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PHGY 209 > 5. Nerve/Synapse > Flashcards

5. Nerve/Synapse Flashcards

1
Q

Central Nervous System (CNS) components

A

brain + spinal cord

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2
Q

Peripheral Nervous System (PNS) components

A

neurons (motor + sensory) and autonomic fibers

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3
Q

motor neurons

A

efferent fibers that give out information to muscles

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4
Q

sensory neurons

A

afferent fibers that receive information

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5
Q

autonomic fibers

A

connect spinal cord to visceral organs

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6
Q

synapse

A

specialised site of communication between neurons

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7
Q

neuron physical characteristics

A
  • cell body = soma
  • branching dendrites
  • a single axon
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8
Q

the action potential starts at the… and propagates down the…

A

initial segment
axon

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9
Q

resting membrane potential

A

small excess of negatively charged ions inside the membrane of neuron

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10
Q

resting membrane potential =

A

-70mV

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11
Q

what creates the resting membrane potential?

A
  • concentration gradients for various ions
  • selective permeability of membrane to K+ ions
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12
Q

membrane potential at rest:

A
  1. neuronal membrane highly permeable to K+ but less permeable to other ions
  2. K+ leak out of the cell down their concentration gradient
  3. unpaired (-) ions accumulate inside the cell, creating an electric gradient: K+ ions pulled back into cell
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13
Q

at equilibrium: electrochemical gradient

A

chemical gradient = electrical gradient

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14
Q

Nernst Equation describes…

A

the membrane potential at equilibrium

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15
Q

Nernst Equation (E)

A

61/z * log([ion]o/[ion]i)

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16
Q

main factor determining the neuron resting membrane potential

A

equilibrium potential for K+

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17
Q

equilibrium potential for K+

A

-90mV

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18
Q

leak channels

A

proteins (ion channels) that form K+ selective pores through the membrane, always open

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19
Q

equilibrium potential for Na+

A

+70mV

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20
Q

equilibrium potential for Cl-

A

-80mV

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21
Q

why is the resting membrane potential slightly more + than the equilibrium potential for K+?

A

small inward leak of Na+

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22
Q

sodium-potassium pump

A

pumps 3 Na out and 2 K in against their concentration gradients by using energy produced by ATP hydrolysis

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23
Q

action potential

A

brief electrical impulse that travels down the axon

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24
Q

action potential spike/peak

A

membrane potential approaches Na equilibrium potential but very briefly

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25
Q

depolarisation

A

when membrane potential peaks at 30mV as sodium channels open

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26
Q

repolarisation

A

membrane potential returning to its resting potential after having spiked

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27
Q

hyperpolarisation

A

when membrane potential decreases below its resting potential

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28
Q

when is an action potential initiated?

A

when the membrane potential depolarises to a threshold level, influenced by voltage-gated sodium channels

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29
Q

can the magnitude of action potential increase/decrease?

A

no, the action potential is an all or nothing mechanism

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30
Q

3 critical properties of voltage-gated sodium channels

A
  • closed at resting membrane potential: open when repolarising
  • selective for Na+
  • open channel rapidly inactivates, stopping the flow of Na+ ions
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31
Q

absolute refractory period

A

sodium channels are inactive and the membrane is completely unexcitable for a few seconds after an action potential

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32
Q

what does speed of propagation depend on?

A

how fast the Na+ channel can be converted back to its closed configuration after repolarisation

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33
Q

relative refractory period

A

membrane potential overshoots its resting potential, making the axon less excitable and unlikely to fire an action potential

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34
Q

action potential is a positive or negative feedback mechanism?

A

positive

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35
Q

action potential steps

A
  1. depolarisation of membrane to threshold activates small fraction of sodium channels: Na+ flows in membrane
  2. inside of neuron gets more positive, further depolarising the membrane: more sodium channels open
  3. all sodium channels open: peak reached
  4. sodium channels inactivated
  5. membrane relaxes back to resting potential
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36
Q

which ion channel is more present in the axon membrane?

A

voltage-gated sodium channels

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37
Q

what is the dominant permeability at action potential peak?

A

Na+

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38
Q

rising phase of action potential:

A
  • sodium channels open
  • potassium channels still closed
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39
Q

falling phase of action potential

A
  • sodium channels close
  • potassium channels open (takes longer)
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40
Q

which ion channels have delayed activation?

A

voltage-gated potassium channels -> take longer to open

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41
Q

when are potassium channels maximally open?

A

during repolarisation phase: K+ can flow out faster to bring membrane potential back to -70mV

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42
Q

Action potential propagation steps

A
  1. depolarisation: sodium ions flow in
  2. (+) charge in this region attracted to - charge in adjacent segment
  3. (+) charge flows into next axon segment
  4. propagation down axon continuously like a wave
  5. (+) charge can only move forward due to rapid sodium channel inactivation
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43
Q

how do neurons send information?

A

through means of frequency and pattern of action potentials

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44
Q

what do neurotoxins target?

A

sodium channels

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45
Q

tetrodotoxin (TTX)

A

produced by puffer fish, extremely potent sodium channel inhibitor

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46
Q

batrachotoxin

A

secreted by frogs, deadly sodium channel activator: irreversibly opens sodium channels so constant AP being fired

47
Q

drugs that can also block sodium channels

A

local anesthetics and antiepileptics

48
Q

local anesthetics

A

injected into the nerve to block its sodium channels so the pain information will be blocked from going up to the brain at this point

49
Q

examples of local anesthetics

A

lidocaine, benzocaine, tetracaine, cocaine

50
Q

anti epileptics

A

prophylactic drugs taken everyday to prevent seizures (without putting you to sleep) by blocking sodium channels

51
Q

anti epileptics examples

A

phenytoin (Dilantin), carbamazepine (Tegretol)

52
Q

propagation rate of action potential is proportional to…

A

axon diameter and myelination

53
Q

Wider axon propages slower or faster?

A

faster

54
Q

How can thinner axons propagate faster?

A

surrounded by Myelin sheets

55
Q

Myelin formed by: (2)

A
  • Schwann cells in PNS
  • oligodendrocytes in CNS
56
Q

nodes of Ranvier

A

periodic gaps in myelin sheets

57
Q

nodes of Ranvier contain a high concentration of…? why?

A

voltage-gated sodium channels to enable signal to be regenerated at periodic intervals due to sodium influx

58
Q

cause of multiple sclerosis

A

loss of myelin due to immune system attacking myelin made by oligodendrocytes

59
Q

white matter

A

regions of the brain and spinal cord containing mostly myelinated axons

60
Q

grey matter

A

comprises cell bodies, dendrites and synapses

61
Q

3 main types of synapses

A
  • axodendritic
  • axosomatic
  • axoaxonic
62
Q

axodendritic synapse

A

between axon and dendrites (most common)

63
Q

2 types of axodendritic synapses

A
  • spine synapse = mainly excitatory
  • shaft synapse = mainly inhibitory
64
Q

axosomatic synapse

A

on neuron body (soma)

65
Q

axoaxonic synapse

A

axon synapses with the axon of another neuron

66
Q

presynaptic refers to…

A

everything upstream a synapse

67
Q

postsynaptic refers to…

A

everything downstream a synapse

68
Q

divergence

A

a single neuron makes synapses with many other neurons through its branching axon

69
Q

presynaptic vesicles

A

contain neurotransmitters

70
Q

synaptic cleft

A

narrow space between presynaptic terminal and postsynaptic spine

71
Q

active zone

A

vesicles docked to the membrane adjacent to synaptic cleft, ready to be released

72
Q

postsynaptic density

A

darker spots on postsynaptic spine, containing proteins for neurotransmitter reception

73
Q

Calcium concentration inside neuron is very…

A

low

74
Q

what triggers neurotransmitter release?

A

activation of voltage-gated calcium channels

75
Q

neurotransmitter release steps

A
  1. action potential invades presynaptic terminal, depolarising the membrane
  2. calcium channels open so Ca moves into presynaptic terminal
  3. synaptic vesicles fuse with presynaptic membrane
  4. neurotransmitters released into synaptic cleft
  5. transmitter activates receptors in the postsynaptic membrane, opening ligand-gated ion channels
76
Q

calcium-dependent fusion of synaptic vesicle at active zone

A
  1. action potential activates voltage-gated calcium channels so Ca enters neuron
  2. calcium binds to receptor on presynaptic terminal
  3. vesicle fuses with the membrane
  4. transmitters in vesicles released into synaptic cleft
  5. membrane reforms
77
Q

toxins that can act on calcium-dependent fusion of synaptic vesicle at active zone

A
  • tetanus
  • black widow spider toxin: too many vesicles fuse with the membrane
  • botox: proteins responsible for neurotransmitter reception chewed up
78
Q

Excitatory Postsynaptic Potential (EPSP)

A

depolarises the postsynaptic membrane, making it more likely to fire an AP
-> involves excitatory synapse

79
Q

Inhibitory Postsynaptic Potential (IPSP)

A

hyperpolarises the postsynaptic membrane, making it less likely to fire an AP
-> involves inhibitory synapse

80
Q

glutamate

A

main excitatory neurotransmitter in the brain

81
Q

ionotropic receptors

A

ion channels that open in response to binding of neurotransmitters to receptor sites on their external surfaces

82
Q

2 types of ionotropic glutamate receptors

A
  • AMPA receptors
  • NMDA receptors
    –> ligand-gated ion channels
83
Q

receptors involved in excitatory transmission

A
  • AMPA receptors
  • NMDA receptors
84
Q

AMPA receptors

A

responsible for fast EPSP at excitatory synapse

85
Q

AMPA receptor activation

A
  1. Glu released from vesicles and diffuse across synaptic cleft
  2. Glu bind to AMPA receptors, opening its ion channel
  3. AMPA is permeable to sodium so Na+ flows into postsynaptic spine, depolarising the post-synaptic cell
86
Q

NMDA receptors

A

have their pore blocked by Mg2+ at resting membrane potential so they can’t conduct current

87
Q

NMDA receptor activation

A
  1. depolarisation expels Mg2+ so pore can conduct
  2. open pore is highly permeable to Ca2+ and noncovalent cations: Calcium flows into neuron
88
Q

2 conditions required for NMDA receptor activation

A

glutamate binding and postsynaptic depolarisation

89
Q

synaptic plasticity

A

idea that synapses can change and become stronger (larger EPSP)

90
Q

Long-Term Potentiation (LTP)

A

model of synaptic plasticity in experimental context

91
Q

3 phases of LTP

A
  1. Control: a single action potential stimulates Glu release
  2. Induction: high frequency action potentials depolarise post-synaptic cleft so Calcium can be conducted, leading to more Glu release
  3. LTP: hours after induction, a single action potential triggers a bigger/stronger EPSP
92
Q

excitotoxicity

A

high concentrations of glutamate are toxic to neurons

93
Q

how is excitotoxicty likely to contribute to neuronal degeneration after a stroke?

A
  1. stroke: neurons die, releasing Glu which diffuses to surrounding regions
  2. over activation of AMPA and NMDA receptors causes too much Calcium to flow into the cell
  3. cell apoptis/suicide
94
Q

2 broad functions of inhibitory synapses

A
  • act as a break on excitatory neurons
  • shape the pattern of excitatory neuron’s action potential
95
Q

which type of synapse is more local?

A

inhibitory synapses

96
Q

Y-aminobutyric acid (GABA)

A

main inhibitory neurotransmitter in the brain

97
Q

GABA A receptor

A

postsynaptic ionotropic receptor responsible for IPSP

98
Q

GABA A receptor activation

A
  1. GABA binds to GABA A receptors, activating it
  2. Influx of Cl- into cell hyperpolarises postsynaptic membrane
99
Q

drugs that can act on GABA A receptors

A
  • xanax makes GABA A receptors stay open longer, accentuating the IPSP and making you sleepy
  • ethanol makes GABA A receptors more receptive, causing more inhibition in the brain, making you sleepy
100
Q

synaptic integration key points (5)

A
  • excitatory inputs usually located on dendritic spines
  • inhibitory inputs usually clustered on/near cell soma
  • action potential fired depending on relative balance of EPSPs and IPSPs
  • each neuron is either excitatory or inhibitory
  • inhibitory neuron can only inhibit other neurons by having excitatory inputs to fire action potentials
101
Q

Metabotropic receptors (GPCRs)

A
  • aka G-Protein Couple Receptors
  • found at synapses but aren’t ion channels
102
Q

GPCR activation

A
  1. Glu release in synaptic cleft
  2. Glu binds to mGluRs (metabotropic Glu receptors), inducing a conformational change, activating mGluRs
  3. 2nd messenger generated by mGluR inside postsynaptic spine
  4. 2nd messenger diffuse inside cell, activating a range of cellular proteins
103
Q

what does 2nd messenger activate when metabotropic receptors activate?

A
  • ion channels: 2nd messenger binds to it on inside of cell, causing it to open
  • protein kinases: proteins that add phosphates to another protein to activate it
  • transcription factors which will regulate gene expression in the nucleus: gene transcription + protein synthesis
104
Q

Glutamate and GABA activate what kind(s) of receptors?

A

both ionotropic and metabotropic receptors

105
Q

neuromodulators

A

substances that aren’t directly involved in fast flow of neuronal information but modulate global neural states, influencing alertness, attention and mood

106
Q

neuromodulators interact mainly with which kind(s) of receptors

A

metabotropic receptors

107
Q

neuromodulators examples

A
  • dopamine
  • serotonin
  • norepinephrine
  • endorphins (neuropeptide)
108
Q

where do neuromodulators originate from?

A

tiny clusters of neurons in small brainstem or midbrain nuclei

109
Q

how are neuromodulators spread out?

A

neuron’s axon in brainstem extend all the way up to cerebral cortex

110
Q

dopamine involved in…

A
  • addictive behaviours
  • connections between + emotion and associate behaviour: reward pathway
111
Q

serotonin influences…

A

mood

112
Q

antidepressant effect on neuromodulators

A

affect serotonergic transmission
-> ie Prozac

113
Q

simulants effect on neuromodulators

A

affect dopamine and norepinephrine transmission
-> ie amphetamines, cocaine

PHGY 209 (8 decks)

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