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PHGY 209 > Nervous system > Flashcards

Nervous system Flashcards

1
Q

What is the role of action potential

A

propagate information from one region of the nervous system to another one (electrical impulses)

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2
Q

Where the action potential start and stop (the travel of an action potential) ?

A

start at the initial segment of the axon and then propagate down the lenght of the axon to the presynaptic terminals

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3
Q

At the action potential peak, the membrane potential apprpaches what?

A

E (Na)

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4
Q

how long is an action potential

A

1 or 2 mms

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5
Q

what is the process of the action potential?

A

1- goes from the resting level (-70mV)
2- to about +30 mV
3- drop back to -70 mV

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6
Q

When the action potential is initiated ?

A

when the membrane potential depolarizes to a threshold level

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7
Q

how the threshold is determined

A

by the properties of ion channels in the axon membrane (especially voltage-gated sodium channels)

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8
Q

Is the action potential is an all or nothing events

A

yes

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9
Q

By what the rising/depolarizing phase of the action potential is caused

A

by sodium (Na+) flowing into the cell through voltage-gated sodium channels.

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10
Q

properties (3) of voltage-gated sodium channels

A

1) They are closed at the resting membrane potential, but open when the membrane depolarizes.
2) They are selective for Na+. opens and lets NA+ flow in
3) The open channel rapidly inactivates, stopping the flow of Na+ ions.

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11
Q

what activates the depolarization of the membrane to threshold

A

a small fraction of sodium channels = depolarize the membrane = activation of more sodium channels

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12
Q

positive feedback mechanism of the action potential process

A

maximal activation of sodium channels, a large sodium influx and depolarizarion of the membrane from the membrane from the resting to near the E(Na+) = inactivation terminates the sodium influx =membrane relax

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13
Q

the dominant at restinf and at the peak

A
  • At rest, the dominant permeability is to potassium, so the membrane is close to the potassium equilibrium. At the peak, there’s more sodium channels = the dominant is sodium = sodium equilibrium. Then, the sodium channels inactivate, and we go back to the potassium equilibrium.
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14
Q

the density of voltage-gated sodium channels in the axon membrane is _ than the density of leak potassium channels

A

much higher
so at the peak of the action potential, the Na+ permeability swamps the resting permeability for K+.

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15
Q

what are the factors contributing to the falling phase of the action potential

A

1- sodium channels
2- the delayed activation of voltage-gated potassium channels

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16
Q

when the voltage gated potassium channels open?

A
  • They are close at the at the resting membrane potential and the open when the membrane depolarized
  • It’s made a hole permeable to potassium
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17
Q

the speed of the sodium-potassium pump

A

The sodium and potassium gradients run down faster when the neuron is firing a lot of action potentials. The pumps must keep up with neuronal activity.

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18
Q

is the potassium leaking ou and the sodium leaking in even at rest?

A

yes, They are constantly maintaining they concentrations gradiets.

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19
Q

action potential propagation is caused by?

A

spread of electrotonic currents from the site of the action potential, which excites adjacent regions of axon.

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20
Q

the process of the propagaation of the action potential

A
  1. We depolarize the membrane to the action potential threshold
  2. The action potential happened at the initial segment
  3. The membrane depolarized (very rapidly up to +- 30 mV
  4. But the charge at the right is -70 mV, then the positive and the negative attract each other
  5. The positive charge is attack and move to the segment
  6. Then, this region will be depolarized = action potential threshold = action potential
  7. … keep propagate (continuous) even if it’s 60 feet’s long
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21
Q

why the sodium charge doesn’t go the other way

A

the voltage gated behind are inactivate; , they can’t open again. Then, they can’t go back and need to go forward.

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22
Q

absolute refractory period.

A

the sodium channels are inactivated, and the membrane is completely unexcitable.

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23
Q

relative refractory period

A

the axon is less excitable and is unlikely to fire an action potential. Over a somewhat longer period, during which the voltage-gated potassium channels are open, the membrane potential overshoots its resting level.

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24
Q

Neurons send information by means of _?

A

the frequency and pattern of action potentials.

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25
Q

size of an action potential

A

always the same

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26
Q

Sodium channels are the molecular targets for

A

naturally occurring neurotoxins. Nature is involve.

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27
Q

Puffer fish

A

make tetrodotoxin, an extremely potent inhibitor of sodium channels

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28
Q

Phyllobates frogs

A

secrete batrachotoxin, a powerful sodium channel activator

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29
Q

Tetrodotoxin:

A

block volage-gated sodium channels. You can die

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30
Q

Batrachotoxin:

A

sodium channel activator; they can’t close. The neuron are going to be crazy.

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31
Q

Sodium channels are also modulated by

A

pyrethroid insecticides, scorpion and anemone toxins.

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32
Q

are sodium channels can be blocked ? if yes, how?

A

yes, by therapeutically important drugs, including local anesthetics and some antiepileptic agents.

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33
Q

local anesthetics (funciton)

A

block voltage-gated sodium channels. They stop there and can’t go through there. The anesthetics is injected in the nerve.

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34
Q

some local anesthetics

A
  • Lidocaine
  • Benzocaine
  • Tetracaine
  • Cocaine
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35
Q

function Antiepileptics

A

block sodium channel

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36
Q

some antipileptics

A
  • Phenytoin (Dilantin): when people have epilepsies (prevent).
  • Carbamazepine (Tegretol)
  • Lamotrigine
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37
Q

the propagation rate of the action potential is proportional to

A

axon diameter

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38
Q

why it’s important to have rapide propagation of action potential?

A

potentials is important for survival, especially in situations that require rapid, reflexive responses.

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39
Q

squid axon potential

A

making giant axons, 1000 times fatter than our axons.

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40
Q

the fastest our action potential can propagate?

A

100m/s

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41
Q

how a propagation of action potential can be faster

A
  • The diameter of the axon; more it’s large, more it’s fast.
  • Insulate de axon
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42
Q

what is the solution to have a small axon that have a high conduction?

A

by wrapping the axon in an insulator called myelin

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43
Q

by what is formed the myelin?

A

by Schwann cells (in the PNS) or oligodendrocytes (in the CNS).

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44
Q

where if the myelin ?

A
  • wraps the axon
  • The myelin is not continuous
  • It’s separate at gaps (1mm) / nodes of Ranvier.
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45
Q

what is the function of the myelin

A

an electrical insulator, enabling charge to travel farther and faster down the axon.

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46
Q

the names of the periodic gaps in the myelin

A

nodes of Ranvier

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47
Q

what containts the nodes of Ranvier

A

These regions of bare axon contain very high concentrations of voltage-gated sodium channels

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48
Q

what is the function of the nodes of ranvier

A

enabling the signal to be regenerated at periodic intervals.

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49
Q

the causes of sclerosis

A

loss of myelin ( the info is not send good)

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49
Q

the causes of sclerosis

A

loss of myelin ( the info is not send good)

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50
Q

where happen most of the sclerosis

A

places of the brain where the myelin is degraded

51
Q

white matter

A

regions of the brain and spinal cord that contain mostly myelinated axons.

52
Q

gray axon

A

comprises cell bodies, dendrites, and synapses.

53
Q

where are the synapses

A

on the dendrites

54
Q

Axodendritic

A

axon making a synapse with a dendrite.

55
Q

Spine synapse

A

the synapses are on spine of the dendrites. They are excitatory synapses.

56
Q

Shaft synapse

A

between the spine, there’s synapse that are directly on the shaft of the dendrites. They are inhibitory synapses

57
Q

Axosomatic:

A

between an axon and the cell body of the neuron. They are inhibitory

58
Q

Axoaxonic

A

when the pre-synaptic terminal of a neuron is making a synapse with a pre-synaptic of another neuron

59
Q

pyramidal cell of the cerebral cortex

A

Dendrites and spines

60
Q

number of synapse and axon for one neuron

A

Each neuron has only 1 axon (connection to the cell body) but have many synapses.

61
Q

is a message can be resend directly to the same neuron that send it

A

yes

62
Q

is a single synpase can have more than one synapse

A

A single neuron, through its branching axon may make synapses with many other neurons

63
Q
  • Presynaptic terminal
A

end of the axon.

64
Q
  • Postsynaptic
A

after the cleft

65
Q

Synaptic cleft

A

: there’s place between the presynaptic terminal and the postsynaptic spine

66
Q
  • Vesicle
A

made of plasma membrane and contain the neurotransmitters.

67
Q

active zone

A

vesicles are line up on the membrane and face up the synaptic cleft. They are involved in the function of the synapse. (Ready to be use).

68
Q
  • The postsynaptic density
A

in the postsynaptic membrane = pack of proteins

69
Q

where are the voltage-gated calcium channel

A

they are in the presynaptic terminal.

70
Q

what triggers the release of neurotransmitter

A

activation of voltage-gated calcium channels

71
Q

ligand-gated ion channels (where and what)

A
  • in the postsynaptic receptors
  • for transmission at brain synapse
72
Q

fundamental steps of chemical synaptic transmission

A

1- The action potential arrives in the presynaptic terminal = depolarize. Calcium channels open, resulting in Ca2+ influx into the terminal (cleft) (the calcium is the signal)
2- Synaptic vesicles fuse with the presynaptic membrane, releasing transmitter into the synaptic cleft.
3- Transmitter diffuses across the cleft and activates receptors in the postsynaptic membrane. (the receptors are activated and ions can flow in)

73
Q

Calcium-dependent fusion of a synaptic vesicle at an active zone

A

When the calcium channel open, calcium flows in and bind to protein. They protein will change of conformation. That drive diffusion of the vesicle with the membrane in the synaptic cleft. The presynaptic terminal pinches the vesicle up again and it’s continued.

74
Q

the differents kind of postsynaptique response to neurotransmitter

A

an excitatory postsynaptic potential, (EPSP) which depolarizes the postsynaptic membrane, or an inhibitory postysnaptic potential (IPSP), which hyperpolarizes the postsynaptic membrane.

75
Q

excitatory synapses

A
  • they make the postsynaptic cell more likely to make action potential.
  • They are the one with the long synapses.
  • to the EPSP threshold
76
Q
  • Inhibitory synapses
A
  • they hyperpolarized the membrane.
  • It pushes the membrane further aways from the threshold.
  • IPSP they tend to have short axon and they are really localize.
77
Q

what is the main ecitatory neurotransmitter in the brain

A

glutamate (what is packed in the vesicle)

78
Q

Rapid excitatory transmission at synapses is primarily due to

A

the actions of glutamate on two types of ionotropic glutamate receptors

79
Q

types of ionotropic receptors

A

1) AMPA receptors
2) NMDA receptors.

80
Q

ionotropic receptors definitions

A

that they are ion channels, that open in response to binding of small molecules (e.g. neurotransmitters) to receptor sites on their external surfaces.

81
Q

AMPA receptors are responsible for

A

the “fast” EPSP at excitatory synapses.

82
Q

the process of the AMPA receptors

A

1- An action potential propagates down the presynaptic terminal and it is depolarized. The calcium channels open and the calcium flow in and bind to the protein that trigger the event.
2- There’s diffusion of one of the vesicleswith the membrane. Is content (glutamite) is in the cleft and will bind to the AMPA receptors
3- The AMPA receptors open. They have a pore permeable to sodium ions (Na+). That make sodium to flows in the postsynaptic spine. The postsynaptic spine will be depolarized.

83
Q

the EPSP is

A

a small, transient depolarization of the postsynaptic spine.
- The depolarization is small; it’s about 1 or 2 mV.

84
Q

In typical brain synapses, the depolarization caused by a single EPSP is

A

> a few millivolts and last around 20 msec.

85
Q

is The depolarization caused by a single EPSP can activate the axon to atteindre the threshold

A

no; too small to depolarize the axon initial segment to threshold.

86
Q

how many EPSP do we need to have initiate an action potential

A

From 50 to 100

87
Q

where the EPSP came from

A

These near-simultaneous EPSPs can come from multiple synapses acting in synchrony and/or from individual synapses, activated at high frequencies.

88
Q

NMDA receptors

A
  • At resting membrane potentials, the pore is blocked by Mg2+; depolarization expels Mg2+, enabling the pore to conduct.
  • The open pore is highly permeable to Ca2+ as well as monovalent cations.
89
Q

At -70 mV almost all the synaptic current at an excitatory glutamate synapse

A

is carried by Na+ through AMPA receptors

90
Q

what happends to the Ca2+ if the postsynapic membrane is depolarized

A

a substantial Ca2+ current flows through NMDA receptors.

91
Q

synaptic plasticity

A

Highly active excitatory synapses become stronger (i.e. the EPSPs become larger

92
Q

what involes the synaptic plasticity (synapse can get stronger)

A

NMDA receptors

93
Q

Model of synaptic plasticity

A

Long-term memory

94
Q

process of long-term memory

A

1- there an action potential
2- the glutamite is release
3- the glutamite binds to the AMPA and the MNDA
4- sodium go in the AMPA receptor = littlem EPSP

high frequency activity
5- depolarized the postsynaptic spine
6- removing the Mg2+ block of NMDA receptors
7- conduct Ca2+

when we come back = larger EPSP = synapse stronger = more AMPA receptors = more sodium flow in …

95
Q

High concentrations of glutamate

A

toxic to neurons

96
Q

excitotoxicity

A

glutamate kill the neuron)

97
Q

if the AMPA receptor have too much glutamate around and the concentration stays high too long

A

the neuron is too much ercitite = too much sodium and calcium that flow in. neurons don’t like calcium for too long.

98
Q

neuronal degeneration after stroke and in some neurodegenerative diseases.

A

excitotoxicity contributes to it

99
Q

Inhibitory synapses

A
  • The pattern of neuron is break by the inhibitory. They determine the pattern
100
Q

The main inhibitory neurotransmitter in the brain

A

-aminobutyric acid (GABA).

101
Q

The postsynaptic receptor responsible for the IPSP

A

GABAa receptor.

102
Q

receptor types of the GABAa

A

ionotropic receptor

103
Q

receptor types of the GABAa

A

ionotropic receptor

104
Q

. Activation of the GABAA receptor causes

A

influx of Cl- , which hyperpolarizes the postsynaptic membrane.

105
Q

When the neurotransmitter (GABA) bien to the receptor GABAa

A

it opens a hole that is permeable to chloride ions (high concentration on the outside and low concentration on the inside) chloride is a negative charge that flows in and will hyperpolarized the cell. It moves through the chloride potential. (Less likely to have action potential)

106
Q

Excitatory inputs tend to be located on

A

dendritic spines

107
Q

inhibitory inputs are often clustered on or near

A

the cell soma

108
Q

on what depends the activation of an actio

A

depends on the relative balance of EPSPs and IPSPs

109
Q

glutamate synapses have _….

A
  • iononotropic receptors (AMAPA and NMDA receptors)
  • metabotropic glutamate receptors (mGluR’s)
110
Q

metabotropic receptors

A

glutamate receptors (mGluR’s)

111
Q

ionotropic receptors

A

AMPA, NMDA receptors

112
Q

how - activation of mGluR’s

A

by glutamate

113
Q

activation of mGluR’s by glutamate relays

A

a chemical signal to the nside of the postsynaptic neuron

114
Q

what happend when the chamical signal is generates (activation of mGluR’s)

A

a seconde messenger is called inside the postsynaptic spine

The AMPA receptor open u and change its configuration. The sodium ions flow in and depolarize.
For the metabotropic receptors: glutamate activate the receptors and will initiate biochemicals events on the inside of the cell that cause to generate the 2nd messengers.

115
Q

the second messengers activates what

A

a range of cellular proteins, indluding ions channel, protein kinases, enzymes and transcription factors ( do a lot of things)

116
Q

Glutamate and GABA activate both

A

ionotropic and metabotropic receptors. (The metabotropic glutamate and GABA receptors are called mGluRs and GABAB receptors, respectively.)

117
Q

the action of neurotranmitter

A

interact mainly, or entirely with metabotropic receptors

118
Q

types of neurotranmitter

A

dopamine, serotonin, norepinephrine, neuropeptides such as endorphins = neuromodulators

119
Q

what is the role of the neuromodulators

A

modulate global neural states, influencing alertness, attention, and mood.

120
Q

Neurons that release neuromodulators often originate

A

small brainstem or midbrain nuclei

121
Q

where the axons af the neuromodulators are diffuse

A

trhoughout the brain

122
Q

dopamine projections in the human brain

A

The neurons that release dopamine are all in a small region of our brain (substantial Nigra and ventral tegmental area). These neurons have axon that goes everywhere and branch.

123
Q

Neuromodulator systems are important targets for

A

a wide range drug

124
Q

antidepressants, such as Prozac, affect

A

serotonergic transmission

125
Q

amphetamines, cocaine and other stimulants typically affect

A

dopamine and norepinephrine transmission.

PHGY 209 (6 decks)

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