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Neuroscience > Lecture 2: Action Potentials + Propagation Synaptic Transmission > Flashcards

Lecture 2: Action Potentials + Propagation Synaptic Transmission Flashcards

1
Q

why are neurons electrically polarized like all cells?

A

Due to an unequal distribution of ions on each side of the plasma membrane

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2
Q

are neurons electrically excitable?

A

yes unlike most cells

the membrane potential can deviate from -70m

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3
Q

what is the change in membrane potential (voltage)

A

the signal neurons use to communicate with other neurons or other targets (muscles, glands).

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4
Q

what are graded potentials (GPs)

A

In some cases, changes in membrane potential are typically small, slow and gradual and either decrease (depolarize) or increase (hyperpolarize) membrane potential

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5
Q

in graded potentials, what is the activity of the neuron related to

A

the voltage at any point in time

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6
Q

what type of communication are neurons capable of only generating GPs involved in

A

local or short distance communication, as signal transmission distance is limited (typically to a few mm).

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7
Q

what are action potentials (APs)

A

changes in membrane potential are large and typically repetitive, with rapid alternating depolarization and hyperpolarization (“spikes”) of membrane potential

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8
Q

in action potentials, what is the activity of the neurons related to

A

not the voltage, but the number of action potential spikes over time

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9
Q

what type of communication are neurons that generate APs capable of

A

long-range signaling

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10
Q

do all neurons that generate APs procuce GP as well?

A

yes because the generation of APs depends on the generation of GPs

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11
Q

How is the resting membrane potential generated?

A

An ion pump moves potassium ions (K+) from the outside (typically 4mN) to the inside of the neurons. K+ concentration inside is elevated (120 mM).

The pump also moves sodium ions (Na+) from the inside, keeping the concentration of Na+ low (14 mM) relative to the outside (140 mM).

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12
Q

what creates the voltage difference between the inside and outside of the cell?

A

ion channels that allow some of the K+ to move from the inside to the outside, down the concentration gradient, and allow some Na+ to move from the outside to the inside, down their concentration gradient.

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13
Q

what would happen if there were no sodium Na channels

A

the resting membrane would be more negative

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14
Q

How are graded potentials generated?

A

with GPs, the permeability of Na+ channels can change (go up or down) by neurotransmitters or mechanical forces.

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15
Q

what happens if we increase the permeability of the Na channel a bit?

A

At rest, Na+ channel permeability is low (resting membrane potential is dominated by K+ channels).

if we increase it, Na+ moves down its concentration gradient (outside to inside) moving the membrane voltage in the positive direction (depolarizing).

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16
Q

how are action potentials generated?

A

Starting from rest (-70 mV), a stimulus first produces a graded depolarization. Then, at a certain voltage, there is a rapid, but brief, depolarization to +35 mV. The voltage drops quickly, and there is a period of calm before it happens again.

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17
Q

during stimulation of an action potential, does the membrane potential return back to -70 mV?

A

not during the period of stimulation, but at the end of the stimulation, there is a gradual hyperpolarization back to rest.

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18
Q

what makes ApPs special?

A

they are produced by ion channels that are “voltage-gated.”

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19
Q

what are voltage-aged ion channels

A

They are activated by a change in membrane potential. When the membrane potential reaches threshold, voltage-gated Na+ channel permeability rapidly increases, greatly depolarizing the
neuron.

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20
Q

why do voltage-gated Na channels drop and not keep increasing

A

they are subject to intrinsic inactivation. Soon after activation, they inactivate, causing the falling phase after the peak

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21
Q

is the falling phase of the AP is due to the inactivation of voltage- gated Na+ channels

A

yes, but also to a delayed activation of voltage-gated K+ channels that produce hyperpolarization.

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22
Q

Does sodium moving into the cell cause depolarization or repolarization

A

depolarize (move towards positive)

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23
Q

Does potassium being pushed out of the cell cause depolarization or repolarization

A

depolarization (bringing it towards resting membrane potential)

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24
Q

what is a refractory period and what are the two types

A

Voltage-gated Na+ channel inactivation imposes a refractory period on AP generation.

absolute refractory period

relative refractory period

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25
Q

what is an absolute refractory period

A

the period during which, no matter how strong the stimulus, another AP cannot be generated. It is due to the inactivation of voltage-gated Na+ channels.

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26
Q

what is a relative refractory period

A

the time following Na+ channel reactivation, but when voltage-gated K+ channel are still sufficiently active to oppose depolarization to threshold. However, a sufficiently strong stimulus could overcome such opposition.

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27
Q

do Voltage-gated K+ channels inactivate

A

No.

it takes quite a long time for voltage-gated K+ channels permeability to return to resting levels, as membrane potential hyperpolarizes. This explains the brief after hyperpolarization of the AP

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28
Q

what 2 things impose limits on the frequency that action potentials can be generated

A

The refractory periods

the after hyperpolarization

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29
Q

Why are graded signals limited to local or short-distance?

A

Electrical current flows passively both down the interior of the axon and leaks through the membrane. With distance, the amplitude of the potential change decreases.

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30
Q

How can we make the action potential travel further?

A

active regeneration of the signal

there are two mechanisms

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31
Q

what is the less ideal mechanism to regenerate the signal?

A

Cover unmyelinated axons with voltage-gated channels so that the action potential is constantly being boosted

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32
Q

what are the disadvantages to Cover unmyelinated axons with voltage-gated channels

A

its slow (takes time for each segment of the axon to reach threshold)

costs a lot of energy (the extensive movement of Na+ and K+ along the axon)

33
Q

what is the ideal mechanism to regenerate the signal?

A

Insulate the axon, with myelin leaving some gaps (nodes), to decrease decay of signal.

34
Q

what happens in the gaps (nodes) of myelinated axons?

A

Voltage-gated Na+ and K+ channels are only found in the nodes. Myelin reduces the decay of the electrical signal so that the voltage is above threshold when it reaches the node. At the node the signal is regenerated.

35
Q

why are myelinated axons faster?

A

fast speed of transmission because only the voltage-gated channels within the nodes need to be activated

36
Q

how fast can myelinated vs unmyelinateed axons can reach conduction velocities

A

80-120 m/sec

0.5-2.0 m/sec

37
Q

how is conduction velocity affected by axon diameter?

A

larger axons have less longitudinal resistance and thicker myelin so they’re faster

38
Q

what are the 2 basic types of synapses

A

Electrical synapses (gap junctions)

Chemical synapses (release neurotransmitter)

39
Q

what are electrical synapses (gap junctions)

A

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

Bidirectional and with essentially no synaptic delay.

40
Q

what are chemical synapses?

A

neurotransmitter released at axon terminals, crosses 20-40 nm wide synaptic cleft, acts on receptors on postsynaptic membrane

41
Q

is neurotransmission unidirectional or bidirectional?

A

unidirectional: presynaptic→postsynaptic.

42
Q

what is step 1 of the synaptic vesicle cycle

A

Newly former vesicle are loaded with neurotransmitter through the action of proton (H+) pump

43
Q

what is step 2 of the synaptic vesicle cycle

A

vesicles are translocated to the presynaptic membrane

44
Q

what is step 3 of the synaptic vesicle cycle

A

Vesicle then dock near release sites waiting for something to happen

45
Q

what is step 4 of the synaptic vesicle cycle

A

Priming occurs, involving the formation of partially assembled SNARE protein complexes.

46
Q

what is step 5 of the synaptic vesicle cycle

A

Fusion exocytosis (Ca2+- dependent)

47
Q

what is step 6 of the synaptic vesicle cycle

A

Endocytosis of vesicle membrane.

48
Q

what is step 7 of the synaptic vesicle cycle

A

Empty vesicles acidify (required for proton pump, step 1)

49
Q

what is step 8 of the synaptic vesicle cycle

A

Synaptic vesicles fuse with endosomes. (This step can be bypassed; go directly to step 1).

50
Q

what is step 9 of the synaptic vesicle cycle

A

New vesicles bud from the endosome.

51
Q

what are endosomes?

A

part of membrane trafficking pathways controlling recycling and degradation of synaptic vesicle membrane proteins.

52
Q

is there ever partial fusing of vesicles

A

no. If a vesicle fuses, all of the neurotransmitter in the vesicle is released.

53
Q

what is a quantum

A

The amount of neurotransmitter released by a single vesicle

quanta-vesicles released over time

54
Q

The total amount of neurotransmitter released by a single action potential corresponds to what?

A

the number of quanta

55
Q

what does the number of vesicles released depend on?

A

a) How much Ca2+ enters the terminal that is related to …

b) the extent of voltage-gated Ca2+ channel activation that is related to …

c) the number and frequency of action potentials that reach the terminal.

56
Q

How is synaptic transmission halted?

A

In most cases transporters on the pre-synaptic or post-synpaptic membrane can remove neurotransmitter from the synaptic cleft and even recycle it.

In some cases, the neurotransmitter is broken down by an enzyme

57
Q

what is excitatory post-synaptic potential

A

The neurotransmitter released from synaptic vesicles produces graded potentials that depolarize the postsynaptic membrane

58
Q

what is an inhibitory post-synaptic potential

A

The neurotransmitter released from synaptic vesicles produces graded potentials that hyperpoleraize the postsynaptic membrane

59
Q

what is Glutamate

A

the most common excitatory neurotransmitter in the CNS.

Vesicles are loaded with glutamate by a vesicular glutamate transporter

60
Q

what are excitatory amino acid transporters

A

remove glutamate from the synaptic cleft to stop the transmission process and convert it to glutamine

61
Q

what happens to the glutamate that is transported by the excitatory amino acid transporters?

A

is then transported back to the presynaptic neuron where it is converted into glutamate and loaded into vesicles.

62
Q

what are the 2 types of post-synaptic receptors that glutamate acts as

A

AMPA receptors

NMDA receptors

63
Q

what happens when glutamate binds to AMPA receptors

A

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

64
Q

what happens when glutamate binds to NMDA receptors

A

are permeable to Na+ and Ca2+. The influx of these cations (especially Na+) can contribute to depolarization

BUT

The Ca2+ can act as an intracellular second messenger, affecting mechanisms (including gene expression) with long term consequences with learning and memory

65
Q

why do NMDA receptors rely on AMPA receptors

A

Under resting conditions, the NMDA receptor channel is blocked by Mg2+. To remove the Mg2+ block requires that the receptor is depolarized by AMPA receptors

66
Q

what is the duration of an excitatory post-synaptic potential produced by AMPA alone vs with AMPA and NMDA

A

Just AMPA = brief

AMPA + NMDA = longer

67
Q

How are Inhibitory post-synaptic potential generated?

A

generated by inhibitory neurotransmitters. The most common inhibitory transmitter is GABA

GABA is synthesized from glutamate and loaded into synaptic vesicles by the vesicular GABA transporter

68
Q

what happens once released GABA is cleared from the synapse by GABA transporters

A

it can be loaded again into vesicles where it converted into glutamine and can be returned for the synthesis of GABA.

69
Q

GABA can exert an inhibitory influence by acting on which two receptors

A

GABA a

GABA b

70
Q

what do GABA a receptors do

A

GABAA receptors (as well as AMPA and NMDA receptors) are ionotropic receptors.

they increase influx of CL-

71
Q

what do GABA b receptors do

A

metabotropic receptors that increase efflux of K+

72
Q

what are inotropic receptors

A

-ions move rapidly across membrane -channels are selective to certain ions -effect requires transmitter to be bound to the receptor (many desensitize even in the continued presence of neurotransmitter, so ion flow is brief)

73
Q

what are metabotripic receptors

A

-typically involves G-protein activation that either directly, or indirectly (second messenger system) influences ion channel permeability or other intracellular processes
-slower than ionotropic
-second messengers may persist after removal of transmitter

74
Q

what does the amplitude of an EPSP depend on

A

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

small signal = small amount of transmitter release

larger signal = larger amount of transmitter release

75
Q

Is an EPSP always sufficient to depolarize the post-synaptic neuron to threshold, required for action potential generation.

A

not always

76
Q

how can EPSPs come together to reach threshold?

A

if sequenced quickly enough (Temporal Summation) or through multiple inputs (Spatial Summation). The summation allows the post- synaptic membrane potential to reach threshold.

77
Q

what happens if there is spatial summation of EPSP and IPSP

A

IPSPs can prevent EPSPs from reaching threshold (postsynaptic inhibition)

78
Q

what do EPSPs at the level of thalamic neurons do

A

they can generate action potentials that then signal neurons in the cortex via thalamocortical projections.

79
Q

how does sensory information to reach the cortex

A

the EPSPs must be sufficient to overcome the inhibition being generated by the IPSPs

Neuroscience (10 decks)

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