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
post-synaptic specialisation
neurotransmitter receptors
26
how is a membrane potential created
by the difference in ion distribution
27
chemical gradient
energy provided by the difference in concentration across the plasma membrane
28
write down the chemical energy equation
triangleu= RT In(inconc)/(outsideconc)
29
electrical gradient
energy associated with moving charged molecules across the membrane
30
write down the electrical energy equation
triangleu=RT In(inconc)/(outconc) +1(F) (-60mV)
31
what are the only two excitable cells in the body
nerve and muscle cells as they generate APs
32
define equilibrium potential
the energy in mV of a concentration gradient of an ion
33
equilibrium potential/ electrical potential
the electrical potential that exactly balances the concentration gradient of an ion
34
Nernst equation
Eion= 60/Z log (concout/concin)
35
RMP for a muscle compared to a nerve cell
RMP muscle -70mV and nerve -90mV
36
why do resting membrane potentials exist
the neuronal membrane at rest is slightly permeable to sodium ions
37
describe the RMP
large potassium ion out flow with a modified by a smaller sodium ion inflow
38
decrement of local potential depends on
length constant of the nerve
39
local potentials are
small ion fluxes across the membrane means that the RMP fluctuates these fluctuations are local potentials
40
local potentials/action potentials
local potentials influence the firing of an action potential
41
describe a local potential in five points
``` decremental in size graded in size summate temporally and spatially depolarise/hyperpolarise influence the generation of an action potential ```
42
describe an action potential in three points
all or nothing self generating- propagate without decrementing has to reach threshold 15mV
43
why is Ena often not reached
because the potassium channels open before its reached causing a decrease
44
what drives the AP
voltage gated sodium channels
45
what allows the sodium channels to shut fast
the inactivation gate
46
what substance can block and inhibit the sodium channels
tetrodotoxin
47
what allows the voltage gated sodium channels to turn on
the voltage sensor
48
where is the voltage sensor of the sodium channel located
in the 4th transmembrane domain of the protein
49
ball and chain model
inactivation gate
50
voltage gate and what are interchangeable
activation gate
51
do potassium channels have an inactivation gate
yes but this is slower than the sodium inactivation gate
52
relative refractory period
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
refractory period
when the AP is repolarising or hyperpolarising
54
how does increasing axon diameter increase conduction velocity in an axon
decreases internal resistance
55
how does insulation/ myelination increase conduction speed
prevents leakage of the electrical current
56
how does insulation/ myelination increase conduction speed
prevents leakage of the electrical current increases the membrane resistance
57
three ways of enhancing conduction speed
increase axon insulation and diameter to reduce internal resistance but increase membrane resistance, also saltatory conduction
58
how does botox work
prevents the fusion of vesicles and blocks the synapse
59
proximal vs distal synapses
the closer the synapse is to the soma the bigger the AP
60
spatial summation of local potentials causes
takes the neuron above threshold and causes an AP
61
temporal summation causes
two APs in quick succession
62
what is subliner summation
also known as shunting
63
the more proximal to the soma the local potential is the
greater the AP
64
subliner summation/shunting
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
facilitation
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
LTP and LTD
post-synapse change in size of local potential
67
name the six types of neurotransmitters
ach, biogenic amines, amino acids, purines, gas and peptides
68
where are the sites of action for Ach
NMJ, autonomic endings, basal ganglia and GI tract
69
what are the types of biogenic amines
adrenaline, nor adrenaline, serotonin and histamine
70
where are the three sites that biogenic amines act
brain, spinal cord and sympathetic ends
71
what are the types of amino acids in the body
glutamate, GABA, aspartate and Gly
72
where in the body do amino acid neurotransmitters act
brain, spinal cord and retina
73
what are the types of purines
adenosine and ATP
74
where in the body do purines act
brain and autonomic ganglia
75
what is the main gas neurotransmitter in the body and where does it act
nitric oxide and brain, spinal cord, GI tract
76
what are the main peptides in the body and where do they act
oxytocin and somatostatin they act in the brain, spinal cord and pituitary gland
77
what is the Ach receptor permeable to
sodium ions
78
what does P do to the body and why is it bad
increases levels of noradrenaline dopamine and serotonin and is neurotoxic
79
what does the GPCR Gs do
stimulates adenylyl cyclase
80
in nicotinic Ach receptors what binds to where to open the pore
Ach binds to the alpha subunit to open the pore
81
what blocks the nicotinic Ach receptor
bungarotoxin
82
three types of glutamate receptors
AMPA, NMDA and Kainate
83
what ion blocks the NMDA receptor
magnesium
84
which glutamate receptor is critical for LTP
NMDA
85
what type of potentials do glutamate receptors produce
EPSPs
86
what does PCP/angel dust do
blocks the NMDA receptor leading to induced psychosis
87
what effects do metabotropic glutamate receptors have
downstream changes in calcium and phosporylation
88
how do metaboptropic glutamate receptors cause an increase in calcium ions
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
how does a LTD occur
coincidence of both temporal and spatial summation causes a rise in calcium release this causes a long lasting strong synapse
90
what kind of response does a GABA-A receptor trigger
IPSP , hyperpolarisation
91
what ion is GABA-A permeable to
chloride
92
what can block the GABA-A receptor
picrotoxin