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Neuro - Week 2 > Cellular Physiology > Flashcards

Cellular Physiology Flashcards

1
Q

The gap between myelin sheaths is named this

A

Node of Ranvier

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2
Q

What is the the Node of Ranvier?

A

The gap between myelin sheats

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3
Q

This is the start area of the axon and the initiation site of action potentials (APs)

A

Axon hillock

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4
Q

These contact neurons and wrap around synapses
They also wrap around the blood vessels in the brain, where they act as a conduit for nutrients from the circulatory system to the neurons

A

Astrocytes

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5
Q

Astrocytes are linked to each other by these

A

Gap junctions

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6
Q

Small mobile cells in the CNS that act as the brain’s host defense system
When parts of the brain are damaged, these accumulate at the site of injury to remove the damaged tissue via phagocytosis

A

Microglial cells

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7
Q

These are responsible for the myelination of axons in the CNS

A

Oligodendrocytes

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8
Q

These are responsible for the myelination of axons in the PNS

A

Schwann cells

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9
Q

Oligodendrocytes form the myelination of axons in the CNS or PNS?

A

CNS

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10
Q

Schwann cells form the myelination of axons in the CNS or PNS?

A

PNS

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11
Q

The cells that line the ventricular areas of the brain and the central canal of the spinal cord, help in the circulation of the CSF

A

Ependymal cells

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12
Q

Refers to the movement of ions through the membrane through ion channels

A

Current

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13
Q

This is the result of the movement of several different ion species through various ion channels and transporters in the plasma membrane

A

Resting membrane potential

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14
Q

This equation defines the equilibrium potential of a specific ion separated by a cell membrane

A

Nernst equation

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15
Q

This is the typical resting membrane potential for neurons

A

-60 to -70mv

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16
Q

In depolarization, is Vm more positive or negative than RP?

A

Positive

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17
Q

In hyperpolarization, is Vm more positive or negative than RP?

A

Negative

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18
Q

Will the membrane potential depolarize or hyperpolarize when the external concentration of K+ is increased?

A

Depolarize
(Vm becomes more positive than RP)

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19
Q

A cell’s resting membrane potential is very sensitive to changes in extracellular concentrations of this ion

A

Potassium

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20
Q

Do changes in extracellular potassium concentrations affect resting membrane potential?

A

Yes!
Increase [K+] = depolarization

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21
Q

Do changes in extracellular sodium concentrations affect resting membrane potential?

A

No
Sodium channels are closed under resting conditions

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22
Q

This refers to the number of channels that are open in a membrane

A

Conductance

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23
Q

This is the membrane potential at which the occurrence of the action potential is required

A

Threshold potential

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24
Q

Resting potential is due to these channels

A

Ungated K+ channels that are almost fully open

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25
Depolarization is due to these channels
Opening of Na+ channels and Na+ entry
26
Repolarization is due to these channels
Delayed opening of K+ channels, and K+ efflux and Na+ channel inactivation
27
After-hyperpolarization is due to these channels
Slow closing of K+ channels, and opening of additional K+ channels
28
Tetrodotoxin blocks this channel
Sodium
29
Tetraethylammonium blocks this channel
Potassium
30
Lidocaine blocks this channel
Sodium
31
This is the period after AP initiation and just after the peak when a stimulus (no matter how strong) will not initiate another AP due to Na+ channel inactivation
Absolute refractory period
32
This is the period when Na+ channels are recovering from the inactivation, but a strong stimulus can produce another AP
Relative refractory period
33
What effect does demyelination have on action potential conduction velocity?
Decreases
34
Do action potentials decay as they travel down the axons?
No
35
Conduction velocity is positively correlated to this characteristic of the fiber
Diameter
36
These form a complex and tether the vesicle to the plasma membrane for docking and priming
SNAREs
37
SNAP-25, syntaxin, synaptobrevin are this type of compound
SNAREs
38
Increased levels of this in the presynaptic terminal stimulates acetylcholine release from synaptic vesicles into the synaptic cleft
Calcium
39
Influx of this causes local depolarization of the postjunctional membrane of the neuromuscular junction
Sodium
40
Bolutinum toxin blocks release of this at the neuromuscular junction
Acetylcholine
41
What effect does botilunum toxin have at the neuromuscular junction?
Total blockade Paralysis of respiratory muscles, death
42
Curare competes with this for receptors on motor end plate
Acetylcholine
43
What is the effect of Curare at the neuromuscular junction?
Decreases size of end plate potential May produce paralysis of respiratory muscles and death
44
Neostigmine is an inhibitor of this
Acetylcholinesterase
45
What is the effect of Neostigmine at the neuromuscular junction?
Prolongs and enhances action of acetylcholine at the motor end plate
46
Hemicholinium blocks reuptake of this into presynaptic terminal
Choline
47
What effect does Hemicholinium have at the neuromuscular junction?
Depletes acetylcholine stores from presynaptic terminal
48
Excitatory synapse releases excitatory neurotransmitters, such as this
Glutamate
49
Excitatory synapse releases excitatory neurotransmitters that triggers opening of these channels
Sodium
50
Inhibitory synapse releases inhibitory neurotransmitters, such as this
GABA
51
Inhibitory synapse releases inhibitory neurotransmitters triggers opening of these channels
Chloride
52
Is glutamate an excitatory or inhibitory neurotransmitter?
Excitatory
53
In this part of the body, acetylcholine is a neuromodulator
Brain
54
In this part of the body, acetylcholine is a neurotransmitter
Neuromuscular junction
55
In the brain, is acetylcholine a neuromodulator or neurotransmitter?
Neuromodulator
56
In the neuromuscular junction, is acetylcholine a neuromodulator or neurotransmitter?
Neurotransmitter
57
Do ionotropic or metabotropic receptors form ion channels? Fast responses
Ionotropic
58
Do ionotropic or metabotropic receptors use second messengers (i.e. G protein)? Slow responses
Metabtropic
59
Are NMDA and AMPA receptors considered ionotropic or metabotropic?
Ionotropic receptors
60
AMPA transports these ions
Sodium and potassium
61
NMDA transorts these ions
Sodium, potassium, and calcium
62
Are NMDA and AMPA receptors excitatory or inhibitory?
Excitatory
63
Is NMDA a ligand-gated or voltage-gated ionotropic receptor?
Both
64
This usually blocks the NMDA receptor during normal function
Magnesium
65
Silent synapse contains this type of receptors only
NMDA (no AMPA)
66
Type of excitatory synapse in the brain that are initially inactive but can become active under certain conditions Contains NMDA receptors only
Silent synapse
67
Is GABA-A or -B considered a ligand-gated ionotropic receptor?
A
68
Is GABA-A or -B considered a metabotropic receptor?
B
69
Benzodiazepines bind to these subunits of GABA-A
Alpha and gamma
70
Barbiturates bind to these subunits of GABA-A
Alpha and beta
71
Alcohol binds to these subunits of GABA-A
Alpha and delta
72
Benzodiazepines, barbiturates, and alcohol have this effect on GABA
Are positive allosteric modulators of GABA-A = enhance receptor function indirectly
73
This is used as an antidote in the treatment of benzodiazepine overdoses
Flumazenil
74
This compound decreases GABA function by blocking the pore
Picrotoxin
75
This compound is a competitive GABA receptor antagonist
Bicuculline
76
Six connexins form a channel (pore) called this
Connexon
77
What forms a connexon?
6 connexins
78
These have an important role in synchronizing neuronal activity and propagation of seizures Are found in neurons and astrocytes Can spread electrical current
Electrical synapses (Gap junctions)
79
Astrocytes maintain homeostasis of this in the CNS
Glutamate
80
These cells provide net synthesis of glutamine
Astrocytes
81
Long-term potential involves insertion of AMPA receptors to these membranes
Postsynaptic
82
Long-term depression involves removal of AMPA receptors to these membranes
Postsynaptic

Neuro - Week 2 (10 decks)

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