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Neuroscience Flashcards

1
Q

What are the three divisions of the nervous system?

A

Central nervous system
Peripheral nervous system
Enteric nervous system

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2
Q

What is the difference between CNS and PNS?

A

CNS - the structures of the brain and the spinal chord

PNS - nerves and cell bodies to and from the brain and spinal chord

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3
Q

What is the enteric nervous system?

A

The neural cells of the viscera and is often classified as the PNS

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4
Q

How many peripheral nerves are there?

A

43

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5
Q

What is a nerve?

A

Bundle of axons/neurone processes
Does not contain dendrites
No neuronal cell bodies

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6
Q

What does mixed mean (in terms of nerves)?

A

Has both motor and sensory roles

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7
Q

What are the layers in the nerve?

A

Each individual axon is surrounded by endoneurium
These are bundled together by perineurium into fascicles
Fascicles are bound together by epineurium

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8
Q

How many pairs of cranial nerves are there?

A

12 pairs

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9
Q

Are cranial nerves mixed, sensory or motor?

A

All of them

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10
Q

What is the most common cranial nerve?

A

Vagus nerve (cranial nerve 10) - 80% of PNS outflow

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11
Q

How many spinal nerves are there?

A

31 pairs (5 sets of pairs)

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12
Q

Are spinal nerves mixed, sensory or motor?

A

Mixed

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13
Q

Are spinal nerves branched?

A

Yes

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14
Q

What are dermatomes and what is their clinical use?

A

The patterns of innervation of spinal nerves.

Help neurologists identify sites of damage

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15
Q

What are the sub-divisions of the PNS?

A

Somatic (voluntary) and visceral (involuntary)
These are split into afferent and efferent
Efferent visceral is Autonomic which is split into sympathetic and parasympathetic

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16
Q

Difference between somatic and autonomic? (in terms of motor axons)

A

Somatic - motor axons go straight to muscle

Autonomic - motor axons synapse with another cell in the ganglion and then to the muscle

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17
Q

Which are axons are usually myelinated?

A

Pre ganglionic axons are usually myelinated and post are not

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18
Q

What are the differences between the parasympathetic and the sympathetic nervous system?

A
  • Both para and sympathetic use acetyl choline and sympathetic uses noradrenaline as well.
  • Sympathetic ganglia lie closer to target as axons are shorter
  • sympathetic axons can connect to multiple ganglion
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19
Q

Name some key historical figures in the study neuroscience

A 
Huong Ti - canon of internal medicine
Galen - First to use animals 
Aristotle - heart
Al Hazen - eye as an imaging system
Al - Zahrawi - Neurosurgery
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20
Q

How and why has the use of the squid giant axon improved neuroscience?

A

Allowed the determination of ion flows in action potentials

It has a large diameter and is easy to dissection

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21
Q

How and why has the use of worms (C.elegans) improved neuroscience?

A

The model system for developmental cell death (apoptosis)

They are fully mapped

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22
Q

How and why has the use of flies (Drosophila) improved neuroscience?

A

Identification of gene regualting (e.g. pax-6 development)

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23
Q

How and why has the use of frogs (Xenopus) improved neuroscience?

A

Usefull for:

  • Nerve conduction velocity
  • Ca2+ release
  • How axons grow
  • How nerves pathfind
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24
Q

How and why has the use of chicks (Gallus) improved neuroscience?

A

Allowed development in transplantation and understanding of nerve growth factor
Allows easy embryonic manipulation

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25
Q

How and why has the use of birds improved neuroscience?

A

Behavioural studies e.g.. imprinting

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26
Q

How and why has the use of mammals improved neuroscience?

A
  • Dogs to map motor cortex, chemical neurotransmission and behaviour (pavlovian classical conditioning)
  • Cats dogs and apes used to understand reflexes and motor control
  • Cats dogs and rabbits used to formulate the autonomic nervous system
  • Rats used for operant conditioning by skinner
  • Mice - Molecular dissection of behaviour and disease
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27
Q

Name some neural tube defects

A

Spina Bidfida - failure of the neural tube to close ( a mild form is dimples at the bottom of the spine)
Anencephaly

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28
Q

How can you prevent most neural tube defects?

A

Folic acid - mother needs to take at very start of pregnancy for an effect

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29
Q

What are the primary brain vesicles? (draw it)

A

Prosencephalon
Mesencephalon
Rhombencephalon
http://droualb.faculty.mjc.edu/Lecture%20Notes/Unit%205
/chapter_15_the_brain%20Spring%2007with%20figures.htm

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30
Q

What are the secondary brain vesicles?

A

Change after 5 weeks
- Telencephalon - develops
- Diencephalon - from the prosencephalon
- Mesencephalon
- Metencephalon and Mylencephalon - from Rhombencephalon
http://droualb.faculty.mjc.edu/Lecture%20Notes/Unit%205
/chapter_15_the_brain%20Spring%2007with%20figures.htm

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31
Q

What is the difference between grey and white matter?

A

White - Myelinated axons

Grey - Neuronal cell bodies

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32
Q

What is the structure of the spinal chord?

A

White and grey matter around a central canal encased in a bony vertebrate. Dorsal and ventral roots which have ganglia (looks like a swelling)
http://www.easynotecards.com/notecard_set/33616

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33
Q

What is the function of the dorsal and ventral roots of the spinal cord?

A

Dorsal - carries sensory input in

Ventral - carries motor commands out

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34
Q

What causes a slipped disc?

A

Cartilage supporting the root may compress the nerve and cause pain

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35
Q

What is an interneuron?

A

They connect between sensory and motor neurones and are important in reflexes

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36
Q

What does crossing over mean?

A

Sensory and motor inputs/outputs on the left of the body may be dealt with on the right side of the brain

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37
Q

What are the meninges of the spinal cord?

A
  • Pia mater (closest to neural tissue)
  • Arachnoid
  • Dura mater
    They are layers of membrane to protect the spinal cord
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38
Q

What are the meninges of the brain

A

Continuous with those of the spinal cord

  • Pia mater
  • Subarachnoid space
  • Arachnoid
  • Subdural space
  • Dura sinus
  • Endosteal

https://www.shutterstock.com/image-vector/meninges-brain-labeled-24964390

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39
Q

What is the cerebrospinal fluid?

A

Fluid found in the central canal, brain ventricles and subarachnoid space

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40
Q

What is the function of cerebrospinal fluid?

A

Moves and cushions the CNS and reduces its molecular weight

Trauma - lose fluid and molecular weight increases - compromise blood flow

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41
Q

How can you sample cerebrospinal fluid?

A

Lumbar puncture between 3rd and 4th vertebrate

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42
Q

Disorders of the cerebrospinal fluid

A

Hydrocephalus - build up of fluid in the brain. If internal can be life threatening

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43
Q

What is the blood brain barrier?

A

A physiological barrier - selective semi permeable membrane that separates the circulating blood from the cerebrospinal fluid

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44
Q

What is the blood brain barrier made up of?

A

Astrocytes, tight junctions and capillary endothelial cells

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45
Q

What are the four divisions of the brain?

A
  • Brainstem
  • Diencephalon
  • Cerebellum
  • Cerebrum
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46
Q

What is the brainstem composed of and where is it located ?

A
  • Medulla oblongata (bottom)
  • Pons (middle)
  • Mesencephalon (top)
    Directly connected to the spinal chord
    http://humannervoussystem2.weebly.com/brain-anatomy.html
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47
Q

Define decussation

A

Crossing over from one side to another: usually in the pyramids in the medulla oblongata

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48
Q

What is the function of the medulla oblongata?

A
  • Respiratory rhythmicity center

- Cardiovascular centre

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49
Q

What are the major features of the medulla oblongata?

A
  • Fibre tracts
  • Nuclei
  • Olives (send presses to cerebellum)
  • Nerve roots - site of origin of many cranial nerves
    Large lesions cause death
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50
Q

What is the function of the pons?

A

Was thought to bridge the sides of the cerebellum
Connects to cerebellum via peduncles
Respiratory centre

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51
Q

What is the function of the mesencephalon/midbrain?

A

Visual and auditory reflexes

connects to cerebral hemispheres by cerebral peduncles

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52
Q

Where is the cerebellum located?

A

At the back of the brain:

http://humannervoussystem2.weebly.com/brain-anatomy.html

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53
Q

What is the structure of the cerebellum?

A
  • Folia
  • Layers - Purkinje cells
  • Deep nuclei (clustered neurones)
  • White matter
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54
Q

What is the role of the cerebellum?

A
  • Muscle tone
  • Co-ordiantion
  • Motor error - checking
  • Learning
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55
Q

What is cerebral ataxia?

A

Loss od cerebral neurones leading to jerky and imprecise movements

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56
Q

What is the reticular formation?

A

Cluster of neurones in the brainstem that controls the cardiovascular centres and reticular activating system (cardiac rhythm, alertness and emotion)

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57
Q

Where is the diencephalon located?

A

Part of the forebrain that links the midbrain and the cerebrum.

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58
Q

What is the structure of the diencephalon?

A
  • Thalamus
  • Hypothalamus
  • Pineal
    https: //s-media-cache-ak0.pinimg.com/736x/49/78/49/49
    7849f7cb770365d631b45b927de7b5. jpg
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59
Q

What is the function of the thalamus?

A

It is the processing and relay centre

  • All special senses except smell
  • Motor role
  • Arousal
  • Emotions
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60
Q

What is the role of the pineal?

A

Its an endocrine organ that secretes melatonin and serotonin

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61
Q

What is the role of the hypothalamus?

A

Wide variety:

  • eating
  • drinking
  • sexual behaviour
  • stress
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62
Q

What are the lobes of the cerebrum?

A
  • Frontal
  • Parietal
  • Occipital
  • Temporal
  • Central
  • Limbic
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63
Q

What are the layers of cerebral cortex?

A
  • Molecular
  • External granular
  • External pyramidal
  • Internal granular
  • Internal pyramidal
  • Fusiform layer
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64
Q

What is the cerebral cortex?

A

The outer cortex of the cerebrum surrounding the white matter and deep nuclei

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65
Q

Who was Phineas Gage?

A

Metal bar went though his frontal lobe

Changed his personality

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66
Q

What is Broca’s Aphasia?

A 
Left frontal damage 
Causes impaired speech 
- grammar
- syntax
- word structure
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67
Q

What is Wernicke’s Aphasia?

A

Posterior temporal lobe damage

affects language comprehension

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68
Q

What is the associating cortex?

A

The most cortical area and is highly developed in man. Input from many sources

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69
Q

What is the left hemisphere responsible for?

A

Speech
Calculation
Analysis

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70
Q

What is the right hemisphere responsible for?

A

Spatial
Conceptual
Artistic

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71
Q

What are basal ganglia?

A

Neuronal cell bodies

Ganglia and nuclei are interchangeable terms

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72
Q

What diseases are related to faults in the basal ganglia?

A

Parkinsons
Huntingtons
Because they are important for movement and switching between tasks

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73
Q

Where are basal ganglia found?

A

Caudate and putamen
Globus pallidus
Subthalamic nucleus
Mesencephalon

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74
Q

What is the role of the limbic system?

A
  • Memory
  • Emotions
  • Motivation
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75
Q

What parts of the brain are involved in the limbic system?

A
  • Limbic lobe
  • Thalamus
  • Hypothalamus
  • Hippocampus
  • Amygdala
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76
Q

What are association fibres?

A

Link areas within a hemispheres

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77
Q

What are commissural fibres?

A

Connect between hemispheres

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78
Q

What are projection fibres?

A

Link to non-cortical areas

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79
Q

Examples of association fibres

A
  • Corpus callosum
  • Anterior commisure
  • longitudinal fasciculi
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80
Q

Name the brain ventricles

A
  • Lateral ventricles (right and left)
  • Third ventricles
  • Fourth ventricles
    https: //schoolworkhelper.net/ventricles-and-meninges/
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81
Q

What are ependymal cells?

A

A type of glial cells that line the cerebrospinal fluid filled ventricles and provide a supporting role

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82
Q

What is a neurone?

A

An excitable cell - will respond to an electrical impulse with an action potential

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83
Q

What is a glial cell?

A

A non excitable support cell

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84
Q

Give an example of a unipolar neurone

A

Dorsal root ganglia

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85
Q

Give an example of a bipolar neurone

A

Retinal bipolar cells

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86
Q

Give examples of multipolar neurones?

A
  • Motor neurones
  • Purkinje cells
  • Pyramidal cells
  • Cerebellar granule cells (axon branches of the dendrites)
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87
Q

Give an example of an oddity

A
  • Olefactory receptor and olefcatory granule cells (smell)
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88
Q

What are the main types of glial cells?

A
  • Macroglia
  • Microglia
  • Ependyma
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89
Q

Give some examples of macroglia cells

A
  • Astrocytes
  • Schwann cells
  • Oligodendrocytes
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90
Q

What is the difference between fibrous and protoplasmic astrocytes?

A

Fibrous - white matter and has many intermediate filaments

Protoplasmic - grey matter, shorter processes and few intermediate filaments

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91
Q

Give some specialised astrocytes

A

Retinal muller cells - columnar cells

Radial glia - span from playing to purkinje cells

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92
Q

Name the three roles of astrocytes

A
  1. Spatial buffering
  2. Neurotransmitter uptake
  3. Glucose metabolism
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93
Q

What is the spatial buffering? (astrocytes)

A

Spatial buffering regulates the [k+] as active neurones release k+ and astrocytes are very permeable to them
For example muller cells up take k+ in the retina to reduce [k+] near the photoreceptors.

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94
Q

How are neurotransmitters taken up in astrocytes?

A

Glutamate into astrocytes which is converted into glutamine and then recycled in neurones

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95
Q

How do astrocytes aid glucose metabolism?

A

Astrocytes store glycogen

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96
Q

Microglia facts

A
  • Short spikes processes
  • Wide distribution
  • Derived from circulatory monocytes
  • Function in phagocytosis
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97
Q

Name types of ependyma cells

A

Ependymocytes (majority)

Tanycytes

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98
Q

How many months into development does myelination begin?

A

5 months in human and 10 days postnatal in rats

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99
Q

When are the basic structures of the nervous system developed?

A

3 months

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100
Q

When are the primary vesicles developed?

A

6 weeks

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101
Q

How does the composition of myelin change in development?

A

Galactolipids increase

Protein components increase

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102
Q

At what age does myelination finish?

A

Mostly over by 2 years but some can continue into late teens

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103
Q

How does rubella affect a developing foetus?

A

Targets cells that are dividing at the time:

  • 6th week - cataracts
  • 9th week - deafness
  • 5th-10th week - cardiac malformation
  • 2nd trimester - CNS disorder
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104
Q

What are the symptoms of fatal alcohol syndrome?

A
  • Facial abnormalities
  • Microcephaly - smaller brain due ti loss of cells
  • loss of fibres
  • Disturbed migration
  • Irritability
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105
Q

What causes fatal alcohol syndrome?

A

Alcohol taken by mother is passed across the placenta

Foetus doesn’t clear alcohol very well so foetal levels are higher

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106
Q

How does drug abuse affect a developing foetus?

A

Opiates - foetus will become dependant
Cocaine - hypoxia, abortion, lower cognition
Ecstasy - long term effects on hippocampus
Cannabis - long term cognitive effects

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107
Q

When does the foetus feel pain?

A

Pain requires connection of receptors, sensory neurones, thalamus and cortex.

  • innervation of dermal skin from 28 weeks
  • Dorsal root ganglia connect to spinal cord from 8 weeks
  • Reflex responses from 23 weeks
  • connections from the thalamus to cortex from 24 weeks
  • Evoked potentials in the cortex from 29 weeks
  • Cortical repossess after 24 weeks
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108
Q

When does taste and smell develop?

A

They are well developed at birth
Evidence:
- Differentiate from mother/non mothers breasts
- Bottle fed babies prefer any lactating female

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109
Q

When is hearing developed?

A
  • Responsive at birth

- Excellent discriminators of language sounds

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110
Q

When does vision develop?

A
  • Vision not well developed at birth
  • Eyes open and sensitive from 7 months
  • Retinal cells sparse and not mature
  • optic nerves mot myelinated
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111
Q

How long does the stepping reflex last?

A

6 weeks

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112
Q

How long does the swimming reflex?

A

4-6 months

Not all babies

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113
Q

What is the babinski reflex?

A

Toes fan when sole is stroked
Adults cured toes
If toes fan in adults then descending motor tract damage

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114
Q

Does myelin surround all axons?

A

No - more non myelinated than myelinated

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115
Q

What glial cells produce myelin?

A

PNS - Schwann cells

CNS - Oligodendrocytes

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116
Q

How do Schwann cells and oligodendrocytes myelinate axons?

A

Schwann cells - membrane of Schwann cells wrapped around individuals axons
Oligodendrocytes - sends out processes and myelinate several axons at once

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117
Q

What is myelin made of?

A

Water - 40%
Dry lipid - 70-85%
Protein - 15-30%

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118
Q

Myelin in the PNS has less…..

A

cerebroside and sulfatide

CNS has more sphingomyelin

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119
Q

What are the the major proteins in myelin?

A

Myelin basic protein - shiverer mice - die early
Proteolipid protein - in Jimpy mutant mouse, there are is little myelin and severe loss of oligodendrocytes
Also enzymes and IG’s

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120
Q

What is multiple sclerosis?

A

An auto immune disease that causes primary demyelination disease. Macrophage and protease activity degrades myelin. Plaques develop

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121
Q

Who gets MS?

A

Onsets 20-40’s
More common in white females
30% concordance in identical twins - not all genetic

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122
Q

What treatments are available for multiple sclerosis?

A
  • Steroids
  • Interferons - target immune response
  • Haemopoietic stem cells
  • Diet - vitamin D
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123
Q

What is Guillan-barre syndrome?

A

An autoimmune disease that causes primary demyelination and occurs after a viral/bacterial infection

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124
Q

How does the nervous system allow an organism to react rapidly to its environment?

A
  • Electrical activity to allow neurones to receive and transmit signals
  • Chemical messengers between and within cells
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125
Q

What are the two types of electrical signals?

A

Action potentials

Graded potentials

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126
Q

What is the difference between an action and a graded potential?

A

Action potentials - fixed size, all or nothing signals, CAN pass either way but tend to go one one, coded by frequency
Graded potentials - variable size, pass both ways and are coded by size and vary according to the strength of a stimulus

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127
Q

Why do neurones have a resting potential?

A

Inevitable consequence of:

  • Selectively permeable membrane
  • Unequal distribution of charged molecules
  • Physical forces
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128
Q

What physical forces control ion movements in generation of an action potential?

A
  • Diffusion - from high to low

- Electrical current - positive to negative

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129
Q

How do you measure membrane potential?

A

Using a KCl electrolyte and a Cl electrode

Negative membrane potential is essential

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130
Q

What ion pumps are used in the generation of an action potential?

A

Ion channels set up ionic concentration gradients found in neurones

  • Na+/k+ ATPase
  • Ca2+ pumps
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131
Q

What is an equilibrium potential?

A

The membrane potential that would `be achieved in a neurone if the membrane was selectively permeable to that ion

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132
Q

How is the equilibrium potential for an ion calculated?

A

The Nernst Equation

do practice questions

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133
Q

The Goldman Equation

A

How you calculate resting membrane potential at equilibrium for k+ taking into account other ions such as Na+ (combined potentials)

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134
Q

What is the purpose of Na+/K+ pump in a resting potential?

A

Na+/K+ pump produces and maintains large K+ concentration gradient across neuronal membrane meaning at rest the membrane is highly permeable to K+ ions

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135
Q

What are the properties of the action potential?

A
  • Rapid and reversible change in membrane potential from negative to positive
  • All the same size and duration
  • Do not decrease as conducted down the axons
  • Different types of excitable cells may have different types of action potentials
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136
Q

What are the characteristic features of an action potential?

A
  • Resting membrane potential = -70mv
  • Depolarisation above threshold level
  • Repolarise and overshoots fall below threshold level
  • Action potential is triggered by Na+ permeability
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137
Q

What is the structure of the voltage gated Na+?

A
  • 6 transmembrane domains
  • Channels open in response to depolarisation
  • Concentration of charge near plasma membrane affects voltage sensors
  • Na+ channels inactivate in a time and voltage dependant manner
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138
Q

Name some poisons that affect the generation of action potentials?

A
  • Tetrodotoxins - inhibits voltage gated ion channels

- Lidocaine - inhibits Na+ channels - lethal

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139
Q

What factors influence conduction velocity?

A
  • How leaky the membrane is
  • Thickness of the axon - less resistance id the axon is bigger
  • Myelination - prevents current loss along an axon
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140
Q

Why are humans axons myelinated?

A

Because humans have a space constraint so the axons can’t be that large

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141
Q

Why aren’t all axons myelinated?

A

Energy and space constraint

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142
Q

What sized axons are myelinated?

A

Greater than 1 micrometer are usually myelinated

Small unmyelinated around 0.2-1.5 micrometers

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143
Q

Dendrites function

A

They have voltage sensitivite channels but don’t usually produce action potentials
Mostly encode information with graded potentials
Many dendrites can respond to the same stimulus - high intensity

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144
Q

What affects the intensity of a stimulus?

A

Action potential frequency

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145
Q

What type of potential can produce a higher intensity?

A

Graded potentials as they can summate

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146
Q

What are the two types of summation?

A

Spacial summation - multiple axons synapsing to the same place
Temporal summation - Multiple stimuli add together to create a response - one stimuli might not be enough to get move the threshold level

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147
Q

What are electrical synapses?

A

Connect two neurones that are dung the same thing

Exist in glial cells and in cardiac and smooth muscle

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148
Q

What is an EPSP?

A

Excitatory postsynaptic potential
More likely for a neurone to fire an action potential
Inhibitory inputs can stop EPSPs

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149
Q

What are the different types of synapse?

A
  • Axodendritic
  • Axosomatic
  • Axoaxomic (often inhibitory)
  • Dendrodendric - rarer
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150
Q

What is often used as a model to study synapses?

A

Neuromuscular junctions

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151
Q

Why are synapses needed?

A

Allows flow of information in different directions

Allows the processing of information that is complex elaborate and flexible

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152
Q

What is the difference between convergence and divergence?

A

Convergence - Cells can have many inputs

Divergence - Cells can send processes to multiple different cells

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153
Q

What are the standard features of chemical synapses?

A
  • Axon with a swelling
  • Secretory vesicles
  • Synaptic cleft with 20-50nm gap
  • Adhesion junction
  • Active zones where neurotransmitters are released
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154
Q

Active zones

A

Synapses can release neurotransmitters from more than one active zone
Large synapses usually have more active zones

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155
Q

Name the types of neurotransmitters

A

Amino acids - GABA, Glysiine
Biogenic amines - Dopamine, Serotinin, histamine
Neuropeptides - B - endorphin

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156
Q

List the steps in neurotransmission

A
  1. Synthesis of transmitters in presynaptic cells
  2. Stored in lipid bound bags
  3. Release of transmitters into synaptic cleft
  4. Post synaptic effect
  5. Inactivate of transmitter to terminate the cell-cell communication
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157
Q

How are neurotransmitters synthesised and stored?

A

Neuropeptides are made by ribosomes and transported in secretory granules to the active zone where they are stored away from the membrane so they don’t fuse with the membrane
Also kept close enough for rapid release

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158
Q

How are neurotransmitters released from the pre synaptic membrane?

A
  • Presynaptic membrane is depolarised by action potential causing an influx of Ca2+ though voltage gated Ca2+ channels
  • Causes restructure of docking the synaptic vesicle causing it to fuse with me membrane
  • Exoctosis
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159
Q

What is the quantal effect?

A

Synaptic vesicles contain 35-30nm of neurotransmitters

Synaptic vesicles are of a similar size so they can be considered as 1 quanta

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160
Q

What are the main types of receptors in the synapse?

A
  • Ligand-gated ion channel

- G-protein coupled receptor - slower transmission

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161
Q

How is an EPSP generated?

A

Na+ channels open
Generates an excitatory post synaptic potential (EPSP)
Individual may not be enough to reach threshold level so summation may occur

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162
Q

How is an IPSP generated?

A

Cl- channels open
Generates a inhibitory post synaptic potential
Hyperpolarises membrane making it harder to reach threshold - less chance of action potential

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163
Q

How is the transmission of an action potential terminated?

A
  1. Post synaptic break down
  2. Diffuse away
  3. Reuptake by postsynaptic terminal
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164
Q

What are the differences between chemical and electrical synapses

A
  • Chemical allows more types of communication
  • Chemical has more flexibility
  • chemical signals of different types being released from a stimulating neurotransmitters
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165
Q

What are the criteria for neurotransmitters?

A
  • Present in presynaptic terminals
  • Released in response to stimulation
  • Able to interact with postsynaptic receptors
  • Rapidly removed from the synapse
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166
Q

What are the characteristics of amino acid and amine neurotransmitters?

A
  • Small molecules
  • stored and released from synaptic vesicles
  • Activate both ligand gated channel receptors and G coupled receptors
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167
Q

What are the characteristics of peptide neurotransmitters?

A
  • Large molecules
  • Stored in secretory granules
  • Only activate G coupled receptors
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168
Q

What is Dales principle?

A

A single neurone has only one transmitter

he was wrong

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169
Q

What is the role of glutamate as a neurotransmitter?

A
  • Binds to various receptors eg. NMDA and AMPA

- AMPA important in fast transmission

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170
Q

What is the most common excitatory transmitter in the CNS?

A

Glutamate

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171
Q

Why do NMDA receptors have to be indirectly activated by another transmitter?

A

Because they have a voltage dependant Mg2+ block

When partially depolarised Mg2+ moves out

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172
Q

What is the most common inhibitory transmitter in the brain?

173
Q

How is GABA formed and where is it found?

A

Glutamate –> GABA using the Glutamic acid decarboxylase enzyme
Found mainly in the cortex and the striatum

174
Q

What happens if there is too much or too little GABA?

A

Too much - Coma

Too little - seizures

175
Q

How does presynaptic inhibition occur?

A

Action potential arrives at neurone causing the release of GABA. This inactivated Ca2+ channels and therefore reduces neurotransmitter released reducing its affect on the post synaptic neurone
One neurone surpasses the action of another

176
Q

How do anxiolytic drugs work?

A

e.g.. alcohol, benzodiazepine

bind to GABA receptors and stimulate its response to GABA

177
Q

What happens due to the loss of GABA receptors?

A

Panic attacks

178
Q

How do opiates have an effect?

A

They bind to opiate receptors in the brain that are present due to natural opiates in the body such as endorphins

179
Q

Where are opiate receptors present?

A
  • Spinal - block pain
  • Amygdala - regulates emotion
  • Frontal cortex - Cognitive
  • Brain stem - depress respiration and cough reflex
180
Q

What type of receptors are opiate receptors?

A

G coupled receptors

181
Q

Name some therapeutic uses of opiates

A
  • Analgesia - reduces perception to pain
  • Intestinal disorders - deceases dehydration
  • Antitussive - cough suppressant
182
Q

Problems with the use of opiates

A
  • Tolerance and dependancy
  • Euphoric effects are linked
  • Relieve dull visceral pain better than sharp pain
  • Analgesia (inability to feel pain) and dependence liability
183
Q

What are the common features of the diffuse modulatory systems of the brain?

A

Core nuclei in the central part of the brain. The neurones may contact large numbers of postsynaptic neurones

184
Q

What neurotransmitters are involved in the diffuse modulatory systems?

A

Catecholamines
Serotonin
ACh

185
Q

Where in the brain is ACh found?

A
  • Autonomic nerves
  • Neuromuscular junction
  • Basal forebrain
  • Hippocampus
186
Q

Name some examples of things that prevent the release of ACh

A
  • Botulism - botox

- Black widow spider

187
Q

Name some AChE inhibitors?

A
  • Nerve gas
  • Insecticides
  • Alzheimers treatments - not much success
188
Q

What are the catecholamine systems?

A

Regions of the nervous systems associated with movement, mood, attention, visceral function

  • Dopamine system - ‘Pleasure centre’
  • Noradrenaline system - memory, anxiety
189
Q

How are catecholamines synthesised?

A

Tyrosin –> dopa –> Dopamine –> Norepinephrine –> Epinephrine

190
Q

How many people does Parkinson’s disease affect?

A

1 in 200 world wide

191
Q

What are the symptoms of Parkinson’s disease?

A
  • Tremor
  • Rigidity
  • Akinesia (loss of voluntary movement)
  • Postural changes
  • Slurred speech
  • No sensory loss
  • Normal cognitive function
192
Q

What part of the brain is affected by Parkinson’s disease?

A

Dopamine containing areas of the brain are lost

193
Q

What is the function of the striatum?

A

Inhibits motor function

194
Q

What is the role of dopamine in the striatum?

A

It inhibits cells of the striatum (decreasing their inhibitory action). In Parkinson’s disease this inhibition is lost from dopamine meaning an increase in motor function

195
Q

Name some drugs that increase dopamine levels

A
  • L-Dopa
  • Amphetamine - increases release
  • Cocaine - blocks reuptake
  • MAO inhibitor
  • D2 agonists
196
Q

What are the problems with the long term uses of L-Dopa as a treatment for Parkinson’s?

A
  • The drug becomes ineffective

- Can lead to chronic L-Dopa syndrome which can cause sudden immobility

197
Q

What are the disadvantages of taking antagonists on dopamine?

A

Dopamine inhibits the production of prolactin and antagonists may results in its overproduction - can cause lactation in males and females

198
Q

How are catecholamines removed?

A
  • reuptake into presynaptic terminals
  • Metabolised by COMT - in the cytoplasm and by MOA - on outer mitochondrial membranes
    MOA -A - noradrenaline
    MOA -B - dopamine
199
Q

What are MOA inhibitors used as treatments for?

A
  • Depression - increase NA

- Parkinsons - increase DA

200
Q

What are the functions of serotonin (5-HT)?

A
  • Arousal
  • Cardiac rhythms
  • Mood
  • Aggression
201
Q

Name some treatments of depression?

A
  • Tricyclics - block uptake of NA and 5 -HT
  • SSRI’s - inhibit serotonin reuptake
  • MOA - A inhibitors
202
Q

What type of receptors are classified based on their modality?

A

Chemo, thermo, mechano

203
Q

What type of receptors are classified based on their origin?

A
  • Interoceptors - internal organs, visceral pain
  • Proprioreceptors - muscles, tendons, joints
  • Nociceptors - Hugh threshold mechano and thermoreceptors
  • Exteroceptors - vision, hearing, touch
204
Q

What type of information do all sensory receptors transmit?

A
  • Modality
  • Location
  • Intensity
  • Duration
205
Q

What is sensory modality?

A

What is perceived after a stimulus

- eg. vision, taste, smell, hearing

206
Q

How is location transmitted by a sensory receptors?

A

Through receptive fields and projection pathways to CNS:

  • stimuli diverge an converge at different synapses
  • lateral inhibition occurs
207
Q

What is the function of inhibitory synapses?

A
  • Prevent unrestricted spread of excitation
  • descending inhibition - higher control - block transmission to concentrate on other stimuli
  • feedback inhibition - gain adjustment
  • lateral inhibition - block neurone next to it - e.g.. increases contrast in the eye
208
Q

How is intensity transmitted in sensory receptors?

A
  • Increases frequency of stimuli = higher intensity
  • Recruitment of more neurones
  • Low threshold fibres for weak stimuli
209
Q

How is duration transmitted in sensory receptors?

A

Phasic receptors - burst, fast adaption (response quickly diminished)
Tonic receptors - slow adaption (produces action potential for long time)

210
Q

Define sensory transduction

A

Conversion of sensory information from one form to another

211
Q

What are receptive fields?

A

Particular region that will cause the firing of a neurone in response to a stimuli eg. body surface (back, fingers)

212
Q

How does sensory transduction occur?

A
  • Stimulus induces local change in membrane permeability
  • Ions flow across the membrane
  • Receptor generates a potential
  • Release of neurotransmitter onto nerve
  • Burst of action potentials from nerve
213
Q

What wavelength is visible light?

214
Q

What are the three layers of the eye?

A
  • Tunica fibrosa
  • Tunica vasculosa
  • Tunica interna
215
Q

What is the tunica fibrosa layer of the eye?

A

The partly transparent collagen layer that surrounds the eye and stops it from bursting when the pressure increases

216
Q

How is the tunica fibrosa layer of the eye transparent?

A

The cornea has to be transparent to allow us to see and it does this by undergoing apoptosis but not enough to actually kill the cells

217
Q

What is the tunica vasculosa layer of the eye?

A

Layer of choroid (full of blood vessels) for nutritional support
Ciliary body
Iris

218
Q

What is the tunica interna layer of the eye?

A
  • Retina

- Optic nerve - papilla and lamina cribrosa

219
Q

What is the role of ciliary body in the eye?

A
  • The ciliary body secretes fluid into the anterior and posterior chambers. The canal of schlemm drains the fluid. The rate of secretion and drainage needs to be equal in order to maintain the pressure.
  • The fluid also provides nutrients required for the lens and the cornea
220
Q

What is the most important part of the eye in forming an image and why?

A
  • Lens - best refractive index of 1.41

However cornea and aqueous humour have similar refractive indexes (around 1.34)

221
Q

What are the most common causes of blindness?

A
  • Cataracts - clouding of lens - treatable with laser eye surgery
  • Glaucoma - increases eye pressure leads to retinal degeneration
222
Q

What is the role of the iris in the eye?

A

Regulates light level

- Pupils constrict and dilate using smooth muscle

223
Q

What is the photopupillary reflex?

A

If you illuminate one eye the other will constrict as well

- responds to a change in intensity

224
Q

Why is the photopupillary reflex tested after an accident?

A

To check that the connection with the CNS is undamaged.

  • The optic nerve goes to the pre-tectal region in the pons
  • Feedback loop back to the iris by ciliary nerves leading to the reflex
225
Q

What occurs in the eye in the near response?

A
  • Convergence - eyes move together
  • Miosis - constriction of the pupils
  • Lens accommodation - ligaments pull and distort shape or the lens so the eye can focus
226
Q

Why do animals have the photoreceptive rod and cone cells at the back of the eye?

A

So that it is close to the pigment epithelium which contain phagocytes - which breakdown damaged photoreceptors and allow its repair

227
Q

How are rod and cone cells structured in the eye?

A

The majority of the cell in a line below the pigment epithelium and then all of the nuclei are in a layer below that together

228
Q

What are the four lingual papillae on the human tongue?

A
  • Filform
  • Foliate
  • Fungiform
  • Valiate
229
Q

What are the characteristics of the filiform on the tongue?

A
  • Spiked
  • No taste buds
  • Texture
  • Most abundant
230
Q

What are the characteristics of the foliate on the tongue?

A
  • least abundant

- gone by 2-3 years of age

231
Q

What are the characteristics of the fungiform on the tongue?

A
  • 3 apical taste buds

- tip and sides of tongue

232
Q

What are the characteristics of the villate on the tongue?

A
  • Large
  • back of tongue
  • contains about half of the taste buds
233
Q

How many taste buds are there?

234
Q

What parts of the tongue are associated with particular tastes?

A
  • sweet - tip of tongue
  • salty and sour middle of the side of the tongue
  • texture -middle
  • bitter at the back
235
Q

Why are the bitter taste buds located at the back of the tongue?

A

To activate the gag reflex as many toxic substances taste bitter

236
Q

Why are the sweet sour and umami taste buds located near the front of the tongue?

A

Because salty foods contain essential electrolytes (Na and K), sweet foods are high in energy, sour foods are often things like citrus fruits and umami foods like meat contain essential amino acids

237
Q

Why does the salt pathway differ to sweet and umami?

A

Salt can transform from appetite stimulus to an aversive one. This allows the regulation of salt intake
- High salt can activate the bitter and sour pathways to stop you from any more intake

238
Q

How many odours can be detected in the olfactory system?

239
Q

Does the olfactory system adapt quickly or slowly to a stimulus?

A

Quickly by synaptic inhibition

240
Q

How does sensory transduction in the olfactory system occur?

A
  • Odorant binding proteins in mucus binds to odorant receptor
  • cAMP is the second messenger
  • Opens Na+ and Ca2+ channels allowing an action potential
    The nerves are unmyelinated
241
Q

What is the olfactory bulb?

A

An extension of the brain from the cerebrum that drops nerves into the nasal cavity

242
Q

What does the amplitude of a sound wave convey?

A

Sound intensity

243
Q

What is the range of human hearing?

A

20-20000Hz

244
Q

What is the speech range of hearing?

245
Q

What is the benefit having two ears?

A

Localises sound - by calculating the delay of sound between the two ears:
- distance between ears/speed of sound = 1/2ms delay

246
Q

What bones are present in the middle ear?

A
  • Malleus
  • Incus
  • Stapes
247
Q

What is the purpose of the middle ear?

A

To focus sound - focuses large amount of sound in a small area

248
Q

Why is there a long coiled basilar membrane in the cochlea?

A

To know the frequency - high if one end vibrates and then low if the other vibrates

249
Q

What is the basilar membrane?

A

The membrane in the cochlea containing the nerves and collagen hair cells

250
Q

What is the organ of corti?

A

Part of the cochlea situated on the basilar membrane and has hair cells protruding from it

251
Q

What is the role of tip links on hair cells?

A

Tip links connect the stereocilia on hair cells together causing them to move together. When hair cells move, the tip links stretches and open K+ channels.

252
Q

What are stereocilia made of?

253
Q

How do hair cells transduce an action potential?

A
  • Vibration from sound causes seterocillia on hair cells to move opening K+ channels
  • K+ moves into the hair cells causing it to depolarise as its resting potential is -70mv
  • Causing action potential
254
Q

What is special about the endolymph section of the cochlea?

A

K+ rich - surrounds organ of corti - providing the K+ that enters the hair cells

255
Q

What is the role of the outer (jumping) hair cells?

A

The inner ear amplifier - it increases the threshold of activity in the basilar membrane allowing to to be amplified and tuned

256
Q

What is the role of the inner hair cells?

A

Primary receptors - receive most of the sensory innervation

257
Q

What is the role of the spiral ganglion?

A

The nerve innervating the hair cell

258
Q

Why is there only one spiral ganglion to one hair cell?

A

No convergence (unlike retina) to maintain the resolution

259
Q

How is a range intensity shown in the ear?

A

Multiple nerves with different thresholds on a single hair cell. One threshold might be met by the action potential but the next might not be

260
Q

What is the role of efferent mediated innervation in the ear?

A

Modifies amplifiers - temporarily lowers thresholds so that the hair cells are less sensitive - a form of proctection

261
Q

What parts of the brain are used to put frequency, intensity and amplification of sound put back together?

A
  • Cochlea nuclei - contains the fastest synapse
  • Superior olivary complex - sound localisation and intensity
  • Inferior colliculus - responsible for reflexes
  • primary auditory cortex
262
Q

What are some differences between auditory system and vestibular system?

A
  • Hair cells are much longer in vestibular

- Modified tectorial membrane called cupulla in vestibular

263
Q

What is the vestibular - ocular reflex?

A

It allows the eye muscles to compensate for head movement

264
Q

What is nystagmus?

A

Constant involuntary movement of the eyes

265
Q

What are the first cells that light hits?

A
  • Ganglion cells
  • Bipolar cells
  • Then photoreceptors (rod and cone cells)
266
Q

What are the differences between rod and cone photoreceptors?

A 
Rod:
- Scotopic - high sensitivity to light
- High convergence - many receptors into one nerve
- Low resolution
- 500nm
Cone:
- Photopic - low sensitivity
- low convergence
- high resolution 
- 420 - 558nm
267
Q

What is the role of ganglion cells in the eye?

A

Main output from retina surface to optic nerve

268
Q

What is the role of horizontal and amacrine cells in the eye?

A

Attach to bipolar cells at the end of processes and do lateral inhibition to allow contrast

269
Q

What is duplicity theory?

A

You can’t have high sensitivity and high resolution in the same receptor. This is why there are separate systems for colour and monochrome systems

270
Q

Are there more rod or cone cells to each optic nerve fibre?

A

Many rod cells to one optic nerve fibre but only one cone cell

271
Q

What are the photopigments in rod and cone cells?

A

Rods - rhodopsin

Cones - Photopsin (red, green, blue)

272
Q

What are the steps in phototransduction?

A

Rhodopsin binds with transducin GTP activating phosphodiesterase causing hydrolysis of cGMP closing the Na+ channels (in the light)
Ca2+ decreases causing the opening of Na+ channels (in the dark)
Glutamate released

273
Q

What happens in ON bipolar cells?

A
  • Glutamate inhibits ON bipolar cells and causes hyperpolarisation in the dark
  • Meaning no signal to the ganglion cells
  • Produces IPSP
274
Q

What happens in OFF bipolar cells?

A
  • Glutamate excites OFF bipolar cells and causes depolarisation in the dark
  • Produces EPSP
275
Q

What is the most common type of cone cell?

A

Red - 64%
Green - 32%
Blue - only 4% - must be the most sensitive

276
Q

What are the types of retinal ganglion cells?

A
  • W type (mainly from rods)
  • X type (mainly from cones)
  • Y type (inputs less types)
  • Melanopsin RGCs
277
Q

What is reflex?

A

A rapid involuntary, yet stereotyped and co-ordianted response to a sensory stimulus

278
Q

Give the characteristics of spinal reflexes?

A
  • Require stimulation
  • Are quick
  • involuntary and automatic
  • stereotyped - occur the same way each time
279
Q

What is the patellar reflex?

A
  • stimulus = tap on the knee
  • response = leg kick
  • travels through dorsal root ganglia to the spinal chord
  • Monosynaptic - one synapse involved
280
Q

What is the stretch (myotactic) reflex?

A
  • important in maintaining body posture
  • reciprocal inhibition - motor neurones contract bicep at the same time as interneurons relaxing triceps
  • e.g. pouring a drink and keeping the glass up right
281
Q

What is the muscle spindle?

A

A proprioceptor - a sense organ that monitors position and movement
Found in most striated muscle and are abundant in muscles involved in fine motor control

282
Q

Define proprioception

A

The sense of the position of parts of the body relative to other parts

283
Q

Waterman had a viral infection that caused loss of proprioceptors, what did this do?

A

He was unable to coordinate movement - he taught himself to move again by visually monitoring his actions. If dark he can’t do this

284
Q

What is the difference in function between the Golgi tendon organ and the muscle spindles?

A

Muscle spindles detect muscle tension due to stretching but GTO detect muscle tension due to contraction

285
Q

What is the Golgi tendon reflex?

A

It is a negative feedback circuit that regulates muscle tension and protects the muscle from damage when a large force is generated

286
Q

What is the flexor reflex?

A

The quick contraction of flexor muscles to withdraw a limb from an injurious stimulus
- polysynaptic reflex despite it being quick

287
Q

What is the parallel after-discharge circuit?

A

Stimulus activates multiple pathways with different number of synapses to cross to reach response
Will take different times for it to pass creating a response for a continuous period

288
Q

What are used to relax extensor muscles in the flexor and stretch reflexes?

A

Excitatory interneurones

289
Q

What is the crossed extensor reflex?

A

provides postural support for another response

eg. in flexor reflex, rapid withdrawal of a leg will result in the extension of the other leg to maintain the balance

290
Q

What are central pattern generators?

A

Local circuits produce a pattern of alternating flexion an extension caused by inhibition across the midline

291
Q

Give an example of a central pattern generator?

A

Animals walking repeatedly, extending an flexing the legs. If spinal cord cut then co-ordiaton between the limbs continue

292
Q

What is the role of meissner (tactile) corpuscles?

A

A sensory receptor whos modality is light touch, texture and is very sensitive
Found in lips, palms

293
Q

What is the role of pacinian corpuscles?

A

Sensory receptor whos modality is eep pressure, vibration

Found in dermis, joint capsules

294
Q

What is the role of ruffuni corpuscles?

A

Sensory receptor whos modality is heavy touch, pressure

Found in dermis, joint capsules

295
Q

What is the role of Merkel (tactile) discs corpuscles?

A

Sensory receptor whos modality is light touch, texture, edges
Found in superficial skin (epidermis)

296
Q

What is the role of free nerve ending corpuscles?

A

Sensory receptors - modality is pain, heat

Found in epithelia

297
Q

What is the difference between a rapidly adapting response (phasic) and a slowly adaptive response (tonic)?

A

A rapidly adapting gives info about changes in stimuli as stimuli quickly stops
A slowly adapting gives info about the persistence of the stimulus as the receptors continue to respond

298
Q

How are primary afferent axons classified?

A

According to conduction velocity (faster larger diameter)

299
Q

How are axons coming from the skin and muscle classified differently?

A

Axons coming from skin are classified by letters and sub classified by greek letters
Axons coming from muscle are classified by Roman numerals

300
Q

How are cell bodies organised in the dorsal root ganglia?

A

The cell bodies of sensory neurones are grouped based on function in the DRG and their projections are in layers in the dorsal horn

301
Q

What is the Medial Lemniscal tracts?

A

One of the two routes that sensory information moves through to get to the brain
- Carry mechanoreceptive and proprioceptive signals to the thalamus

302
Q

What is the Spinothalamic tract?

A

One of the two routes that sensory information moves through to get to the brain
- Carries pain and temperature signals to the thalamus

303
Q

What is the role of the three neurones that sensory information travels through to reach the brain?

A
  • First-order neurones detect the stimulus and transmit to the spinal cord
  • Second-order neurones relay the signal to the thalamus - gateway to the cortex
  • Third-order carry the signal from the thalamus to the cortex
304
Q

Are 1st, 2nd and 3rd order axons for upper and lower body lateral or medial as they move up the medial lemniscal system?

A
  • In 1st order axons from the upper body - lateral and from lower body - medial (closest to the midline)
  • 2nd order - they cross the midline and swap over (upper is medial)
  • 3rd order - they cross over each other again returning their topology to original (upper is lateral and lower is medial)
305
Q

What does the axons pathways in the medial lemniscal system?

A

A topographic map

306
Q

What is a dermatome?

A

Each sensory ganglion innervates a specific region of skin called a dermatome

  • can be used clinically to see CNS damage
  • develop from a somite in an embryo
307
Q

What is a receptive field?

A

The area that a sensory neurone can receive a stimulus

308
Q

How can you measure the size of a receptive field?

A

If a person can differentiate between two small sharp points close together then they are different receptive fields

309
Q

Which parts of the body has larger/smaller receptive fields?

A

Finger tips - small - more precision

Arms/legs - large

310
Q

Is the cortical representation proportional to the physical size of the body part?

A

No hands in humans have large cortical representation but aren’t that large same for whiskers in some mammals
However they are linked to the behavioural significance of the area

311
Q

Why does pain differ to the other senses?

A

Because it’s behavioural and not actually physical

312
Q

Why is pain essential for survival?

A

Because without it, the individual would not know that what they were doing or experiencing was damaging them

313
Q

What are the two theories of pain?

A
  • Specificity theory

- Convergence theory

314
Q

What is the specifiicity theory?

A

Says that pain is a distinct sensation that is transmitted by specific receptors to pain areas in the brain

315
Q

What is the convergence theory?

A

Says that pain is an integrated plastic state represented by a pattern of convergent somatosensory activity within a distributed network

316
Q

What are nociceptors?

A

Afferents with free nerve endings - pain receptors

317
Q

Give an example of evidence for nociceptors as a receptor for pain?

A

Thermoreceptors are stimulated at a low temperature. As the temperature rises (stimulus increases) nociceptors start to become active - feel pain

318
Q

What is the difference between fast and slow pain?

A
  • Fast pain is sharp and immediate and can be mimicked by stimulation of Adelta nociceptors
  • Slow pain is more delayed and longer lasting and can be mimicked by stimulation of C nociceptors
319
Q

What is a molecular pain receptor?

A

A specific molecular receptor associated with nociceptors nerve endings that are activated by heat

320
Q

Give an example of a molecular pain receptor

A

The capsaicin receptor (TRPV1) - activated at 45ºc and by capsaicin ( a component in chilis)

321
Q

What are the two components in the pathways carrying nociceptive info to the brain?

A
  • Sensory discriminative (signals location and intensity)
  • Affective - motivational
    (signals unpleasantness)
322
Q

What does the activity in the cortex indicate about pain?

A

That this region of the cortex does respond to a painful stimuli and that the response correlates to the intensity of pain

323
Q

What parts of the brain are involved in the pain response as shown on an MRI?

A
  • A painful stimuli activates the same region of the cortex that is activated by a non painful stimuli in the same place of the skin
  • Parts of the insula and cingulate cortex are also activated - they are connected to the limbic system
  • Limbic system is known for emotional responses
324
Q

What are some problems with the specificity theory?

A
  • Pain perceived is not always proportional to intensity of stimuli
  • Phantom limbs
  • Placebo effect
  • Modulation by other stimuli
  • Referral of pain from viscera to skin
325
Q

Define hyperalgesia

A
  • Increased response to a painful stimulus

e. g. hypersensitivity in an area that has already been damaged like pricking sunburnt skin

326
Q

Define allodynia

A
  • Painful response to a normal innocuous stimulus

e. g. touching sunburnt skin

327
Q

What causes hyperglasia?

A

When skin is damaged inflammatory substances are released which increases sensitivity of nociceptive molecular receptors as the threshold for nociceptors has lowered

328
Q

What is the role of prostaglandins in central sensitisation (pain lecture)?

A
  • Lower the threshold for action potential generation so cause hyperglasia
  • Can also cause neurones to become sensitive to non nociceptive inputs - allodynia
329
Q

What is hyperpathia (in pain lecture)?

A

Axonal loss causing the detection threshold to increase meaning that when it is detected it is very large resulting in an explosive pain

330
Q

What is a phantom limb?

A

Amputees can feel the limb even though it is not there and can even feel pain in it.
Attempts to block pain do not work

331
Q

What is referred pain?

A

When damage in the viscera is perceived from coming from an area of the skin depending on what organ is affected
- e.g. pain in left arm when having a heart attack

332
Q

What is procedural memory?

A
  • Skills and associations largely unavailable to conscious mind e.g. motor learning
333
Q

What is declarative memory?

A
  • Available to the conscious mind can be encoded I’m symbols an language
334
Q

What is the duration of the different types memory?

A
  • Immediate memory - few seconds
  • Short -term memory - seconds or minutes
  • Long-term memory - days, months, years
335
Q

What are the important structures of the brain involved in memory?

A
  • Pre-frontal cortex
  • The hippocampus (essential for converting short term memory to long term memory)
  • Amygdala (multiple processed sensory inputs)
  • Cerebellum (sensorimotor)
336
Q

What can hippocampal lesions lead to?

A

Memory loss and unable to form new memories

337
Q

Why does synapse strength change?

A
  • They have plasticity
  • Facilitation - stronger with stimulus
  • Depressions weaker with stimulus
  • Ca2+ availably affects its plasticity
338
Q

Define long term potentiation

A
  • The increasing strength of a synapse
339
Q

How is a long term potentiation used to create an association?

A

The long term potentiation pathway is stimulated at the same time as as a cell producing a strengthen response e.g. pavlovian dogs

340
Q

What is habituation?

A

The diminishing of an innate response due to a repeated stimulus

341
Q

What is short-term sensitisation?

A

Repeated gentle stimuli causing habituation

Response returns after a short period of time

342
Q

What is long-term sensitisation?

A

Repeated stimuli which causes long term habituation

343
Q

What do long term potentiation, long term depression and short and long term sensitisation require?

A
  • Receptor activation
  • Altered synaptic responsivity
  • Require protein phosphorylation changes in early stages
  • Require protein synthesis for late stages
344
Q

What pathologies affect memory?

A
  • Amnesia
  • Head injury, tumour surgery
  • Alzheimers
345
Q

What is different about an Alzheimers brain?

A
  • Enlarged temporal horns
  • Senile plaques
  • Tangles - protein phosphorylation
  • Loss of cells
346
Q

What is Kluver-Bucy syndrome?

A
  • Amygdala lesions

- symptoms: visual agnosia, hyperorality, hypersexuality, hyperphagia

347
Q

What is the Hebbian synapse concept?

A

Suggests that synapses are actively modifiable (plastic) allowing them to change as new memories form

348
Q

What type of motor neurones are responsible for all movements by skeletal muscles?

A

Lower motor neurones

349
Q

What is a central pattern generator?

A

When the spinal cord generates complex behaviours without the input from the brain

350
Q

What is the primary motor cortex?

A

Gerentes the electrical impulses that cause the contraction of the contralateral body muscles (motor control)

351
Q

What type of motor neurones are responsible for motor function?

A

Upper motor neurones

352
Q

What is a motor pool?

A

Where the cell bodies of motor neurones lie

353
Q

How are motor pools organised?

A

Somatotopically - point of the body corresponds to a specific part of the spinal cord. Motor pool made up of the cell bodies from all the neurones that innervate a particular muscle

354
Q

What do motor cortex upper motor neurones primarily control?

A

Fine control of more distal structures

355
Q

What do brainstem upper motor neurones primarily control?

A

Control with postural movement

356
Q

What layer of the cortex are responsible for motor input and motor output?

A

Input - layer 4 (Internal granula)

Output - layer 3 (external pyramidal)

357
Q

What are the difference between upper motor neurones of the motor cortex and of the brainstem?

A

Motor:
- voluntary movements
- Contralaterally - e.g. praises limb movements
Brainstem:
- Maintenance of posture and balance
- Located it several nuclei e.g. reticular formation

358
Q

What s the difference between upper and lower motor neurones?

A

Upper - always synapse on lower motor neurones

Lower- always synapse on muscle fibres

359
Q

What is the anticipatory mechanism?

A

When the body preadjusts its posture in order to compensate for forces generated from another movement

360
Q

What is motor neurone disease?

A

A degenerative disease of the motor neurones

361
Q

What is the difference between upper and lower motor neurone disease?

A 
Lower 
- Muscle weakness/paralysis
- Loss of stretch reflexes
- Muscle atrophy
-Usually die from lung dysfunction
Upper
- Muscle weakness
- Spasticity
- Hyperactive reflexes
- Loss of fine voluntary control
usually die from tongue and pharynx involvement
362
Q

What is the role of the basal ganglia in movement?

A

Regulates the function of the upper motor neurones - motor loop

363
Q

What are the basal ganglia composed of?

A
  • Caudate/Putamen (striatum)

- Globus pallidus

364
Q

How does the basal ganglia initiate movement?

A
  • The striatum activates the Globus Pallidus which inhibits VLo. Inputs from many cortical regions converges on the striatum
  • When activated by this the striatum inhibits the Globus Pallidus releasing the VLo to activate and initiate movement
365
Q

What causes Huntington disease?

A

Due to the degeneration of the striatum and leads to hyperkinesis

366
Q

What causes Parkinson’s disease?

A

Due to the degeneration of the substantial nigra and leads to hypokinesis

367
Q

What is the roll of the cerebellum in movement?

A
  • Detects and corrects differences between intended and actual movement - motor error checking
368
Q

What are the two types of routes for cortical control of lower motor neurones?

A
  • Direct - activation of voluntary movement direct to spinal cord
  • Indirect - anticipated by indirect projection via reticular formation to muscles
369
Q

What does EEG stand for?

A

Electroencephalogram

370
Q

What field potentials are used in an EEG?

A

20-100microV

371
Q

Does an EEG have good resolution?

A
  • Poor spatial resolution

- Good temporal resolution

372
Q

What does an MEG do?

A

Measures the magnetic field evoked by current flow

373
Q

What type of rhythm do relaxed awake individuals with their eyes closed show from an EEG?

A

Alpha rhythm - 8-13Hz

374
Q

What type of rhythm do aroused awake individuals with their eyes open show from an EEG?

A

Beta rhythm - 14-25Hz

375
Q

What is gamma rhythm in an EEG?

A

Normal wake individuals show it with eyes open and shows intermittent bursts of synchronous 30-80Hz in sensory and motor regions

376
Q

Give examples of regional variations in alpha rhythms

A

Kappa - alpha like in auditory cortex
Nu - alpha like in sensorimotor cortex e.g.. Mirror neurones (electrical activity when watching someones elves movements)

377
Q

What are mirror neurones?

A

Electrical activity when watching someones elves movements

Lack of mirror neurones could be related to autism

378
Q

What is theta rhythm in an EEG?

A
  • Early stage sleep
  • 4-8Hz
  • Found in children and frustrated adults
  • Spatial memory tasks
379
Q

What is REM sleep?

A

Random eye movement sleep - dream sleep

380
Q

What are the stages of non-REM sleep?

A

Stage 1: alpha rhythm slows, drowsy
Stage 2: sleep spindles, light sleep
Stage 3: Higher amplitude, lower frequency, slowing
Stage 4: delta waves - High amplitude low frequency less than 4Hz, deep sleep - sleep walking can occur in this stage

381
Q

What are the roles of non-REM sleep?

A
  • Restorative

- Loss evokes homeostatic break down (takes weeks in animals)

382
Q

What animals have REM sleep?

A

Mammals and young birds

Reduces with age

383
Q

What is the role of REM sleep?

A

Laying down of memories
Dream sleep
Deprivation doesn’t have much affect, maybe an increase in irritability

384
Q

What parts of the brain are used to control sleep?

A
  • Reticular activating systems (brain stem regions)
  • Hypothalamus
  • Basal forebrain
  • Pineal gland
  • Cortex
385
Q

What is the role of the hypothalamus in the control of sleep?

A

Secretes hypocretin

Decrease in this compound can lead to narcolepsy

386
Q

What is the role of the pineal gland in the control of sleep?

A

Secretes melatonin which influences the sleep/wake cycle

  • Secretion is affected by light levels
  • Serotonin in the day and melatonin at night
387
Q

What are the symptoms of Parkinson’s disease?

A
  • Decrease in spontaneous movements
  • Gait difficulty
  • Postural instability
  • tremor
  • initiation/termination of movements very difficult
388
Q

What causes Parkinson’s disease?

A

Degeneration of the pigmented neurones in the substance nigra of the brain, resulting in decreased dopamine availability

389
Q

How common is Parkinson’s disease?

A

1-2% of the population

Increases after age of 60

390
Q

What are the treatments for Parkinson’s disease?

A
  • Ca voltage channel blockers - reduces over excitation that causes loss of dopamine producing cells
  • Transplantation, stem cells
  • Smart stimulators
391
Q

What are the symptoms of Huntington’s disease?

A
  • Progressive
  • Hyper/dyskinesias
  • Akinesia and dystonia
  • Dementia
392
Q

What causes Huntington’s disease?

A
  • Striato -GPe and striato-gli neurones die followed by more neurodegeneration
  • Associated with nuclear and cytoplasmic inclusions containing mutant Huntingtin
  • Increase in CAG repeats in Huntingtin gene
393
Q

What are the treatments for Huntington?

A
  • Memantine
  • Tetrabenazine
  • Deep brain stimulation
  • RNA interference
  • Stem cell transplantation
394
Q

What are the symptoms of schizophrenia?

A
  • Positive (extra things that experienced)-
    hallucinations, delsions
  • Negative - Flat affect, alogia, anhedonia (not outgoing)
  • Often associated with depression, substance abuse and suicide
395
Q

What are the causes of schizophrenia?

A
  • Increased levels of dopamine
  • 50% concordance in momozygotic twins
  • substance abuse - cause or effect??
  • infection in utero
396
Q

What are the treatments of schizophrenia?

A
  • Antipsychotics
  • intense psychotherapy, social support
  • Recovery and improvement in symptoms over 50%
397
Q

What are the symptoms of depression?

A
  • Lowered mood
  • Anhedonia
  • Altered appetite
  • Worthlessness and guilt
  • Reduced ability of concentration
  • Recurrent thoughts of death
398
Q

What are the causes of depression?

A
  • Reduced hippocampal volume
  • Genetic serotonin transporter abnormalities
  • social affects - poverty, stress, absue
399
Q

What are the treatments of depression?

A
  • Light therapy
  • Psychotherapy
  • Tricyclic antidepressants
  • Prozac
  • Exercise
  • ECT
400
Q

What are the two types of the stroke?

A
  • Ischaemic stroke (due to embolus clot)

- Haemorrhagic stroke (entry of blood into CNS via a rupture of a blood vessel)

401
Q

How long does a stroke need to be for there to be irreversible brain damage?

402
Q

What are the types of haematomas that affect the brain?

A
  • Epidural (trauma to meningeal artery)
  • Subdural (rapid movement of head)
  • Subarachnoid (damage to cerebral artery)
403
Q

What is the incidence of stroke?

A

10% deaths worldwide

404
Q

What are the treatments of stroke?

A
  • Anticoagulant
  • Diet /lifestyle
  • Thrombolysis - break up clots if given quickly
  • Stents
  • Surgery
405
Q

What are the types of epilepsy?

A

Childhood absence epilepsy
- 4-12 years of age
- Mutations in low threshold voltage dependant Ca channels
- Resolves without pathology during puberty
Temporal lobe epilepsy
- late childhood and adolescence
- Most common type of epilepsy in adults
- complex partial seizures often preceded by aura

406
Q

What is the incidence of epilepsy?

407
Q

What are the causes of epilepsy?

A
  • Reflex seizures - flashing lights
  • genetic - mutations in Na+ channels
  • alcohol/drugs
  • Infection
  • 2/3 spontaneously in nature
408
Q

What are the treatments of epilepsy?

A 
Acute 
- Benzodiazepines 
- Recovery position
Chronic 
- Pharmacological 
- Electrical 
- Surgical - removal of tumour
409
Q

What are the symptoms of Alzheimers disease?

A
  • Short term memory loss
  • Confusion
  • Irritability
  • Long term memory loss
  • Death within 7 years of diagnosis
410
Q

What causes Alzheimers disease?

A
  • age
  • Genetic (ApoE4)
  • Trauma
  • High blood pressure
  • Environmental factors
411
Q

What is the incidence of Alzheimers disease?

412
Q

What are the treatments of Alzheimers disease?

A
  • AChesterase inhibitors
  • NMDA receptor antagonists
  • Intellectual stimulation
  • diet
  • not many treatments
413
Q

What part of the brain is used to control eating behaviour?

A

Hypothalamus

414
Q

What does anabolism mean?

A

Building up macromolecules for energy storage

415
Q

What does catabolism mean?

A

Breaking down macromolecules for energy usage

416
Q

What experiments were used to investigated the role of the hypothalamus in eating behaviour?

A
  • A lesion to both sides of hypothalamus causes anorexia

- If you cut the ventromedial part of the hypothalamus then it causes obesity

417
Q

What is the role of Leptin protein in eating behaviour?

A

Leptin is released by fat cells in order to decrease eating behaviour
In the absence of leptin, eating behaviour is stimulated

418
Q

What does the binding of Leptin on receptors activate?

A
  • Activates the release of alpha-MSH and CART neurotransmitters
  • They send projections to hypothalamus which release TSH and ACTH from the pituitary gland
  • TSH and ACTH act on the adrenal glands to increase basal metabolic rate
419
Q

What does the injection of alpha-MSH and CART do?

A
  • Suppresses appetite by mimicking the effect of raised leptin levels
420
Q

What does falling leptin levels stimulate?

A

Stimulate the release of NPY and AgRP

421
Q

What is the role of NPY and AgRP in eating behaviour?

A

Stimulated by falling leptin levels

  • This inhibits TSH and ACTH
  • Stimulate feeding behaviour
  • Activates the parasympathetic nervous system
422
Q

What is the role of Gherelin?

A

Released into bloodstream from an empty stomach and stimulates the role of NPY and AgRP

423
Q

What short term factors affect regulation of feeding?

A
  • Cultural meal times

- Motivation to continue eating depends on how much you have already eaten

424
Q

What is monogamy?

A
  • One male and female form an exclusive relationship

- 12% of primates

425
Q

What is polyandry?

A
  • One female mates with many males

- Rare in mammals

426
Q

What is polygyny?

A
  • One male mates with many females

- Many mammalian species

427
Q

How does the human brain show sexual dimorphism?

A
  • Males have larger brains than females
  • More neurones in the Onuf’s nucleus in males
  • Pre-optic area of the hypothalamus is larger males
428
Q

How does the menstrual cycle affect behaviour?

A
  • Spatial reasoning tests when oestrogen is lowest
  • Sexual encounters increase prior to ovulation
  • Sexual attractiveness changes throughout the menstrual cycle
  • Synaptic density in hippocampus changes with levels of oestrogen
429
Q

How and why has the use of non-human primates improved neuroscience?

A

Non human primates - immense knowledge gained on Schizophrenia, Alzheimers and Parkinson’s

BMS 1 (6 decks)

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