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202 Neuroscience & Behaviour > Theme 1 - Neuroscience & The Brain > Flashcards

Theme 1 - Neuroscience & The Brain Flashcards

1
Q

What are the 3 different locations of chemical synapses?

A

axodendritic
axosomatic
axoaxonic

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2
Q

What 2 types of response can be generated by a receptor upon recognition of a neuroreceptor?

A
  • Direct excitatory or inhibitory neurotransmission

- Neuromodulation

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3
Q

Define neuromodulation?

A

alters the presynaptic cell’s ability to release more transmitter or the postsynaptic cell’s ability to respond

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4
Q

During brain development, from where do neuroectoderm cells receive their induction signals?

A

Notochord

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5
Q

During brain development, the neural plate folds to form what?

A

Neural tube

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6
Q

Label day 24 of brain development. (4)

A

Neural crest cells
Mantle layer
Ependymal layer
Lumen

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7
Q

In terms of neural tube defects, what condition is the failure of the anterior neuropore to close?

A

Anencephaly

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8
Q

In terms of neural tube defects, what condition is the failure of the posterior neural tube to close?

A

Spina bifida

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9
Q

What does the forebrain develop from?

A

Prosencephalon

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10
Q

What does the midbrain develop from?

A

Mesencephalon

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11
Q

What does the hindbrain develop from?

A

Rhombencephalon

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12
Q

What are the primary vesicles? 3

A

Prosencephalon
Mesencephalon
Rhombencephalon

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13
Q

What are the secondary vesicles and what do they become? 5

A 
Telencephalon - Cerebral hemispheres
Optic vesicles - eyes
Diencephalon - Thalamus/hypothalamus
Metencephalon - Pons/cerebellum
Myelencephalon - Medulla
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14
Q

What’s grey and white matter made from?

A

Grey - neuronal cell bodies

White - myelenated axons

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15
Q

What are the 4 lobes of the cerebral hemispheres?

A

Frontal
Temporal
Occipital
Parietal

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16
Q

What feature divides the frontal and parietal lobes?

A

Central sulcus

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17
Q

What features lie either side of the central sulcus?

A

Precentral gyrus - motor

Postcentral gyrus - ssensory

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18
Q

What feature divides the parietal and temporal lobes?

A

Lateral lobes

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19
Q

Label the following areas of the cortex (5)

A 
Prefrontal
Primary motor
Somatosensory 
Visual
Motor speech area of Broca
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20
Q

What is the name of the white matter tract linking the two cerebral hemispheres?

A

Corpus callosum

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21
Q

What brain system is associated with emotions and memory?

A

Limbic system

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22
Q

What deep brain structure is associated with posture and movement?

A

Basal ganglia

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23
Q

What are the main components of the limbic system?

A 
Cingulate cortex
Fornix
Hypothalamus
Mamillary bodies
Amygdala
Hippocampus
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24
Q

What two structures are connected by the fornix?

A

Mamillary bodies

Hippocampus

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25
Q

What structures make up the basal ganglia?

A

Lentiform nucleus

Caudate nucleus

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26
Q

Label the caudate and lentiform nucleus on slide 20 lecture 2

A

Slide 20 lecture 2

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27
Q

What structures does the hypothalamus lie between?

A

Mamillary bodies and optic chiasm

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28
Q

What senses are the superior and inferior colliculi associated with?

A

Superior - vision

Inferior - auditory

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29
Q

What is the function of the pons?

A

Relay information to the cerebellum

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30
Q

Label features of medulla oblongata 4

A

Pyramid
Olive
Cuneate tubercle
Gracile tubercle

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31
Q

Afferent from/to?

A

To brain/spinal cord

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32
Q

Efferent from to?

A

From brain to effector organ

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33
Q

What is a ganglion?

A

Group of neural cell bodies outside the CNS

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34
Q

Characteristics and example of motor ganglion

A

Autonomic
Smaller neurons
Parasympathetic ganglion

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35
Q

Characteristics and example of sensory ganglion

A

Larger neurons

Dorsal root ganglion

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36
Q

Label the directions of the human prefrontal cortex

A

Rostral
Cortex
Dorsal
Dorsal

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37
Q

What is the purpose of myelin sheathing of a neuron?

A

Increase conduction velocity

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38
Q

What are the 3 classifications of neurons?

A

multipolar
bipolar
unipolar

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39
Q

How many axons do neurons have?

A

1

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40
Q

Where are pyramidal and Purkinje cell neurons found?

A

Neocortex

cerebellum

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41
Q

An example of where Pseudo-unipolar neurons found?

A

Dorsal root ganglion

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42
Q

In terms of signalling what term is used when a single neuron sends its output signal to many neurons and give an example

A

Divergent

Skin

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43
Q

In terms of signalling what term is used when multiple inputs influence a single neuron and give an example

A

Convergent

Retina

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44
Q

In what nervous system do inter neurons occur and are they motor or sensory?

A

CNS

Neither, they process signals

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45
Q

4 features of glia

A

No action potentials
Do not form synapses
Able to divide
From myelin sheaths

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46
Q

What is the ratio of glia to neurons?

A

10-50:1

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47
Q

Purpose and site of oligodendrite

A

production / maintenance of myelin sheath

CNS

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48
Q

Purpose and site of astrocyte

A

Support
Development
Protection from harmful substances
CNS

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49
Q

Purpose and site of microglia

A 
immune cells, protect 
neurons from disease, migrate 
to injury sites, engulf microbes 
/ debris, mesodermal origin
CNS
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50
Q

Purpose and site of ependymal cells

A

line brain’s ventricles and central canal of spinal cord,
form CSF
CNS

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51
Q

Purpose and site of Schwann cells

A

production / maintenance of
myelin sheath
PNS

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52
Q

Purpose and site of satellite cells

A

support neurons, regulate exchange of materials between neurons and interstitial fluid
PNS

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53
Q

What is a glioma and 4 characteristics that give them such a shit prognosis.

A 
largest group of primary tumours 
  derived from glial cells
• usually highly malignant
• grow rapidly
• difficult to remove completely with surgery
• Usually inside cranium
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54
Q

What is a neuroblastoma and 4 characteristics

A 
Tumor
most common in children & infants
outside cranium
derived from neural crest cells from sympathetic NS
increased Catecholamine levels (often)
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55
Q

5 features of electrical synapses

A 
faster
bidirectional
smaller gap
no plasticity 
no ampliafication
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56
Q

What is A neuron determines whether to fire based on the “add together” of all the tiny signals it is receiving from several other neurons synapsing on it (from both excitatory and inhibitory inputs). In this way small depolarisations (if there are many) can reach threshold known as?

A

Spacial summation

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57
Q

What is When the input neuron is firing fast enough so that the receiving neuron can “add together” the many tiny signals, ultimately reaching threshold known as?

A

Temporal summation

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58
Q

Label action potential graph

A 
Resting state -70mV
Threshold -55mV
Depolarisation until +40mV
Repolarisation
Hyperpolarisation 
Refactory period
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59
Q

What channels keep the neuron at resting potential?

A

Inward rectifier K+ channels

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60
Q

What channels does initial depolarisation open?

A

Na+ channels

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61
Q

How is depolarisation a positive feedback loop?

A

Na+ going into the cell causes more depolarisation

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62
Q

At what point during depolarisation does overshoot occur?

A

Vm above 0mV

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63
Q

What two channels are involved in repolarisation?

A

Na+ channels become inactivated

Delayed rectifier K+ channels open (so more K+ goes out)

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64
Q

At what voltage do inward rectifier channels open?

A

below -60mV

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65
Q

Why does after-hyperpolarisation occur in terms of channels open/shut/activated?

A

The delayed rectifier channels are slow to close.

At the same time the inward rectifiers open and Na+ are inactivated

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66
Q

In what 2 ways can neurons code for the intensity of synaptic input?

A

Firing frequency

Different neurons for different strength stimuli

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67
Q

What term describes how easy it is to start nervous signalling (overall, in sensory and muscle?

A

Excitability
Sensitivity
Irritability

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68
Q

How does lidocaine work? 3

A

Blocks sodium ion channels
Raises theshold
Lowers excitability

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69
Q

What type of drug is cabamazepine and how does it work?

A

Anticonvulsant

blocks sodium channels and reduces excitability

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70
Q

Equilibrium potentials for Na, K, Ca, Cl

A

Na +50
K -90
Na +123
Cl -40/-65 in neurons

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71
Q

5 characteristics of action potentials

A 
Stereotyped
Short duration
A spike
Always the same - all or none
Require time to start
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72
Q

5 characteristics of graded potentials

A 
*Decrease as they move along*
Electrically localised  
Last a long time
much Flatter in shape
Are conducted almost instantly
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73
Q

What is the term that describes when an action potential jumps from node to node?

A

Saltatory conduction

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74
Q

Give the 5 steps of a typical chemical synapse transmission from the transmitter being synthesized and stored in vesicles to the transmitter being released into the synaptic cleft.

A

Action potential invades the presynaptic terminal
Depolarisation causes opening of voltage gated Ca2+ channels
Influx of Ca2+
Ca2+ causes vesicles to fuse with pre-synaptic membrane
Transmitter released into presynaptic cleft via exoxytosis

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75
Q

Give 5 steps of a typical chemical synapse transmission from when the transmitter is released into the cleft through to retrieval of vesicular membrane

A

Transmitter binds to receptor molecules in post synaptic cleft
Opening/closing of post synaptic vesicles
Post synaptic current causes excitation/inhibition potential that changes excitability of post synaptic cell
Removal of transmitter by glia/enzyme
Retrieval of vesicular membrane

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76
Q

Where are the pool of synaptic vesicles located and what are they anchored by?

A

Cytoskeleton

synapsin

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77
Q

How does Ca2+ release the vesicles from the cytoskeleton?

A

Ca2+ activates CaMKII which phosphorelates synapsin

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78
Q

What complex docks vesicles to the plasma membrane?

A

SNARE

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79
Q

Give the 4 steps of exocytosis during neurotransmitter release.

A

Vesicle docks
SNARE complexes pull membranes together
Entering Ca2+ binds to synaptotagmin
Synaptotagmin the catalyses membrane fusion

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80
Q

Via what process are vesicles recoverd

A

Endocytosis

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81
Q

How does Botulinum affect the synaptic terminal?

A

Affect SNARE and dont allow the vesicle to fuse
Acts directly on the neuromuscular junction to inhibit release of Ach. Muscles have no input so become permanently relaxed

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82
Q

How does tetanus afect he synaptic terminal?

A

Affect snare and don’t allow the vesicle to fuse
Acts upon the interneurons in the spinal cord.
Inhibits the release Gly and GABA st inhibitory neurons so muscles become permanently contracted

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83
Q

5 examples of ways in which diseases can affect the presynaptic terminal?

A 
Impair vesicle recycling - myasynthenic 
Vesicle fusion - latrotoxin
Bind to SNARE - BoTX/TeTX
Impair transynaptic sugnalling
Attack presynaptic Ca2+ channels - LEMS
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84
Q

What type of gradient powers vesicular membrane and plasma membrane transporters?

A

vesicular - protein

plasma - electrochemical

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85
Q

4 categories of neurotransmitters

A

Amino acids
monoamines
acetylcholine
neuropeptides

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86
Q

3 characteristics of monoamine, acetylcholine and neuropeptides.

A

Synthesized locally in presynaptic terminal
Stored in synaptic vesicles
Released in response to local increase in Ca2+

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87
Q

3 characteristics of neuropeptides

A

Synthesized in the cell soma and transported to the terminal
Stored in secretory granules
Released in response to global increase in Ca2

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88
Q

Will a low frequency stimulation and localised increase in Ca2+ result in small molecule neurotransmitter or neuropeptide?

A

Small molecule neurotransmitter

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89
Q

What is the difference between the vesicles that smallmolecule transmitter and neuropeptide are stored in?

A

Small molecule - small clear vesicles

Neuropeptide - large dense vesicles

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90
Q

What is the excitatory neurotransmitter in the CNS?

A

glutamate

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91
Q

2 inhibitory neurotransmitters in the CNS and thir specific location.

A

GABA - brain

Glycine - spinal cord and brain stem

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92
Q

From what two sources is glutamate synthesised from?

A

from glucose via the Krebs cycle

from glutamine converted by glutaminase into Glutamate

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93
Q

What loads and stores glutamate into vesicles?

A

VGLUTs

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94
Q

What facilitates the reuptake of glutamate?

A

excitatory amino acid transporters (EAATs

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95
Q

What role do glia play in the reuptake of glutamate?

A

glial cells convert Glu to glutamine and this is transported from the glia (“ball boys”) back to nerve terminals where it is converted back into Glutamate

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96
Q

From what id GABA synthesised?

A

synthesized from glutamate (Glu)
in a reaction catalyzed by
glutamic acid decarboxylase (GAD)

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97
Q

What loads and stores GABA and glycine into vesicles?

A

vesicular GABA transporter, GAT

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98
Q

What facilitates the reuptake of GABA?

A

transporters on glia and neurons including non-GABAergic neurons

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99
Q

What will too much Glu / too little GABA result in?

A

hyper-excitability – epilepsy excitotoxicity

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100
Q

What will too much GABA result in?

A

sedation coma

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101
Q

Mechanism of action of GHB?

A

a GABA metabolite that can be converted back to GABA
Increases amount of available GABA
too much leads to unconsciousness and coma

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102
Q

Two subcategories of monamines and an example of each

A

Catecholamines - dopamine, adrenaline

Indolamines - serotonin

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103
Q

5 steps of Catecholamine synthesis

A 
Tyrosine
(L-dopa)
Dopamine
Norepinephrine
Epinephrine
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104
Q

What is L dopa used to treat?

A

Parkinson’s

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105
Q

What are Catecholamine’s loaded and stored in vesicles by?

A

Vesicular monoamine transporters (VMATs)

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106
Q

What facilitates the reuptake of catecholaines?

A

reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters (DATs), Norepinephine transporters (NETs) etc.)

107
Q

What 3 things can happens to catechloamines once they are back in the cytoplasm?

A
  • reloaded back into vesicles
  • enzymatically degraded by Monoamine oxidases (MAOs)
    or
  • inactivated by Catechol-O-methyl-transferase (COMT)
108
Q

How do amphetamines affect catecholamines?

A

reverses transporter so pumps out transmitter and blocks reuptake (DA & NE)

109
Q

How does cocaine and ritalin affect catecholamines?

A

(Ritalin) block DA reuptake into terminals. More DA in synaptic cleft – extended action on postsynaptic neuron.

110
Q

How does selegiline affect catecholamines?

A

MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations

(treatment of early-stagePD,depression anddementia).

111
Q

How does entacapone affect catecholamines?

A

COMT inhibitor

treatment of PD

112
Q

What is the chemical orogin of seretonin?

A

thyptophan

113
Q

How is serotonin stored, uptaken and destroyed?

A

Stored in vesicles
reuptaken by transporters on presynaptic membrane
destroyed by MAOs

114
Q

3 drugs that affect serotonin and how

A

Fluoxetine (Prozac) blocks reuptake of serotonin (SSRI – selective serotonin reuptake inhibitor)

Fenfluramine stimulates the release of serotonin and inhibits its reuptake

MDMA, methylenedioxymethamphetamine (ecstasy) causes NE and serotonin transporters to run backwards releasing neurotransmitter into synapse/extracellular space

115
Q

What packs Ach into vesicles?

A

vesicular acetylcholine transporter (VAChT).

116
Q

Where is Ach degraded and by what?

A 
in synaptic cleft 
by acetylcholinesterase (AChE)
117
Q

What drugs affect Ach and how?

A

AChE (Acetylcholinesterase) inhibitors

block the breakdown of ACh, prolonging its actions in the synaptic cleft

e.g. Neostigmine (treatment of myasthenia gravis, MG)
118
Q

Which type of receptors are responsible for fast and slow transmission respectively?

A

Ionotrophic - fast

Metabotropic - slow

119
Q

What is a ligand gated ion channel and how does it work?

A

An ionotrophic receptor
Neurotransmitter binds
central pore opens
ions flux through

120
Q

What type of ions do glutamate and GABA ionotrophic receptors flux and what is the effect?

A

Glutamate ionotropic receptors in general flux Na+, which causes an EPSP (Excitatory Post Synaptic Potential)
GABA ionotropic receptors flux Cl-, which causes an IPSP (Inhibitory Post Synaptic Potential)

121
Q

What are the three types of ionotrophic receptor that respond to glutamate?

A

NMDA
AMPA
Kainate

122
Q

Two characteristics of Non-NMDA receptors (AMPA and Kainate)?

A

Fast opening channels permeable to Na+ and K+

Responsible for early phase EPSP

123
Q

Characteristics of NDMA receptor?

A

Slow opening channel – permeable to Ca2+ as well as Na+ and K+
BUT also
2) requires an extracellular glycine as a cofactor to open the channel
3) it is also gated by membrane voltage – Mg2+ ion plugs pore at resting
membrane potentials. When membrane depolarizes Mg2+ ejected from
channel by electrostatic repulsion allowing conductance of the other
cations, activity-dependent synaptic modification.
NMDA receptors responsible for a late phase EPSP
Activated only in an already depolarized membrane in the presence of glutamate

124
Q

What does PCP (angel dust) affect?

A

NMDA receptors also inhibited by phencyclidine (PCP, angel dust) and MK801; both bind in the open pore.

Blockade of NMDA receptors in this way produces symptoms that resemble the hallucinations associated with Schizophrenia.

125
Q

6 ionotrophic receptors and what effect they have

A

Glutamate - excitatory
GABA(A) - inhibitory (brain)
Glycine - inhibitory (spinal cord and brain stem)
Nicotine - excitatory at NMJ (neuromuscular junction)
- excitatory or modulatory in the CNS
Serotonin -excitatory or modulatory
ATP - excitatory

126
Q

How do metabotrophic receptors work?

A

They transduce signals into the cell not directly through an ion channel but through activation of a G-protein which in turn triggers a series of intracellular events (that can lead to ion channel opening)

G-protein coupled receptors (GPCRs)

127
Q

Draw how the three G protein subunits interect following the binding of a ligand

A

lecture 7 slide 26

128
Q

What is the shortcut pathway?

A

receptor to G-protein to ion channel

129
Q

How do G protein receptors influence the synthesis of the second messenger cAMP?

A

Gs and Gi have opposite effects on adenylyl cyclase, thus stimulating or inhibiting the synthesis of cAMP and the subsequent activation of protein kinase A (PKA).

130
Q

4 steps of the second messenger PIP2 cascade?

A

Gq activates phospholipase C (PLC)
which converts PIP2 into IP3 and diacylglycerol (DAG).
DAG activates protein kinase C (PKC) and IP3 releases Ca2+ from internal stores which activates Ca2+-dependent enzymes.

131
Q

How can the amount of neurotransmitter that is released be modulated by the presynaptic receptors??

A

autoreceptors - regulate release of transmitter by modulating its synthesis, storage, release or reuptake

heteroreceptors - (axoaxonic synapses or extrasynaptic)
regulate synthesis and/or release of transmitters other than their own ligand

132
Q

7 types of metabotrophic receptors

A

GABA(B) receptor

muscarinic acetylcholine receptors

dopamine receptors

noradrenergic and adrenergic receptors

serotonin receptors

neuropeptide receptors
metabotropic glutamate receptors

133
Q

Draw modal model of memory

A 
Stimulus
Sensory
(attention)
Short term - rehearsal
(encoding/retrieval)
Long term
134
Q

What is the evidence for the dual sketchpad model of memory?

A

Visula-spacial sketchpad - - Central execuitive - - Phonological store

Dual test showed that numbers could be remembered whilst reasoning applied

135
Q

What is then evidence for the phonological store? 3

A

Greater error rate in remembering words that are phonologically similar as well as syllables and how quick the word is to say
But semantic similarity has no effect on error rate

136
Q

What is the lesion localisation for short-term memory patients?

A

Left hemisphere

Usually affecting the parietal and temporal lobes

137
Q

What are the two subdivisions of the visuospatial sketchpad and what do these store?

A

Visual cache - form and colour

Inner scribe - spacial and movement and can rehearse visual cache

138
Q

What actively refreshes the contents of the phonological store?

A

Articulatory loop

139
Q

What is the evidence for the visuospatial sketch pad?

A

Subject performs a visual task and a spacial task. Each task is run with visual interference and spatial interference. If the interference is the same then they do shit

140
Q

What are the three types of processing, how deep is it and what is the retention like?

A

Orthographic - Shallow - Poor
Phonological - Medium - Average
Semantic - Deep - Good

141
Q

What is the study/test vs study/study experiment evidence of?

A

Retrieval practice effect

142
Q

What is transfer appropriate processing?

A

A “shallow” processing task might be better if retrieval uses the same type of processing

143
Q

What is amnesia?

A

Ability to take in new information is severely and usually permanently affected. Intelligence and personality intact.

144
Q

What effect does amnesia have upon Verbal and visual short-term memory?

A

Nothing, it remains intact

145
Q

What type of amnesia comes after the brain injury and what types of memory are affected?

A

Anterograde

episodic memories are severely affected

146
Q

Draw the divisions of long term memory

A

Declarative - Episodic (events) Semantic (facts)

Implicit - Priming effects Procedural memory

147
Q

What is the dedicated system for procedural memory and inn what type of patients is procedural memory effected?

A

Basal ganglia

Huntington’s

148
Q

What type f amnesia affects memories before brain injury?

A

Retrograde amnesia although to what extent episodic memories are affected is highly contested.

149
Q

What is the Standard Model on consolidation?

A

Over time, declarative memories become consolidated to other brain regions

150
Q

What does semantic dementia refer to?

A

A poor knowledge of meaning of words or concepts

151
Q

What region of the brain is associated with semantic knowledge?

A

lateral temporal cortex on the LEFT side of the brain

152
Q

What is confabulation?

A

erroneous memories, either false in themselves or resulting from ‘true’ memories misplaced in context an inappropriately retrieved or interpreted

153
Q

What is the difference between provoked and spontaneous confabulation?

A

Provoked - a normal response to a demand for information which is not available
Spontaneous – the person acts on their erroneous memories

154
Q

Spontaneous confabulation may result from damage to what region of the brain?

A

Usually a result of frontal lobe damage

155
Q

What does and EEG measure?

A

synchronous fields in pyramidal cells

156
Q

What are the 4 basic EEG phenomena and when do these occur?

A

Alpha - awake with eyes closed
Beta - awake eyes open
Theta - drowsiness/sleep/pathology
Delta - drowsiness/sleep/pathology

157
Q

In what two ways can synchronous rhythms be generated in the brain?

A

Led by pacemaker thalmic cell

Or the timing arises from the collective behaviour of the neurons themselves

158
Q

4 behavioural criteria of sleep

A

Reduced motor activity
Decreased response to stimulation
Stereotypic postures
Relatively easy reversibility

159
Q

What are the three function states of sleep?

A

Awake
Non REM I,II,III,IV
REM sleep

160
Q

4 possible functions of sleep/dreaming?

A

Conservation of metabolic energy
Cognition
Thermoregulation
Neural maturation and mental health

161
Q

What is the difference between PET and fMRI in terms of what they measure?

A

PET measures change of blood flow to a region.

fMRI is sensitive to the concentration of oxygen in the blood.
Therefore an indirect measure of neuron activity

162
Q

What is BOLD fMRI?

A

BOLD signal: blood oxygen-level –dependent contrast, is the signal measured in fMRI that relates to the concentration of oxy- and deoxyhaemoglobin in the blood.

163
Q

How does MRI work?

A

Protons initially aligned randomly
magnetic field causes come of them to align
Pass radiowave through them causes them to spin 90 degrees
This spinning causes a resonance that can be measures

164
Q

Draw and label the 4 components of the lateral ventricles and state what lobe they are located in.

A

Anterior horn - frontal
Body - parietal
Posterior horn - occiptal
Inferior horn - temporal

165
Q

What separates the lateral ventricles?

A

Septum pellucidum

166
Q

What sits on the roof, lateral wall and floor of the lateral ventricles?

A

Corpus callossum
Caudate nucleus
Hippocampus

167
Q

What connects the lateral and third ventricle?

A

Foramen of Monro

168
Q

What does the third ventricle sit between and what forms it’s roof?

A

Thalami

Fornix

169
Q

Label slide 12 of the ventricular system

A 
Caudate nucleus
corpus callossum
Septum pellucidum
Fornix
Thalamus
Lentiform  nucleus
Hippocampus
170
Q

What connects the third and fourth ventricle?

A

cerebral aqueduct

- Also called Aqueduct of Sylvius

171
Q

What surrounds the cerebral aqueduct/ Aqueduct of Sylvius?

A

Midbrain

172
Q

What surrounds the fourth ventricle?

A
  • Cerebellum posterior
  • Pons and medulla anterior
  • Cerebellar peduncles lateral
173
Q

The fourth ventricle has 3 foramen, what are these nad what do they drain into?

A

Two Foramen of Luschka (lateral)
One Foramen of Magendie (middle)
- Into Cisterna Magna

174
Q

What produces CSF and where is it?

A

Choroid plexus

lining of ventricles

175
Q

Outline the basic structure of the choroid plexus

A

Fenestrated capillaries - filter

Cuboidal epithelium - transport

176
Q

What barrier is formed by the cuboidal epithelium?

A

Blood-CSF barrier

177
Q

What is the percentage breakdown of CSF by location?

A

60% vebtricles

40% Other sites in the brain

178
Q

What must CSF pressure exceed and why?

A

Venous pressure

Otherwise tips of villi close off to prevent reflux of blood into subarachnoid space

179
Q

What is the total and produced daily volume of CSF?

A

140ml

500ml per day

180
Q

4 functions of CSF

A
  1. Hydraulic buffer to cushion brain against trauma
  2. Vehicle for removal of metabolites from CNS
  3. Stable ionic environment for neuronal function
    (communicates with brain interstitial fluid via pia)
  4. Transport of neurotransmitters and chemicals
181
Q

What does yellow or cloudy CSF indicate?

A 
Yellow (Xanthocromia)
E.g. Subarachnoid haemorrhage
Coudy
e.g. MS
Bacterial meningitis
182
Q

From where is a lumbar puncture taken?

A

At lumbar cistern
L3/4 in children
L4/5 in adults

183
Q

What is hydrocephalus and 3 possible causes?

A

Dilation of brain ventricles
blocked CSF circulation
, impaired absorption
, or over secretion

184
Q

What is non-communicating hydrocephalus and how is it treated?

A

Blockage within the ventricular system

Surgery to insert shunt

185
Q

What is Dandy Walker syndrome?

A

Congenital malformation of the cerebellum
Caused by obstruction in the foramina of the fourth ventricle
In infancy child’s head may become enlarged

186
Q

What is communicating hydrocephalus and 3 possible causes?

A

Obstruction in the arachnoid villi

Movement of CSF into venous sinuses is impeded

  • E.g. Impaired absorption following subarachnoid haemorrhage, trauma or bacterial meningitis
187
Q

What are the two main families of GABA receptor?

A

GABA(a) ionotropic

GABA(b) metabotropic

188
Q

What are the differences between GABA(a) and GABA(b) receptors?

A 
a - ionotropic
     Ligand gated Cl-
     fast
     mainly GABAergic
b - metabotropic
     G protein coupled receptors
     indirectly coupled to K or Ca channel
     Slow
     pre and post synaptic
189
Q

Two examples of GABAa agonist/antagonist and where do these bind to?

A

Muscimol - agonist
Bicuculline - antagonist
They bind to GABA binding site

190
Q

Three examples of indirect GABAa agonists

A

Benzodiazepine - Increases receptor affinity for GABA so channel opens more frequently
Barbiturates - increase duration of channel openings
Alcohol - agonist

191
Q

Example of a benzodiazapine and 5 effects

A 
Diazepam (Valium)
reduce anxiety
cause sedation
reduce convulsions
relax muscles
cause amnesia
192
Q

What happens of you combine alcohol and Valuim?

A

Valium is a benzodiazapine and so increases the effectiveness of the receptor. Alcohol also acts as an indirect agonist> the effects are therefore additive and can be fatal.

193
Q

Give an example of a GABAb receptor agonist and its use?

A

Baclofen

used as a muscle relaxant to reduce spasticity e.g. in Huntington’s disease)

194
Q

What are the 6 diffuse modulatory systems?

A 
(Specific populations of neurons that project diffusely and modulate the activity of Glutamate and GABA neurons in their target areas.)
Dopaminergic (DA)
Serotonergic (5-HT)
Noradrenergic (NA/NE) 
Adrenergic
Cholinergic (ACh)
Histaminergic
195
Q

What are the 3 subdivisions of the dopaminergic system and what are they associated with?

A

Nigrostriatal - motor control (parkinsons)
Mesolimbic
Mesocortical - behaviour

196
Q

What are the subtypes of dopamine receptors and what are the differneces?

A

D1 & D2
both metabotropic
D1 - excitatory - stimulate adenyl cyclase
D2 Inhibitory - Inhibit adenyl cyclase

197
Q

What 2 diseases result from dysfunction of the nigrostriatal system and what is the diffference?

A

Parkinson’s disease
destruction of DA projections from SN to basal ganglia
Huntington’s disease
destruction of DA target neurons in striatum

198
Q

What is the result of dysfunction of the mesolimbic and mesocortical system?

A

Mesolimbic - addiction

Mesocortical - Schizophrenia

199
Q

Where is serotonin produced?

A

Raphei Nuclei in brainstem

200
Q

Where is noradrenaline produced and what type of receptors does it affect?

A

Locus Coeruleus

metabotrophic

201
Q

4 disorders of the cholinergic system

A

Myasinthnia gravis
Alzheimers
Addiction
Epilepsy

202
Q

Two characteristics of coma

A

Characterised by complete loss of wakefulness and reactivity

A state of unresponsiveness to external stimuli with eyes closed

203
Q

5 causes of coma

A 
Sedation / anaesthesia
Epilepsy
Electrolyte / metabolic disturbance
Disturbance of thermoregulation
Structural damage to brainstem / thalamus / cortex
204
Q

What is the difference between a coma, vegetative state and minimally conscious state

A

C - Absent wakefulness absent awareness
VS - Wakefulness absent awareness
MCS - Wakefulness minimal awareness

205
Q

Timeline for types of vegetative state

A

Continuing - 4 weeks
Permanent - non-trauma 6 months
- trauma 1 year

206
Q

4 Non progressive causes of dementia

A

Head injury
Stroke
encephalitis
meningitis

207
Q

5 causes of dementia that are apparently progressive but non damaging to the brain

A 
systemic disease (metabolic, endocrine), 
prescribed drugs, 
psychiatric illness, 
poor sleep, 
chronic pain, etc.
208
Q

6 causes of dementia that are damaging to the brain but not neurodegenerative

A 
cerebrovascular disease (vascular dementia),
 MS, 
alcohol,
 brain tumours or hydrocephalus,
 HIV, 
B12 deficiency
209
Q

5 neurodegenerative diseases

A

Alzheimer’s disease,
dementia with Lewy bodies
(DLB, LBD — closely related to Parkinson’s);
also fronto-temporal lobar degeneration spectrum, Huntington’s,
Creutzfeldt-Jakob (prion) disease

210
Q

What is the threshold for raised intercranial pressure and what are 3 possible causes?

A

Above 200mm H2O
Increased CSF volume (hydrocephalus)
Intracranial space occupying lesion (neoplasm, haemorrhage, abscess)
Cerebral oedema

211
Q

Other than a huge cranium in infants what is the likely consequence of hydrocephaly?

A

Herniation

212
Q

Three types of herniation, whats the worst one and why?

A

Subfalcial (cingulate)
Central/transtentorial
Tonsillar/cerebellar - the worst
Because can compress medulla and impair respiratory/cardiac functions

213
Q

4 types of haemorrhage

A

Extradural/epidural haemorrhage
Subdural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

214
Q

Other than haemorrhage, 3 other types of space occupying lesions.

A

Ischaemic infarct with subsequent oedema or haemorrhage
Neoplasm
Abscess

215
Q 
What type of vessel is injured in each of these vascular injuries?
Extradural
Subdural
Subarachnoid
Interperenchymal
A

Extra - artery (MMA)
Sub - vein
Subarachnoid - berry aneurysm circle of willis
Inter - hypertension capillary

216
Q

Two types of cerebral oedema

A

Vasogenic Increased vascular permeability

Cytotoxic Neuronal, glial or endothelial cell damage

217
Q

7 types of neural neoplasms

A

Gliomas (astrocytoma, oligodendroglioma, glioblastoma)
Neural tumours (ganglion cell tumours)
Meningiomas
Poorly differentiated neoplasms (medulloblastoma)
Primary CNS lymphoma
Metastasis (lung, breast, skin/melanoma, kidney, GI tract)
Peripheral nerve tumours (schwanoma, neurofibroma, MPNST)

218
Q

4 types of infection associated with the CNS

A

Meningitis
Encephalitis
Abscess
Localised

219
Q

How does the body discriminate types of mechanical sensation?

A

It uses different types of sensor

220
Q

5 types of mechanosensory receptors

A 
Shear - Meissner corpuscle
Contact - Merkel disc
Tension/folding - Ruffini corpuscle
procking - bare nerve endings 
Pressure/vibration - Pacinian corpuscle
221
Q

3 mechanisms of sensory stimulus discrimination

A

Different types of sensor for the same modality
Spacial distribution of sensors
Windows of response intensity (hot/cold)

222
Q

What are the motor neurons in the spinal cord known as which can generate a motor response independent of the brain?

A

Lower motor neurons

223
Q

What type of neurons are the final common path for all neuronal information from the CNS to the skeletal muscles?

A

Lower motor neurons

224
Q

What will destruction of a SINGLE ventral root or spinal nerve result in and why?

A

Paresis
Lower motor neurons arranged in columns
Each column extends through more than one segment of cord.
Each muscle receives input from more than one ventral root or spinal cord

225
Q

What are the two proprioceptive sensory organs and what do they regulate?

A

muscle spindles - length

golgi tendon - tension

226
Q

How does that arrangement of tendon organs differ from that of muscle spindles?

A

tendon organs arranged in series so detect the tension from contraction
spindles in parallel so detect passive stretch

227
Q

What vest describes the type of neural phenomenon whereby connections that are active together become stronger?

A

Hebbian connection

228
Q

2 rules of synaptic modification

A

Neurons that fire together wire together

Neurons that fore out of synch lose their link

229
Q

What mechanism underlies synaptic strengthening?

A

Long Term Potentiation

230
Q

Three characteristics of LTP

A

Temporal
Associative
Specific

231
Q

Two characteristics of Neural Stem cells / Neural precursor cells?

A

Infinitely self –renewing
After terminal division and differentiation they can give rise to the full range of cell classes within the relevant tissue

232
Q

Two characteristics of Neural progenitor cell?

A 
Incapable of continuing self – renewal
Capable to give rise to only one class of differentiated progeny, e.g. an oligodendroglial progenitor cell will give rise to oligodendrocytes until its mitotic capacity is exhausted.
233
Q

What is a neuroblast?

A

Postmitotic, immature nerve cell that will differentiate into a neuron

234
Q

Example of chemoattractant and chemorepellent

A

Netrin

Slit

235
Q

What is the critical period concept and two important factors for its completion

A

A variable time window for different skills and behaviours.

Availability of appropriate influences (e.g. exposure to language, or species-specific songs for songbirds)
Neural capacity to respond to them

236
Q

Difference between PNS and CNS in terms of regeneration.

A

Schwann cells in PNS aid in regeneration.

Does not happen in CNS, results in glial scar

237
Q

Where does adult neurogenesis occur

A

Subventricular zone to olfactory bulb

Hippocampus

238
Q

Why does alcohol affect memory in terms of receptors?

A

It is an NMDA antagonist therefore prevents LTP

239
Q

What is Korsakoff syndrome?

A

loss of recent memory, and tendency to fabricate accounts of recent events (confabulation).

240
Q

Memory related side affect of benzodiazapines?

A

anterograde amnesia

241
Q

What is the hierarchial order order of the 5 sensory systems

A 
Association cortex
Secondary sensory cortex
Primary sensory cortex
Thalmic relay nuclei
Receptors
242
Q

What are the three main multimodal association areas and what do they process?

A

Posterior - language/perception
Temporal - emotion and memory
Prefrontal - executive functions

243
Q

What is the Wada procedure used for?

A

To determine which hemisphere is dominant for speech

244
Q

What is the difference between Broca’s and Wernicke’s aphasia?

A

Broca’s - difficulty in speaking. non fluent but comprehends

Wernicke’s - fluent but without comprehension

245
Q

What is prosopagnosia?

A

Difficulty recognising faces

246
Q

What is visual agnosia?

A

Inability to recognise objects

247
Q

What is anosognosia?

A

inability to recognise own illness

248
Q

What is the difference between agnosia, apraxia and aphagia i terms of disorder?

A

Agnosia - disorder of high level sensory function
Apraxia - disorder of high level motor ccordination
Aphagia - disorder of communicating/symbols

249
Q

In terms of brain activity at onset what are the 2 types seizure?

A

Global

Focal/partial

250
Q

5 types of idiopathic (primary) generalised seizures

A 
tonic-clonic seizures (“grand mal”)
absences (“petit mal”)
tonic seizures
atonic seizures
myoclonic seizures
251
Q

3 features if idiopathic primary generalise seizures

A

onset in childhood or adolescence
usually no focal symptoms/signs
often a number of seizure types cluster

252
Q

6 features of juvenile myoclonic epilepsy

A

commonest form of primary generalized epilepsy
juvenile onset, probably lifelong
early morning myoclonic jerks (ask)
photosensitive, sleep deprivation triggers
+/- absences
generalized tonic clonic seizures occur without warning

253
Q

3 phases of tonic clonic seizures

A

tonic - continous muscle spasm
clonic - jerking that slows
post-ictal - coma, drowsiness, muscle pain

254
Q

do pts get a warning of a tonic clonic (grand mal seizure)?

A

No

255
Q

6 features of absences (petit mal)?

A

abrupt
short, 5-20 seconds
multiple times/day, can lead to learning difficulties
unresponsive, amnesia for the gap, rapid recovery
tone preserved (or mildly reduced)
eyelid flickering

256
Q

2 types of partial/focal onset seizures?

A

simple partial seizure - aware aura

complex partial seizure - some awareness aura

257
Q

6 features of secondary generalise tonic/clonic seizures

A

warning/aura –eg epigastric rising sensation, altered smell, déjà vu, fear
cannot abort attack
onset sudden
duration 1-3 minutes
then falls , loses consciousness as seizure generalizes
rigidity/ convulsive jerks/ excess salivation
incontinence/tongue bite common
red/blue, wakes in ambulance/A&E

258
Q

a partial seizure most often relates to which lobe of the brain?

A

Temporal

259
Q

Brain structure most commonly related to epilepsy?

A

Hippocampus

260
Q

6 physical symptoms of temporal lobe epilepsy?

A

hallucination of taste, speech and /or smell, visual distortion

epigastric rising sensation (over humpback bridge)

pallor / flushing / heart rate changes (can mimic panic/hyperventilation attacks)

automatisms- semi-purposeful movements

oral- lip smacking, chewing movements

dystonic posturing (limb rises)

261
Q

4 cognitive/affective symptoms of temporal lobe epilepsy?

A

déjà vu / jamais vu

speech arrest (dominant hemisphere)

formed words during the seizure implies non-dominant hemisphere focus

affective

fear, elation, depression, anger

262
Q

3 features of frontal lobe epilepsy

A

brief 10-30 seconds

rapid recovery, frequent

predominantly nocturnal

263
Q

4 features of parietal lobe epilepsy

A

positive sensory symptoms (unlike TIA/stroke)

tingling, pain

distortion of body shape/image

Jacksonian march of positive sensory symptoms

264
Q

4 features of occiptal lobe epliepsy

A

typically simple visual hallucinations -balls of coloured or flashing lights

amaurosis (blackout or whiteout) at onset -25%

202 Neuroscience & Behaviour (5 decks)

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