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PHSL231 > Ruth Epsom lectures > Flashcards

Ruth Epsom lectures Flashcards

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1
Q

thalamus function

A

gateway to the cortex

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2
Q

reticular formation controls

A

level of consciousness

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3
Q

pre-frontal cortex controls

A

agression and emotion

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4
Q

hypothalamus is responsible for

A

hormonal integration

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5
Q

cerebellum controls

A

sensory feedback to the motor system

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6
Q

Brocas area

A

motor speech area

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7
Q

what is stored in the hippocampus

A

memory language and emotion

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8
Q

basal ganglia controls

A

voluntary and selection of movement

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9
Q

corpus callosum

A

joins both hemispheres of the brain

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10
Q

nervous tissue is made up of

A

neuron and glia cells

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11
Q

role of neurons

A

communication, carry electrical signal from brain to spinal cord or from spinal cord to effectors

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12
Q

example of a neuron

A

synapses

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13
Q

role of glia cells in nervous tissue

A

support

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14
Q

example of glia cells

A

myelin and CSF

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15
Q

another name for glia

A

neuroglia

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16
Q

four zones of an axon

A

input zone, summation zone, conduction zone and output zone

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17
Q

are neurons or glia excitable

A

neurons

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18
Q

glia are

A

non excitable but do still have a resting membrane potential

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19
Q

name the five steps involved in electrical excitability

A

1- stimulus gated sodium channels open which causes the MP to reach threshold
2- voltage gated sodium channels open and the stimulus gated channels close an AP is being fired
3-voltage gated sodium channels close at the peak of the AP
4- voltage gated potassium channels open causing the AP to be repolarised
5- voltage gated channels close causing hyperpolarisation and the MP is now restored.

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20
Q

what are two way conduction velocity can be increased in an axon

A

myelin sheath and increasing axon diameter

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21
Q

What junction on an electrical synapse allow the flow of current

A

gap junctions as they act as a pore to join two cells

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22
Q

how can synapse strength be modified in chemical synapses

A

changing the amount of receptors on the post synaptic membrane and the change in amount of neurotransmitter released from the pre synaptic vesicles.

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23
Q

are chemical or electrical synapses faster

A

electrical because chemical synapses rely on a series of events to occur

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24
Q

pre-synaptic specialisation

A

vesicles containing neurotransmitter

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25
Q

post-synaptic specialisation

A

neurotransmitter receptors

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26
Q

how is a membrane potential created

A

by the difference in ion distribution

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27
Q

chemical gradient

A

energy provided by the difference in concentration across the plasma membrane

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28
Q

write down the chemical energy equation

A

triangleu= RT In(inconc)/(outsideconc)

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29
Q

electrical gradient

A

energy associated with moving charged molecules across the membrane

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30
Q

write down the electrical energy equation

A

triangleu=RT In(inconc)/(outconc) +1(F) (-60mV)

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31
Q

what are the only two excitable cells in the body

A

nerve and muscle cells as they generate APs

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32
Q

define equilibrium potential

A

the energy in mV of a concentration gradient of an ion

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33
Q

equilibrium potential/ electrical potential

A

the electrical potential that exactly balances the concentration gradient of an ion

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34
Q

Nernst equation

A

Eion= 60/Z log (concout/concin)

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35
Q

RMP for a muscle compared to a nerve cell

A

RMP muscle -70mV and nerve -90mV

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36
Q

why do resting membrane potentials exist

A

the neuronal membrane at rest is slightly permeable to sodium ions

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37
Q

describe the RMP

A

large potassium ion out flow with a modified by a smaller sodium ion inflow

38
Q

decrement of local potential depends on

A

length constant of the nerve

39
Q

local potentials are

A

small ion fluxes across the membrane means that the RMP fluctuates these fluctuations are local potentials

40
Q

local potentials/action potentials

A

local potentials influence the firing of an action potential

41
Q

describe a local potential in five points

A 
decremental in size
graded in size
summate temporally and spatially
depolarise/hyperpolarise
influence the generation of an action potential
42
Q

describe an action potential in three points

A

all or nothing
self generating- propagate without decrementing
has to reach threshold 15mV

43
Q

why is Ena often not reached

A

because the potassium channels open before its reached causing a decrease

44
Q

what drives the AP

A

voltage gated sodium channels

45
Q

what allows the sodium channels to shut fast

A

the inactivation gate

46
Q

what substance can block and inhibit the sodium channels

A

tetrodotoxin

47
Q

what allows the voltage gated sodium channels to turn on

A

the voltage sensor

48
Q

where is the voltage sensor of the sodium channel located

A

in the 4th transmembrane domain of the protein

49
Q

ball and chain model

A

inactivation gate

50
Q

voltage gate and what are interchangeable

A

activation gate

51
Q

do potassium channels have an inactivation gate

A

yes but this is slower than the sodium inactivation gate

52
Q

relative refractory period

A

when another action potential is possible, however must work against potassium gradient as the potassium channels are open, therefore this is difficult and rare because the membrane potential is driving in a different direction.

53
Q

refractory period

A

when the AP is repolarising or hyperpolarising

54
Q

how does increasing axon diameter increase conduction velocity in an axon

A

decreases internal resistance

55
Q

how does insulation/ myelination increase conduction speed

A

prevents leakage of the electrical current

56
Q

how does insulation/ myelination increase conduction speed

A

prevents leakage of the electrical current increases the membrane resistance

57
Q

three ways of enhancing conduction speed

A

increase axon insulation and diameter to reduce internal resistance but increase membrane resistance, also saltatory conduction

58
Q

how does botox work

A

prevents the fusion of vesicles and blocks the synapse

59
Q

proximal vs distal synapses

A

the closer the synapse is to the soma the bigger the AP

60
Q

spatial summation of local potentials causes

A

takes the neuron above threshold and causes an AP

61
Q

temporal summation causes

A

two APs in quick succession

62
Q

what is subliner summation

A

also known as shunting

63
Q

the more proximal to the soma the local potential is the

A

greater the AP

64
Q

subliner summation/shunting

A

the first AP causes the membrane to be depolarised before the second AP reaches it, this makes it harder for the second AP to reach the cell body causing a summation of the APs smaller than what they would be if added together

65
Q

facilitation

A

occurs in the pre synaptic terminal, EPSP gets bigger due to repetitive inputs of APs and a build up of calcium in the terminal meaning more vesicles get released at each AP

66
Q

LTP and LTD

A

post-synapse change in size of local potential

67
Q

name the six types of neurotransmitters

A

ach, biogenic amines, amino acids, purines, gas and peptides

68
Q

where are the sites of action for Ach

A

NMJ, autonomic endings, basal ganglia and GI tract

69
Q

what are the types of biogenic amines

A

adrenaline, nor adrenaline, serotonin and histamine

70
Q

where are the three sites that biogenic amines act

A

brain, spinal cord and sympathetic ends

71
Q

what are the types of amino acids in the body

A

glutamate, GABA, aspartate and Gly

72
Q

where in the body do amino acid neurotransmitters act

A

brain, spinal cord and retina

73
Q

what are the types of purines

A

adenosine and ATP

74
Q

where in the body do purines act

A

brain and autonomic ganglia

75
Q

what is the main gas neurotransmitter in the body and where does it act

A

nitric oxide and brain, spinal cord, GI tract

76
Q

what are the main peptides in the body and where do they act

A

oxytocin and somatostatin they act in the brain, spinal cord and pituitary gland

77
Q

what is the Ach receptor permeable to

A

sodium ions

78
Q

what does P do to the body and why is it bad

A

increases levels of noradrenaline dopamine and serotonin and is neurotoxic

79
Q

what does the GPCR Gs do

A

stimulates adenylyl cyclase

80
Q

in nicotinic Ach receptors what binds to where to open the pore

A

Ach binds to the alpha subunit to open the pore

81
Q

what blocks the nicotinic Ach receptor

A

bungarotoxin

82
Q

three types of glutamate receptors

A

AMPA, NMDA and Kainate

83
Q

what ion blocks the NMDA receptor

A

magnesium

84
Q

which glutamate receptor is critical for LTP

A

NMDA

85
Q

what type of potentials do glutamate receptors produce

A

EPSPs

86
Q

what does PCP/angel dust do

A

blocks the NMDA receptor leading to induced psychosis

87
Q

what effects do metabotropic glutamate receptors have

A

downstream changes in calcium and phosporylation

88
Q

how do metaboptropic glutamate receptors cause an increase in calcium ions

A

when glutamate is released into the synaptic cleft it binds to both the AMPA receptor and the glutamate receptor which drives a signalling change leading to more calcium release

89
Q

how does a LTD occur

A

coincidence of both temporal and spatial summation causes a rise in calcium release this causes a long lasting strong synapse

90
Q

what kind of response does a GABA-A receptor trigger

A

IPSP , hyperpolarisation

91
Q

what ion is GABA-A permeable to

A

chloride

92
Q

what can block the GABA-A receptor

A

picrotoxin

PHSL231 (3 decks)

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