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Neuroantomy > Action Potentials & Synapses > Flashcards

Action Potentials & Synapses Flashcards

1
Q

what causes a neutron to be polarized?

A

unequal distribution of ions on either side of the plasma membrane

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2
Q

what is the charge of neurons measured in?

A

millivolts

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3
Q

how are neutrons different than most cells?

A

they are electrically excitable

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4
Q

what is the resting membrane potential of a neuron?

A

-70mV

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5
Q

what is the signal neurons use to communicate with other neurons or other targets like muscles and glands?

A

a change in membrane potential (voltage)

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6
Q

what is it called when the membrane potential decreases?

A

depolarization

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7
Q

what is it called when the membrane potential increases?

A

hyperpolarization

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8
Q

what are neurons only capable of generating GPs involved in?

A

local or short distance communication (typically a few mm)

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9
Q

what are the characteristics of graded potentials?

A

typically small, slow, gradual, and either decrease or increase membrane potential

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10
Q

what are the characteristics of action potentials?

A

large, typically repetitive, with rapid alternating depolarization and hyper polarization (spikes) of membrane potential

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11
Q

what are neurons that generate action potentials capable of?

A

long range signalling

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12
Q

where do the longest neurons in the body receive input from and travel to?

A

distal lower limb (like the big toe) and travel to the brainstem, a distance of ~ 1m

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13
Q

what does the generation of action potentials depend on?

A

the generation of graded potentials. Therefore all neurons that can produce APs can also produce GPs

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14
Q

what does an ion pump require to move potassium from the outside to the inside?

A

energy, ATP

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15
Q

what is the function of an ion pump?

A

it moves potassium from the extracellular space to the inside of a neutron

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16
Q

what is the typical concentration of K in the extracellular space?

A

4mM

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17
Q

what is the potassium concentration inside the neuron?

A

120mM

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18
Q

what else does the ion pump do?

A

it also moves sodium ions from inside the neuron to the outside

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19
Q

what is the sodium concentration outside the neuron?

A

140mM

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20
Q

what is the sodium concentration inside the neuron?

A

14mM

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21
Q

what is the function of an ion channel?

A

they allow some of the potassium to move from the inside to the outside down the concentration gradient

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22
Q

what does potassium travelling outside the neuron via an ion channel result in?

A

a voltage difference between the inside and outside of the cell

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23
Q

what does the voltage produced depend on

A

the extent of the concentration difference between the inside and the outside

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24
Q

what is the function of a sodium ion channel?

A

they allow some sodium to travel inside the neuron down their concentration gradient causing the inside to become more positive

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25
Q

is the influence of potassium or sodium much greater?

A

potassium because their channels are 25X more permeable than sodium channels

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26
Q

how are ion channels different in graded potentials?

A

the permeability of sodium channels can change

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27
Q

how does sodium channel permeability change for GPs?

A

at rest the permeability is low

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28
Q

what happens when sodium ion channel permeability increases?

A

Na moves down its concentration gradient moving the membrane potential in the positive direction (depolarizing)

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29
Q

what makes action potentials special?

A

the are produces by ion channels that are voltage gated

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30
Q

what happens when an AP reaches threshold?

A

voltage gated Na channel permeability rapidly increases, greatly depolarizing the neuron

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31
Q

what is the falling phase of the action potential due to?

A

the intrinsic inactivation of voltage gated Na channels and a delayed activation of voltage gated K+ channels

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32
Q

what causes a refractory period on AP generation?

A

voltage gated Na channel inactivation

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33
Q

what is the absolute refractory period?

A

the period when no matter how strong the stimulus, another AP cannot be generated

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34
Q

what is the relative refractory period?

A

the time following Na+ channel reactivation but voltage gated K+ channels are still sufficiently active to oppose depolarization to threshold

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35
Q

could a strong stimulus generate another action potential during the relative refractory period?

A

yes

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36
Q

do voltage gated K+ channels inactivate?

A

no. In fact it takes a long time for their channels permeability to return to resting levels as membrane potential hyper polarizes

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37
Q

what explains the brief after hyper polarization of the action potential?

A

it takes a long time for voltage gated K+ channels to return their permeability to resting levels

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38
Q

what imposes limits on the frequency at which APs can be generated?

A

the refractory periods and the after hyperpolarization

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39
Q

why are GPs limited to local or short distance?

A

the electrical current flows passively down the inferior of the axon and leaks through the membrane. So, if there was along distance, the amplitude of the potential change decreases

40
Q

how can you make an AP travel further?

A

1: have voltage gated channels along the fiber so the AP is always being boosted

2: insulate the axon with myeline to decrease the decay of signal

41
Q

what is the area in between balls of myeline called?

A

nodes of ranvier

42
Q

how spaced apart are the nodes of ranvier?

A

every 1-2 mm

43
Q

where are voltage gated Na+ and K+ channels found on a myelinated axon?

A

only at the nodes

44
Q

why is the speed of transmission greatly increased on a myelinated axon?

A

because only the voltage gated channels within the nodes need to be activated

45
Q

what conduction velocities can the fastest myelinated axons reach?

A

velocities of 80-120 m/sec

46
Q

what is saltatory conduction?

A

the node to node transmission that occurs in myelinated axons

47
Q

what also affects conduction velocity?

A

axon diameter - larger axons have less longitudinal resistance and thicker myelin

48
Q

how do neurons communicate with eachother or with other targets like muscles and glands?

A

via synapses

49
Q

what are the 2 basic types of synapse?

A

1: electrical synapses (gap junctions)
2:chemical synapses (release NT)

50
Q

what are gap junctions or electrical synapses?

A

transmembrane channels that join to connect the interior of one cell with the interior of another

51
Q

what is the direction of gap junctions?

A

they are bidirectional

52
Q

is there a synaptic delay with gap junctions?

A

no

53
Q

where may you find gap junctions?

A

they exist between cardiac and smooth muscle and various types of neurons

54
Q

what is a chemical synapse (NT release)?

A

Its are released at axon terminals which then cross a 20-40nm wide synaptic cleft, acting on receptors at the post synaptic membrane

55
Q

what direction is neurotransmission?

A

unidirectional : presynaptic-> postsynaptic

56
Q

what are NTs contained within?

A

synaptic vesicles

57
Q

what do synaptic vesicles fuse with?

A

the presynaptic membrane then contents are released into the synaptic cleft

58
Q

list the sequence of events for synaptic transmission:

A

1: AP arrives at axon terminal
2:Voltage gated Ca2+ channels open
3: Ca2+ enters the presynaptic neuron
4:Ca2+ signals to NT vesicles
5:vesicles move to the membrane and dock
6:NTs release via exocytosis
7:NTs bind to receptors
8:signal initiated in post synaptic cell

59
Q

how are newly formed vesicles loaded with NTs?

A

through the action of proton (H+) pump transporters

60
Q

what forms the SNARE complex?

A

syntaxin and SNAP-25 in the plasma membrane and synaptobrevin in the synaptic vesicle

61
Q

is there partial fusion of synaptic vesicles?

A

no. if a vesicle fuses all NTs in the vesicle are released

62
Q

what is a quantum or quanta?

A

the amount of NT(s) release by a single vesicle

63
Q

how is synaptic transmission halted?

A

1: transporters on the presynaptic membrane can remove NT from the synaptic cleft and recycle it

2:at the neuromuscular junction a NT (acetylcholine) can be broken down by an enzyme (acetylcholinesterase) and the choline is then transported and used to synthesize more acetylcholine

64
Q

what does the action of NTs on the postsynaptic membrane lead to?

A

synaptic integration

65
Q

what does the NT released from synaptic vesicles produce?

A

graded potentials that can either transiently depolarize (EPSP) or hyper polarize (IPSP)

66
Q

what is the most common excitatory NT in the CNS?

A

glutamate

67
Q

what is glutamate synthesized from?

A

the amino acid glutamine

68
Q

what loads vesicles with glutamate?

A

vesicular glutamate transporter

69
Q

how is glutamate removed from the synaptic cleft?

A

it is transported by excitatory amino acid transporters (EAATs) into astrocytes

70
Q

what do astrocytes convert glutamate into?

A

glutamine (via the enzyme glutamine sythetase)

71
Q

how is glutamine then transported back to the presynaptic neuron where its converted into glutamate?

A

by the enzyme glutaminase

72
Q

where does glutamate primarily act at for excitatory NT?

A

the post-synaptic AMPA receptors

73
Q

what happens when glutamate binds to AMPA?

A

a channel allows Na+ to enter the post synaptic neuron, leading to depolarization

74
Q

what is another type of glutamate receptor?

A

NMDA receptors

75
Q

what are NMDA receptors permeable to?

A

Na+ and Ca2+

76
Q

what can Ca2+ act as? and what can it affect?

A

an intracellular second messenger. it can affect mechanisms (including gene expression)with long term consequences (ex. long term potentiation that has been associate with learning and memory)

77
Q

under resting conditions what is the NMDA receptor blocked by?

A

Mg2+

78
Q

how does the NMDA receptor get unblocked?

A

to remove the Mg2+ requires that the receptor is depolarized (e.g by AMPA receptors)

79
Q

what does activation of NMDA receptors require?

A

the presence of a co-transmitter glycine

80
Q

what do EPSP produced only by AMPA receptors look like?

A

brief

81
Q

what do EPSP produced by AMPA and NMDA receptors look like?

A

longer duration

82
Q

what is the most common inhibitory transmitter?

A

GABA

83
Q

what is GABA synthesized from?

A

by the enzyme GAD

84
Q

how is GABA loaded into synaptic vesicles?

A

by the vesicular GABA transporter (VGAT)

85
Q

what do GABAa receptors do?

A

increase the influx of Cl-

86
Q

what do GABAb receptors do?

A

increase the influx of K+ through K+ channels

87
Q

what type of receptors are GABAa, AMPA, and NMDA receptors?

A

inotropic receptors

88
Q

what type of receptors are GABAb?

A

metabotropic receptors

89
Q

what is required for an effect to occur for inotropic receptors?

A

requires transmitter to be bound to the receptor

90
Q

how does a metabotropic receptor work?

A

it typically involved G-protein activation that either directly or indirectly influences ion channel permeability or other intracellular processes

91
Q

what are the sites on GABAa receptors where drugs can bind and have effects?

A

benzodiazepineszepenes (tranquilizers)

barbiturates (anesthetic effect)

alcohol

92
Q

what does the amplitude of a EPSP depend on?

A

the strength of the signal arriving at the synaptic terminal which affects the amount of NT (glutamate release)

93
Q

how can EPSPs summate?

A

if they are produced quickly enough this is called temporal summation

94
Q

what is spatial summation?

A

multiple inputs

95
Q

what effect can IPSPs have on EPSPs?

A

they can prevent EPSPs from reaching threshold (postsynaptic inhibition)

Neuroantomy (4 decks)

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