptor

336
Q

What is the mechanism of action of mGlut receptors?

A

Bound to G protein - activation activates adenylate cyclase - phospholipase C - involved in increasing Ca2+ in cytoplasm

337
Q

What is the mechanism of action of AMPAR receptors?

A

Na+ channel

- Bind glutamate - Na+ influx - depolarisation

338
Q

What is the mechanism of action of NMDAR receptors?

A

Selective for Ca2+
- Has a Mg2+ bound to the pore region - needs to depolarise membrane to move it - just binding of glutamate is not sufficient

339
Q

What are the advantages of studying memory in invertebrates?

A

Large neurones
Circuit complexity
Temperature- dependance
Genetically mapped

340
Q

What are the two forms of simple memory?

A

Habituation - Responds less after repeat stimuli

Sensitisation - Nervous system responds to stimulus more and more

341
Q

Give some examples of habituation in humans?

A

Habituation of eye blink reflex

Habituation of relative non harmful stimulus - e.g. living on a busy road

342
Q

What Is the gill and siphon reflex?

A

Reflex in aplysia - snails
2 organs - Responsible for withdrawal reflex requires 2 neurones - sensory neurone activated with touching the siphon - glutamate - motor neurone contraction to remove

343
Q

How was the cellular basis of habituation researched in aplysia and the gill siphon reflex?

A

Test which neurone becomes desensitised by recording from each neurone

  • From sensory neurone - same response overtime - terminals are not desensitised
  • Record from motor neurone - same
  • Record from both and you can see response getting smaller with repeated stimulus
  • Concluded that it is the synapse that desensitises
344
Q

Why does the response get smaller in habituation?

A

Synapse desensitises

- Less than 50% of neurotransmitters are released

345
Q

How can sensitisation lead to increased gill withdrawal reflex?

A

Addition of painful stimulus just after

  • Sensory neurone activated by touching siphon
  • L29 neurone stimulated by a shock
  • L29 activation leads to the release of serotonin - activates receptors and G proteins - adenylate cyclase converts ATP and CAMP - activates protein kinase A which inactivated K+ channels in synapse
  • Prolongs depolarisation - more vesicles released during one depolarisation
  • Bigger contraction of muscle
  • Sensitisation
346
Q

How can aplysia show pavlovian conditioning?

A

Weak siphon touch paired with strong shock

  • Paired stimulus - withdrawal reflex is very large - lasts long
  • Timing is critical
347
Q

What is the simple bear model?

A

Ca2+ influx due to depolarisation

Serotonin release

348
Q

What was the key message shown from the Lymnaea - Kemenes 2006 research paper?

A

In addition to synaptic plasticity, other mechanisms can directly involve the synapse

349
Q

What was the experimental model for the Lymnaea - Kemenes 2006 research paper?

A
  • Single trail associative learning
  • Present attractive feeding stimulus stimulus (sucrose) - snails will eat it because its sweet
  • Also a neutral stimulus present (amyl acetate)
  • Pair them
  • Then snail shows feeding behaviour to amyl acetate alone - association
350
Q

What is the role of serotonergic cerebral giant cells?

A

Serotonergic cerebral giant cells contact many cell types and permit feeding but not involved in feeding behaviour - if it fires feeding is possible if It doesn’t its not

351
Q

How does association of the two stimulus occur in the Lymnaea - Kemenes 2006 research paper?

A

24 hours after the trial the resting potential of the serotonegic cerebral giant cells had raised by 10mv

  • Only change seen
  • The depolarisation lasted for weeks
  • Depolarisation occurs after the behavioural change
352
Q

What were the conclusions of the Lymnaea - Kemenes 2006 research paper?

A

Depolarisation needed for long term memory but not short term
Long term memory at least partially encoded at a site distant to the neurones

353
Q

How could we test that depolarisation is necessary and sufficient for memory?

A

Necessary: Hyperpolarise neurones and train the animals
Sufficient: Depolarise neurones on untrained animals
Results showed it was sufficient

354
Q

What are the three types of neurones found in the hippocampus?

A

Dentate gyrus
CA1
CA3

355
Q

What synapse in the hippocampus was studied for long term potentiation?

A

CA1 and CA3 synapse

356
Q

What does tetanic stimulation of CA3 neurone in a CA1 CA3 synapse lead to?

A

High frequency stimulation - causes summation of EPSP’s

Causes long term potentiation

357
Q

What is the main input to the hippocampus?

A

The entorhinal cortex

358
Q

What neurone produces the longest lasting potentiation in the hippocampus after stimulation?

A

CA3

359
Q

How is associative memory formed?

A

Two pathways converging on the same target can both be strengthened if they fire together as long as membrane is depolarised

360
Q

Is tetanic stimulation required for long term potentiation?

A

No stimulus just needs to depolarise the membrane

361
Q

Does long term potentiation occur pre or post synaptically?

A

Evidence suggests post

362
Q

What are the two glutamate receptors involved in long term potentiation?

A

AMPA - depolarise post synaptic neurone

NMDA - Selective for Ca2+

363
Q

Give the main characteristic of on NMDA receptor?

A

Mg2+ ion binds to the pore of the receptor and blocks the channel from glutamate
In order to remove glutamate, the membrane of the post synaptic neurone must be depolarised
This is a key mechanism for long term potentiation

364
Q

Give the mechanism of removal of the Mg2+ block on NMDA receptors?

A

Tetanic stimulation —> glutamate release —> AMPA receptor activation —> Depolarisation —> Mg2+ removal —> NMDA activation

365
Q

What are the two stages of long term potentiation?

A

Early - Does not require protein synthesis

Late - requires protein synthesis

366
Q

Give the mechanism of early phase long term potentiation

A

NMDAR mediated

  • Ca2+ released and activated calmodulin kinase II - CaM
  • NMDA receptor is opened and autophosphorylated so that it remains open even after Ca2+ is gone
  • Prolongs the activity of calmodulin kinase II
367
Q

Give an experiment investigating how phosphorylation of NMDA receptors enhance AMPA currents

A

Apply glutamate for short term and wash it out
Trigger long term potentiation
Apply glutamate again
Saw that AMPA currents increases

368
Q

What is the advantage and disadvantage of using inhibitors to research enzymes involved in long term potentiation?

A
  • They allow the animal to develop properly first and then add them
  • Not 100% specific - usually inactivate something else as well
369
Q

What is the advantage and disadvantage of using knockout mice to research enzymes involved in long term potentiation?

A

Specific

Don’t develop properly as effected many processes

370
Q

What are the two ways to increase the activity of AMPA receptors?

A
  • Change the open probability of the AMPA receptors - open more
  • May involve amplification - increased number of AMPA receptors on the post synaptic site
371
Q

When does late phase long term potentiation occur?

A

1 hour after stimulation

372
Q

What is the role of cAMP signalling in late phase long term potentiation?

A

Important in the regulation of gene expression

  • Activates protein CREB-2 (calcium response element) - blocks expression of gene
  • CREB1- Replaces CREB 2 and activates gene expression and is phosphorylated by protein kinase A
373
Q

What is the key mechanism of late phase long term potentiation?

A

Glutamate activates AMPA
Depolarises post synaptic membrane
Removes Mg2+ block
Ca2+ moves in through NDMA
Activates calcium calmodulin
Activates adenylate cyclase and calcium calmodulin kinase
Activates protein kinase A - gene expression —> proteins go to synapse
Calmodulin kinase 2 phosphorylates AMPA receptors –> increased numbers due to exocytosis

374
Q

How would you test if long term potentiation is memory?

A

Behavioural test

  • Animal model had to learn something
  • Then inhibit LTP by inhibiting NDMA receptor
  • Check if animals memorise less
  • Inject inhibitor in hippocampus
  • Could also over express something required in LTP and see if animals learn better
375
Q

What are the problems with studying long term potentiation?

A

There are different types of synapses - some don’t use NMDA receptors, some don’t use CamK11
- LTP varies in non hippocampal areas

376
Q

Give an experiment linking LTP to memory

A

Hidden platform in water for mice - First time they look for it, second time they know where it is
Use knockout mice of CaMKII or NMDA receptors - cant find it as quick

377
Q

Is long term potentiation sufficient for memory formation?

A

No

It is only necessary for some memory formation

378
Q

What is long term depression?

A

Active evoked long-lasting reduction in synaptic efficacy

379
Q

What are the two main types of long term depression?

A 
Depotentiation
- Removal of previous potentiation 
- Reversal of long term potentiation 
Long term depression de novo
- No previous potentiation
380
Q

What are the general mechanisms for long term depression?

A
  • Often requires NMDA receptors but not always
  • Often evoked by low frequency stimulation but not always
  • Often requires Ca2+ influx and activation of serine, threonine phosphotases
  • Often involves glutamate but also diffusible transmitters eg. 5-HT
381
Q

Explain the connections in the cerebellum

A

The cerebellum receives in pt from two fibres

  • Mossy fibres - synapse with granula cells
  • climbing fibres which synapse with one purkinje cell
382
Q

Why is there a strong depolarisation in the cerebellum?

A

Because there are many synapses to one purkinje cell

- Main output of cerebellum is purkinje cell

383
Q

Explain what happens when you stimulate a climbing fibre and parallel fire together?

A

If stimulate just parallel - ESPS

If stimulate both - the amplitude of ESPS in purkinje cells is much smaller - Long term depression

384
Q

What is the Albus Marr model?

A

Climbing fibre input indicates a motor error and therefore weakens the parallel fibres so synapse between parallel fibre and purkinje cell is weakened

385
Q

What receptors are involved in cerebellar long term depression mechanisms?

A

metabotropic glutamate receptors and voltage gated Ca2+ channels are involved

386
Q

What is the mechanism of cerebellar long term depression?

A

Climbing fibres activated - release glutamate depolarisation of purkinje cells - activation of post synaptic Ca2+ cells - Ca2+ influx
Parallel fibres activated - GPCR cascade activated phospholipase C - DAG - activates protein kinase C
The two pathways interact with each other - increases protein kinase C more
Protein kinase C then phosphorylates AMPA receptor on a different side to the LTP
Leads to endocytosis of AMPA and reduction in AMPA receptor current

387
Q

How is hippocampal long term depression thought to occur?

A

If the synapse of the cell is active but the rest of the cell is not depolarised then it becomes weakened

388
Q

What decides whether long term depression or long term potentiation is going to occur in the hippocampus?

A

The degree of NMDA receptor activation
If activated a small amount then LTD and if more than LTP
- because LTD has mainly phosphatsaes which are triggered by NMDA receptors response to a small increase in Ca2+
- LTP has mainly kinases - large increases of Ca2+ lead to more kinases to increase AMPA efficacy

389
Q

Give an experiment investigating whether long term potentiation and depression are memory?

A

On group of marmosets are in enriched environments and another not

  • Looked at morphology of neurones
  • Counted numbers and density of post synaptic boutons
  • Increased number of dendritic spines
  • Not only change strength of synapses but change shape and number of them too
  • So memory is not just LTD and LTP but it is involved
390
Q

What is the difference between anterograde and retrograde amnesia?

A

Retrograde - previous memories not intact

Anterograde - inability to form new memories

391
Q

What is needed to transmit signals?

A 
Transmitters eg. glutamate or GABA
Receptors
ECM - 'glues' synapse
other neurones 
Glial cells - control the extracellular environment eg.ion concentrations
392
Q

Why is a negative membrane potential required? for action potential?

A

So that Na+ channels can open when membrane potential increases and to keep them closed when needed

393
Q

What is required for a resting membrane potential to be generated?

A

Pumps/transporters - to regulate ionic gradients
Na+, Ca2+ channels - depolarisation
K+ channels - to terminate action potential

394
Q

How can the complexity of neurones excitability vary?

A

By changing what channels and transporters are present in the membrane of the neurone

395
Q

How can the resting potential of neurones change during development?

A

By changing the channels present in the membrane
Also by glial cells
- Astrocytes increase causing extracellular [K+]to decrease from 35mM to 3mM

396
Q

Does the ability for a neurone to produce an action potential occur at the same time during development?

A

No action potentials are seen early as well as neurones. develop at different stages

397
Q

What is input resistance?

A

The measure of the ability of the cells for current to flow across the membrane - can be changed due to channels being inserted into the membrane

398
Q

What is the membrane time constant?

A

How quickly the neurone can respond to a cell

399
Q

What does the membrane time constant depend on?

A

Resistance and the capacity (ability to store charge) of the neurone

400
Q

Why does the membrane time constant of neurones decrease during development?

A

Because neurones get bigger

401
Q

What occurs to input resistance and membrane time constant when the resting membrane potential becomes more negative?

A

They both decrease

402
Q

What are the two principle routes for action potential development?

A

Long Ca2+ dependant then short Na+ dependant action potentials
Short Na+ dependant

403
Q

What are Rohon-Beard cells?

A

They are a transit population of mechanosensory neurones found in the spinal cord

404
Q

What are the properties of an early action potential in a Rohon-Beard cell?

A

Looks like a cardiac action potential because it is Ca2+ driven

  • Calcium is let in and the channels don’t shut quickly
  • Not many K+ channels present to terminate so action potential appears elongated
405
Q

What are the properties of an action potential that has started to mature in a Rohon-Beard cell?

A

Delay rectifier K+ channels are inserted into the membrane - open after a delay after activation
So after Ca2+ open, K+ channels ope after a delay so action potential is still a bit elongated

406
Q

What are the properties of an action potential in a mature Rohon-Beard cell?

A

Normal action potential as Na+ channels have been inserted
More sensitive
Fast firing
- Occurs due to Na+ channels will snap shut quickly after it depolarises and also allows K+ channels to open to allow it to repolarise

407
Q

What are delayed rectifiers?

A

Channel that allows current through one way
A delayed rectifier is a channel that opens some time after its voltage threshold is reached
Outward delayed K+ rectifiers allow positive charge out of neurones after an action potential
Appearance of such channels shortens the action potential

408
Q

Apart from the addition of channels into the membrane, how else is complexity of excitability achieved?

A

Mouse cortex
- Different spiking activity as neurones develop
- fast spiking cells increase Kv3.1 expression the mature allowing to depolarise quicker
Purkinje cells bursting pattern
- Regulated by KCa channels increased expression
- Opens in response to influx of Ca2+
- Blocking these K channels stops the mature bursting pattern

409
Q

What is the role of T current calcium channels?

A

Give the action potentials in early development

410
Q

What is the role of N current calcium channels?

A

found in axon terminals ad control neurotransmitter release

411
Q

What is the role of L current calcium channels?

A

Controls transcription

412
Q

What are the spontaneous Ca2+ waves caused by calcium channel used fro in development?

A

Process growth

Involved in differentiation

413
Q

What changes occur in receptors in neuronal development?

A

Neuronal development

  • Populations
  • Subunits
  • Localisation
  • Efficacy
414
Q

How can some GABA be excitatory in developing neurones?

A

There is high intracellular [Cl-] in immature neurones

  • Cl- channels on membrane have changed meaning that it pumps Cl- out instead of in
  • GABA still activates these receptors meaning it has an excitatory role
415
Q

Why is regeneration in the mature nervous system important?

A

Traumatic injuries in PNS, spinal cord and brain
Stroke
Loss of neurone in disease eg. Alzheimers

416
Q

What is regeneration in the newt like?

A

Can regenerate whole limb with or without the presence of a nerve

417
Q

What is regeneration in the xenopus like?

A

Tail regeneration is dependant on BMP signalling
Has a critical window of response
- At 47 hours of development - ail will not regrow

418
Q

What is regeneration in the starfish like?

A

Needs the radial nerve to be intact for limb to regrow

419
Q

How are nerve injuries classified?

A 
Neuropraxia
- Mildest
- No physical peak but block of conduction 
Axonotmesis
- Sectioning of axon but preservation of nerve itself
Neurotmesis
- Severe
- Whole nerve is sectioned
420
Q

How does the position of the nerve sectioning affect the likely head for cell survival?

A

If it is close to the cell soma - likely for cell death
Away from cell soma - cells might survive but will undergo changes such as reorganisation and re expression of the immature features eg. tubulins

421
Q

What is Wallerian degeneration?

A

Discovered in 1840 and is the first state of regeneration in mature nervous system

  • Part of the damaged axon furthest away from the soma (distal end) degenerated by macrophages trying to remove dying Schwann cells
  • The part closest to the soma remains the same
  • Occurs quite quickly so a new one can be made
422
Q

What happens if a muscle becomes denerved?

A

Muscle atrophy

  • AChR start to change to a immature form
  • Muscle specific kinases increase
  • If external electrical input is added it my help to prevent atrophy
423
Q

How does regeneration of nerves that have minor damage happen in the PNS?

A

Wallarian regeneration
Mitosis of Schwann cells
- To cover area to help axon grow
- Also form bands of bunger to guide the new axon
Sprouting may also occur
- Another nerve tries to innervated the muscle to prevent loss of function

424
Q

How do compression and cut injuries affect nerves differently?

A 
Compression
- Basal lamina damaged and ECM unaffected
Cut
- Disrupts both basal lamina and ECM
- May not regrow accurately
425
Q

What happens when the spinal cord is damaged?

A

Sprouting may be attempted but the fibres cannot find where they need to be so - failed regeneration
Formation of cysts and glial scars

426
Q

Outline an experiment showing how regeneration in the spinal cord is difficult due to its environment?

A

Damaged axons from CNS where put in the environment of the PNS
They were able to regenerate unlike in the CNS
Suggesting environmental factor and not intrinsic

427
Q

Give evidence for myelin inhibiting CNS regeneration

A

CNS neurones were trying to avoid oligodendrocytes
Removing myelin/oligodendrocytes improved regeneration
If you auto-immunise a micr to myelin proteins - enhances regeneration

428
Q

What is present in CNS myelin which inhibits regeneration?

A

NOGO -a (protein)

429
Q

What types of NOGO are there?

A

NOGO - a - large and donut in oligodendrocytes
NOGO b - Many cells
NOGO - c - muscle

430
Q

Give evidence for the role of NOGO- a in inhibiting regeneration in the CNS

A

NOGO a is not found in the fish and salamanders or in human PNS which can regenerate

431
Q

How does NOGO-a block regeneration in the CNS?

A

Works on P75 receptors interfering with the roles of neurotrophins which support the development of new fibres

432
Q

What objections are there to NOGO a being responsible for the inhibition of regeneration in the CNS?

A

Knockout mice showed variable results
No correlation between NOGO receptor level and regenerative capacity
Transplanted hippocampal neurones grow axons
Much myelin is removed by macrophages after damage

433
Q

How are scarred glia though to inhibit regeneration in the CNS?

A

When astrocytes are damaged they change in other to contain the inflammation
This causes a scar which fibres can not grow through

434
Q

How are sectioning of nerves in both CNS and PNS surgically treated?

A

Gap in nerve that is too big
Scaffold tube inserted which connected the nerve and allows fibres to grow inside it
- Can be synthetic or biological
- If synthetic it wold have to be filled with ECM

435
Q

What diseases have transplanted foetal cells been used to treat?

A

Parkinsons and Huntingtons

- Little success

436
Q

What research into regeneration of nerves currently undergoing?

A

Transplanted foetal cells
Transplanted human embryonic stem cells
Transplant umbilical cells
Transplant autologous NS cells

437
Q

Give evidence to suggest that neurogenesis can occur in the adult brain normally

A

Canaries
- In their high vocal centre, new neurones are formed as the canary learns to sing
- Suggests that neurogenesis can occur in mature animals
Mammals
- In dentate gyrus (in hippocampus) and olfactory bulb, neurogenesis can occur naturally

438
Q

If there are parts of the adult brain that can undergo neurogenesis naturally, what is a new idea that can be researched for regeneration in the adult nervous system?

A

if there are stem cells capable of neurogenesis then they could be used for spontaneous regeneration under the right conditions

439
Q

What are olfactory ensheathing cells?

A

Supporting cells

- Support and encourage regeneration

440
Q

When studying commissural axons what is the problem with knocking out Shh and how can it be overcome?

A

Without Shh, mouse wouldn’t live long enough to reach the stage where commissural axons cross the midline
Cre recombinase can be used to knockout shh just from the tissue being studied so that the rest of the development is normal

441
Q

How do BMPs and Shh guide commissural axons?

A

BMPs are released from roof plate and BMP is a repellant

Shh is released from floor plate and Shh is an attractant

BMS 2 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions