intro to the nervous system Flashcards

1
Q

what is the CNS composed of?

A

brain + spinal cord

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2
Q

what is the PNS composed of?

A

all sensory and motor neurones across our body

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3
Q

what is the autonomic nervous system?

A

outputs from its fibers are directed to the hear and other internal organs (involuntary)

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4
Q

what are efferent fibers?

A

motor neurons

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5
Q

what are afferent fibers?

A

sensory neurons

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6
Q

how many neurons compose the nervous system?

A

100 billion

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7
Q

what are neurons

A

they are electrical cells

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8
Q

how do neurons talk to each other?

A

communication occurs are the synapses, a specialized site in the cell

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9
Q

what is the shape and size of a neuron?

A

they come in multiple and various shapes and sizes which are all extremly complex

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10
Q

what are the common morphologic elements found in all neurons?

A
  • cell body (soma)
  • dendrites (branches)
  • axon (single)
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11
Q

what can the branching of a neuron say about that specific neuron?

A

the greater the branching the greater the input for that neuron will/can be

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12
Q

can there be small branches found at the ends of the axons?

A

yes, these act with specialized structures of the presynaptic terminals

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13
Q

how does information go across a neuron to another?

A

the output is given to the dendrite of an adjacent neuron and becomes the input of that neuron which passes through the cell body into the axon which can then transfer it as an output to presynaptic terminals or to dendrites of other neurons

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14
Q

what is the typical resting potential of a neuron?

A

between -60 and -70 mV

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15
Q

what is the negative charge of the resting potential caused by?

A

due to the small excess of negative ions inside the cell

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16
Q

how is the resting membrane potential of neurons created?

A

by the concentration gradients of various physiological ions
potassium is high on the inside and strives to exit the neuron, Chloride and sodium are high on the outside and want to come in

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17
Q

then why is their a slighlt negative imbalance?

A

when the membrane is at rest, it is more permeable to potassium than to the other ions allowing to flow out (selective permeability of the membrane)

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18
Q

what happens when K+ leaks out of the membrane?

A

it leaves behind impermeant, negatively charged ions which give the negative membrane potential

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19
Q

why does not all the K+ exit the cell due to its higher permeability?

A

the accumulation of unpaired negative ions will cause for an electrical gradient to pull back k+ into the cell

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20
Q

what happens when the chemical and electrical gradient of the cell are equal?

A

the system is in equilibrium and so is the membrane potential

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21
Q

what is the membrane potential at equilibrium described by?

A

Nernst equation

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22
Q

what is the equilibrium potential for K+

A

-90 mV

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23
Q

what is the resting permeability to k+ caused by? how does that happen?

A

leak channels

they form k+ selective pore through the membrane

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24
Q

when are the K+ leak channels open?

A

they are open all the time, however ions can pass through at resting membrane potential

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25
Q

why is the resting membrane which is permeable to K+ at -70 mV rather than -90 mV?

A

-each ion has an equilibrium potential that is determined by its charges and internal/external concentration, hence if the equilibrium potentials for each ion is calculated this is how the -70 is obtained

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26
Q

what other ion leaks in the membrane and in what direction?

A

very small leakage for Na inwards

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27
Q

what is the membrane potential determined by?

A

concentration gradients and relative permeability

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28
Q

which of the 2 can change more? relative permeability or concentration gradients?

A

relative permeability

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29
Q

which relative permeability makes the greatest contribution to the membrane potential?

A

the dominant permeability, hence the permeability for potassium

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30
Q

how are the sodium and potassium gradients maintained?

A

by the Na-K-pumps

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31
Q

what type of energy is used by the Na-K pump?

A

energy produced by ATP hydrolysis

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32
Q

what is the net movement that results from Na-K pumps?

A

3 Na outwards

2 K+ inwards

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33
Q

what is the action potential?

A

it is the brief potential impulse that causes for axons to propagate info from one region of the NS to another

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34
Q

where do action potentials usually start off?

A

initial segment of the axon

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35
Q

where do action potentials end?

A

they propagte down the length of the axon and into presynaptic terminals

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36
Q

what is the action potential?

A

it is a transient depolarizing spike that moved swn the axon

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37
Q

at the action potential peak, what does the membrane potential approach?

A

Ena

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38
Q

when is the action potential initiated?

A

when the membrane potential depolarizes to a threshold level

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39
Q

what determines the threshold?

A

the properties of ion channels in the axon membrane, especially the voltage gated sodium channels

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40
Q

what is the depolarizing phase of the action potential cased by?

A

the sodium ions flowing into the cell through the voltage gated channels

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41
Q

what are the 3 critical properties of the sodium channels?

A
  • closed at membrane potential, open when it depolarizes
  • selective for Na+
  • the open channel rapidly inactivates stopping the flow of Na+ ions
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42
Q

what type of process is the rising phase of the action potential?

A

a regenerative process

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43
Q

what positive feedback mechanisms is caused by depolarization?

A

depolarization to the threshold activates a small fraction of Na channels which further depolarizes the membrane resulting in the activation of more sodium channels

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44
Q

what does the positive feedback mechanism result in?

A

maximal activation of the sodium channel, a large sodium influx, and depolarization of the membrane from resting to new level

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45
Q

the density of the which higher?

leak potassium channels or voltage gated sodium

A

the density of the voltage gated sodium channels is higher

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46
Q

what factors contribute to the falling phase of the action potential?

A
  • sodium channel inactivation

- the delayed activation of voltage gated potassium channels

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47
Q

when does sodium and potassium gradientrun down faster?

A

when the neuron is firing lots of action potentials because the pumps have to keep up with the neuronal activity

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48
Q

what is the propagation of the action potential caused by?

A

the spread of electronic currents from the site of the action potential which excites adjacent regions in the axon

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49
Q

why does the sodium not go back the other way?

A

since the voltage gated channels inactivate and don’t open again until the membrane returns to resting potential its allows for the impulse to move in only one direction

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50
Q

what is the period where sodium channels are completely unexcitable called?

A

the absolute refraction period

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51
Q

what happens during the absolute refraction period?

A

the axon is less excitable and is unlikely to fire an action potential

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52
Q

how could you describe the function of action potentials?

A

all or none event

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53
Q

how do neurons send information

A

by means of the frequency and pattern of the action potentials

54
Q

sodium channels are the molecular targets for what?

A

naturally occuring toxins

  • tetrodotoxin in pufferfish
  • batrachotoxin in phyllobate frogs
  • scorpions, anemonae, insecticides
55
Q

what can block sodium channels?

A

therapeutical drugs such as local anesthetics and antiepiletic drugs

56
Q

what feature of action potentials is important for survival?

A

the rapid propagation of the action potential

57
Q

what strategry was adopted by squids to ensure rapid propagation of the action potential?

A

their body developped an axon 1000 times fatter than our axons

58
Q

why does having a fatter axon improve the rate of propagation?

A

the rate of the action potential is proportional to the diameter of the axon

59
Q

what did vertebrae neurons accomplish to have small axons with a high conductance velocity?

A

the axons are wrapped with myelin

60
Q

what is myelin formed with?

A

schwann cells (PNS) and oligodendrocytes in the CNS

61
Q

how does myelin function?

A

it acts as an electrical insulator, enabling electrotonic currents to travel farther and faster down the axon

62
Q

what periodically interrupts myelin?

A

nodes of ravier

63
Q

what is contained in the nodes of ravier?

A

these are regions of bare axons that contrain very high concentrations of voltage gated sodium channels

64
Q

what do the nodes of ravier enable?

A

they enables that the signal gets regenerated at periodical intervals

65
Q

are myelinated axons generally longer or shorter?

A

longer

66
Q

what is a commun immune disease caused by the loss of myelin?

A

multiple sclerosis

67
Q

which matter contains the most myelinated axons?

A

white matter

68
Q

what matter is comprised of cell bodies, dendrites and synapses?

A

gray matter

69
Q

what are the 3 main synapses?

A

axodendritic
axosomatic
axoaxonic

70
Q

generally what type of synapses are spine synapses?

A

excitatory synapses

71
Q

generally what type of synapses are shaft synapses?

A

inhibitory synapses

72
Q

can a cell only make a single or multiple synapses with other neurons?

A

multiple, due to the branching axon

73
Q

what is the purpose of presynaptic vesicles?

A

they serve as the back up vesicles and are stored in the presynaptic terminal

74
Q

what are the active zones found in presynaptic terminals

A

the active zones contain vesicles that are release to release the chemicals into the synaptic cleft

75
Q

what is the name of the dark regions found in the postsynaptic spine?

A

these are the postsynaptic density which are regions with high protein concentration

76
Q

what is found between the presynaptic terminal and the post synaptic spine?

A

an extracellular space known as the synaptic cleft

77
Q

what type of channel is found in the presynaptic terminal?

A

voltage gated calcium channels

78
Q

how do voltage gated calcium channels function?

A

Ca in < Ca out causing for gradient to move inwards

79
Q

when are the voltage gated calcium channels open?

A

at resting membrane potential

80
Q

what is the function of voltage gated calcium channels in the presynaptic terminal?

A

they trigger the release of neurotransmitters

81
Q

what type of channel can be found in the postsynaptic spine?

A

ligand gated ion channels

82
Q

ligand gated ion channels are receptors for transmission where?

A

at the brain synapses

83
Q

what are the fundamental steps of chemical synaptic transmission?

A

1- the action potential invades the presynaptic terminal Ca moves inwards
2- synaptic vesicles fuse with the presynaptic membrane and release transmitters into the synaptic cleft
3- transmitters diffuse across the clef and activate receptors of the postsynaptic membrane

84
Q

what can the postsynaptic response to a neurotransmitter be?

A
  • excitatory postsynaptic potential

- inhibitory postsynaptic potential

85
Q

what does the excitatory postsynaptic potential do?

A

it depolarizes the postsynaptic membrane (less negative)

86
Q

what does the inhibitatory postsynaptic potential

A

it hyperpolarizes the postsynaptic membrane (more negative)

87
Q

what is the main exictatory NT in the brain?

A

glutamate

88
Q

what are the 2 types of ionotropic glutamate receptors?

A

AMPA

NMDA

89
Q

What are ionotropic receptors?

A

these are receptors that these are ions channels that will open in response to biunding of small molecules on their external surface

90
Q

what are AMPA receptors responsible for at the excitatory synapse?

A

the fast EPSP

91
Q

what is the first step so that allows the fast EPSP occurs at the excitatory synapses?

A

glutamate is released from the presynaptic terminals and binds to AMPA receptors
their

92
Q

what does the binding of the glutamate to AMPA cause?

A

it allows for sodium cations to flow into the postsynaptic spine causing for a small transient depolarization

93
Q

what is the voltage and duration of a single EPSP in typical depolarized brain synapses?

A

greater than a few milivolts

lasts around 20 mili seconds

94
Q

is the depolarization caused by a single EPSP sufficient to depolarize the axon segment to the threshold?

A

no

95
Q

how many EPSP needs be be fired in order for their sum at the initial segment be sufficient to initiate action potential?

A

50-100 EPSPs

96
Q

what can the EPSPs come from?

A
  • multiple synpases acting in synchrony

- individual synapses activated at high frequencies

97
Q

what binds to NMDA receptors and opens them up?

A

glutamate

98
Q

what are the key properties of NMDA receptors?

A

at resting membrane potential Mg2+ blocks the pore

the pore is highly permeable to Ca2+

99
Q

how is Mg2+ expelled from the pore?

A

depolarization

100
Q

at -70 mV the majority of the synaptic current is carried how?

A

by Na+ through the AMPA receptors

101
Q

at -70 mV what happens if the postsynaptic membrane is depolarized?

A

a substantial Ca2+ current will flow inwards through the NMDA receptors

102
Q

what is synaptic plasticity?

A

when highly active excitatory synapses become stronger

103
Q

what receptor is involved in synaptic plasticity?

A

NMDA receptors

104
Q

long term potentiation (LTP) is a model of what?

A

synaptic plasticity

105
Q

what happens when there is a burst of action potentials?

A

the high frequency activity depolarizes the postsynaptic spine and removes Mg2+ enabling Ca2+ to pass through

106
Q

when are the EPSPs larger before, after or during the induction of LTP

A

hours after

107
Q

what are the 3 phases of LTP?

A

control
induction
LTP

108
Q

high concentrations of what can be toxic for neurons?

A

glutamate

109
Q

what does excitotoxicity involve?

A

Ca2+ influx through NMDA receptors

110
Q

what can excitotoxicity contribute to?

A

neuronal degeneration after a stroke or in cases of neurodegenerative diseases

111
Q

what is the main inhibitory neurotransmitter?

A

GABA

112
Q

what receptor is involved in the IPSP?

A

Gaba A receptor

113
Q

what type of receptor si the GABA a receptor?

A

ionotropic

114
Q

what does the activation of the Gaba A receptor cause?

A

influx of Cl- which hyperpolarizes the postsynaptic membrane

115
Q

where are inhibitory inputs usually located?

A

neat the cell soma because that is where they can have the maximal effect

116
Q

where are excitatory inputs usually located?

A

located on the dendritic spines

117
Q

what determines if a neuron fires an action potention or not?

A

the relative balance between EPSP and IPSP

118
Q

how does the output of the neuron differ on its firing of an action potential

A

the output follows a all of none firing of action potential

119
Q

what do glutamate synapses have?

A
ionotropic receptors (AMPA and NMDA)
metabotropuc glutamate receptors (mGluRs)
120
Q

what does the activation of mGluRs do?

A

it is activated by glutamate and will relat chemical signals to the inside of the postsynaptic neuron

121
Q

what is generated by the activation of mGluRs by glutamate?

A

a chemical signa (second messenger) inside the postsynaptic spine

122
Q

what is the function of second messengers?

A

they activate a range of cellular proteins such as ion channels, protein kinases and transcription factors

123
Q

does GABA also activate a metabotropic receptor?

A

yes Gaba B receptor

124
Q

what substances act mainly or entirely with metabotrophic receptors?

A

dopamine, serotonin, norephinephrine, neuropeptides (endorphins)

125
Q

what is the name given to substances that interact with metabotrophic receptors?

A

neuromodulators

126
Q

are neuromodulators directly involved in the fast flow of neural information?

A

no

127
Q

what is the fct of neuromodulators?

A

they modulate global neural states, influence alertness, attention and mood

128
Q

where do the neurones that release neuromodulators originate from?

A

in the brainstem or midbrain neuclei

129
Q

neuromodulators are important targets for what?

A

a wide range of drugs

130
Q

what does antidepressents such as prozac cause the transmission of?

A

serotonin

131
Q

what does amphetamines such as cocaine affect the transmission of?

A

depamine and norepinephrine