Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 STEP UWorld neuro+psycho > Neuro physio > Flashcards

Neuro physio Flashcards

1
Q

After resolution of HSV-1 (herpes labialis), where virus stays?

A

virus enters a latent phase - viral particles lay dormant in neural SENSORY ganglia (most commonly trigeminal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What induces HSV-1 reactivation?

A

Stress, illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is called transport when HSV-1 goes from skin to neurons?

A

virus enters nerve terminals –> dynein-dependent (retrograde) trasnsport in neuron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is called transport when HSV-1 goes up from neurons to skin?

A

kinesin-dependent (anterograde) transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In which part of the neuron stays HSV-1?

A

Latent virus integrated in DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The function of kinesin?

A

motor protein, that moves intracellular cargo (organelles, viral particles) away from nucleus, down to the axon and toward the nerve terminal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Kinesin-mediated movement is powered by …………….. and guided by …………………….

A

ATP hydrolysis;

guided by microtubule filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Direction of cargo in dynein and kinesin transport?

A

Dynein - toward the nucleus;

Kinesin - away from the nucleus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What protein is respondible for herpes labialis recurrence?

A

kinesin - it moves viral particles away from nucleus. Dynein - is not responsible, because it moves particles to neural sensory ganglia - important in establishing the latent phase following primary HSV infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do lamins?

A

It helps to form the fibrillar network that lines the inside of the nuclear envelope.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lamins provide structural support. What other 2 functions related to cell genetics?

A

Help to organize genome and regulate gene transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is located spectrin?

A

intracellularly along the plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

For which cell is important spectrin?

A

RBCs - maintains distinct shape. When defect - hereditary elliptocytosis and spherocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In which cells is expressed vimentin?

A

In mesenchymal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of vimentin?

A

Securing organelles inside the cytosol and provides resistance to mechanical stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the role of second messengers in release of ACh in synapsis in NMJ?

A

None. It does not play any role in synapsis in NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What stains Nissl stains in neuron?

A

RER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Kinesin is …………………….. protein

A

microtubule assoc motor protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is direction of transport in kinesin in relation to microtubules?

A

Away from nucleus - toward the plus ends of microtubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the result of toxic insult to kinesin?

A

impaired anterograde transport –> results in deficiency of synaptic vesicles at the nerve terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Microvilli and microtubules?

A

Microvilli do not contain microtubules or microtubule associated proteins. It contains actin thin filaments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Function of desmosomes?

A

mediate cell-cell adhesion between epithelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Location of T-tubules?

A

junction of the A and I brands of striated myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Function of T-tubules?

A

they are open to extracellular space and facilitate the spread of the depolarization to the inside of the cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the primary excitatory neurotrasmiter in the brain?

A

Glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

The glutamate NMDA receptor is a ……………….. and ……………….. ion channel

A

Potential-dependent and ligand-gated ion channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What ion form a plug in glutamate NMDA receptor?

A

magnesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are two events that opens glutamate NMDA receptors?

A

Displacement of magnesium and binding of glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What initiates displacement of magnesium in glutamate NMDA receptor?

A

initial depolarization impuls (non-NMDA mediated) –> loss of negative potential –> displaced magnesiujm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why in dying neurons can occur displacement of magnesium in glutamate NMDA?

A

loss of the ATP-dependent sodium-potassium gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

glutamate bind glutamate NMDA receptors along with ………………….

A

glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What allow unrestricted flow of calcium, sodium and potassium via glutamate NMDA receptors?

A

conformational changes that occurs after glutamate binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why there is depolarization in glutamate NMDA receptors if there is also potassium efflux?

A

influx of Sodium + calcium (depolaryzation) > efflux of potassium (hyperpolarize) –> NET = depolarization overcome hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What and where changes of magnesium concentration induces glutamate mediated neuron depolarization?

A

Higher extracellular magnesium levels block the NMDA channes –> decr. influx of calcium and sodium –> inhibited glutamate-mediated neruon depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

During acute ischemic stroke, a sudden, massive rise in ……………………………. occurs within the infarct zone.

A

extracellular glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

High extracellular glutamate levels in acute ischemic stroke leads to ……………..

A

glutamate NMDA receptor excessive activation –> increased calcium influx –> intracellular calcium overload.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens when there is increased intracellular calcium concentration in neuron? eg in acute ischemic stroke?

A

It accumulates in mitochondria –> triggered apoptotic neuronal death (excitotoxicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What and where release dying neurons?

A

they release more glutamate into the extacellular space –> increased excitation in neighboring neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Calcium overload (cytotoxicity) leads to 3 outcomes in CNS.

A

Mitochondrial dysfunction;
inc. ROS;
protease activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

modulation of the ………… receptor is an emerging frontier in neuroprotection

A

NMDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What cases loss of membrane potential in CNS injury?

A

decreased ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

WHat initiates depolarization in damaged CNS?

A

initial nonspecific depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What ion is used therapeutically to block depolarization in CNS?

A

Magensium. It blocks glutamate NMDA receptors –> prevent passage of calcium and sodium.
Magnesium itself does not pass through the NMDA receptors!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Excessive activation of the glutamate NMDA receptor causes ………………

A

Excitotoxic neuronal death through uncontrolled calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

By what depolarization is released magnesium from glutamate NMDA?

A

by non-NMDA-mediated depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

at what stage of the cell NMDA receptors are blocked by magnesium?

A

at the hyperpolarized resting membrane potential

47
Q

NMDA channels are impermeable to …………………

A

anions

48
Q

NMDA channels are ……………… to anions

A

impermeable

49
Q

The influx of chloride and bicarbonate anions induces ………………

A

hyperpolarization

50
Q

Influx of chloride and bicarbonate mediates …………………. ………… potential, generated by ………….. channels.

A

inhibitory postsynaptic; GABA-A channels.

51
Q

Neurons can also be hyperpolarized by ……………………. …………….., mediating inhibitory potentials generated by GABA-B channels.

A

potassium efflux

52
Q

Influx of chloride and bicarbone —> …………….. channels.
Efflux of potasium –> …………… channels.

A

GABA-A;

GABA-B

53
Q

Excitatory postsynaptic potential (EPSP) is a small ……………………………………… that moves the ………………… neuron closer to the threshold for full action potential firing

A

depolarization;

postsynaptic

54
Q

The EPSP occurs with rising …………………..

A

Intracellular calcium

55
Q

EPSP and calcium conductance relation?

A

The EPSP occurs with rising intracellular calcium (bottom panel), indicating that the involved postsynaptic receptor acts, at least in part, by increasing calcium conductance.

56
Q

What receptors participate at least in part in EPSP by increasing calcium conductance?

A

postsynaptic receptors

57
Q

What regulates synaptic plasticity?

A

increased calcium influx –> second-messenged signaling cascades –> regulation of synaptic plasticity

58
Q

repetitive excitation of postsynaptic neurons renders them more …………………, producing ………………. …………………. over time

A

responsive; stronger EPSPs

59
Q

repetitive excitation of postsynaptic neurons renders them more responsive, producing stronger EPSPs over time. How is called this process?

A

long-term potentiation (LTP) - dictates synaptic strength between hippocampal neurons

60
Q

Long-term potentiation is important in hippocampal neurons. LTP function in these neurons?

A

plays a critical role in the molecular basis of memory, learning, and addiction.

61
Q

Acute blockade of glutamate NMDA receptors confers the ………………….. of certain medications (eg, ketamine) and some drugs of illicit use

A

amnestic property

62
Q

Chronic blockade (eg, memantine) can exert ………………………………… effects by dampening glutamate-induced excitotoxicity

A

neuroprotective

63
Q

What is process of exitotoxicity?

A

neuron apoptosis due to calcium overload

64
Q

Dopamine can be either ………… or …………….. depending on the receptor subtype

A

excitatory or inhibitory

65
Q

Dopamine can be either excitatory or inhibitory depending on the …………….

A

receptor subtype

66
Q

D2 receptors are generally coupled to Gi proteins that inhibit protein kinase A, leading to the opening of potassium channels that …………… neuronal depolarization.

A

inhibit

67
Q

D2 receptors are generally coupled to ……… proteins.

A

Gi

68
Q

Gi proteins inhibits ………….

A

protein kinase A

69
Q

Inhibition of protein kinase A leads to ………………

A

opening of potassium channels –> inhibited neuronal depolarization

70
Q

GABA is the chief ………………….. neurotransmitter

A

inhibitory

71
Q

GABA causes postsynaptic hyperpolarization via ………………………………

A

Increased chloride and bicarbonate influx (ie, ionotropic GABA-A ion channel) or increased potassium efflux (ie, metabotropic GABA-B receptor.

72
Q

increased potassium efflux (ie, ………………………… GABA-B receptor

A

metabotropic

73
Q

increased chloride and bicarbonate influx (…………………. GABA-A ion channel)

A

ionotropic

74
Q

The glycine receptor causes inhibitory …………………… via increasing membrane permeability to chloride.

A

postsynaptic hyperpolarization

75
Q

The glycine receptor causes inhibitory postsynaptic hyperpolarization via increasing membrane permeability to ……………

A

Chloride

76
Q

What receptor mediates inhibitory interneuron transmission in the spinal cord?

A

glycine receptor

77
Q

Glycine receptor mediates inhibitory interneuron transmission in the ……………

A

spinal cord

78
Q

The norepinephrine alpha2 receptor is located predominantly on ………………………………………. in neuron

A

presinaptic nerve temrinals

79
Q

In what systems is located alpha 2 receptor?

A

CNS and PNS

80
Q

Activation of alpha2 receptors inhibits ……………………….. from the nerve terminal, inducing sympatholytic effects (eg, reduced heart rate, vasodilation).

A

norepinephrine release

81
Q

What is the main excitatory neurotransmiter of the CNS?

A

glutamate

82
Q

Calcium entry programs the neuron to depolarize more robustly to ………………..

A

repeated stimulations

83
Q

The resting membrane potential shown in the graph is negative, indicating that at rest, the membrane is permeable to an ion with a ……………………..

A

negative equilibrium potential (potassium or chloride)

84
Q

Opening of ligand-gated ion channels in response to ………………………………. binding, causes an increase in membrane potential to above zero.

A

neurotransmiter

85
Q

Membrane potential increases to above zero. This indicates that the membrane has become permeable for an ion with a …………………….

A

positive equilibrium potential (sodium or calcium)

86
Q

Opening of voltage-gated ion channels in response to the change in membrane potential, causes a drop in membrane potential, indicating that the membrane becomes permeable to an ion with a ……………………….

A

negative equilibrium potential (potassium or chloride

87
Q

If the membrane were permeable for sodium at rest, the resting membrane potential would be………………….

A

positive as the equilibrium potential of sodium is +60 mV.

88
Q

Membrane become more permeable for calcium or sodium following the opening of the voltage-gated ion channels. membrane potential would be ……………..

A

positive as both ions have positive equilibrium potentials.

89
Q

Permeability to ion and total membrane potential relation?

A

The more permeable the membrane becomes for a cellular ion, the more that ion’s equilibrium potential contributes to the total membrane potential.

90
Q

Glutamate binding leads to opening of ……………. in postsynaptic neurons and leads to ……………………….. influx

A

ligand-gated sodium channels;

leads to sodium influx –> membrane depolarization

91
Q

What part merges neuron body and axon?

A

axon hillock

92
Q

What substances are contained in axon hillock?

A

large number of voltage-gated sodium channels.

93
Q

When an action potential is triggered and propagates along the axon via a steady influx of sodium ions?

A

Once the axon hillock becomes sufficiently depolarized

94
Q

Once the axon hillock becomes sufficiently depolarized …………………..

A

an action potential is triggered and propagates along the axon via a steady influx of sodium ions

95
Q

What happens when action potential reaches the axonal terminal?

A

voltage gated calcium channels opens –> influx of calcium –> leads to fusion of vesicles containing neurotrasmitter and release of this neurotrasmiter

96
Q

Seizures occur due to ………….., ………………….. firing of ………………….. neurons in the brain

A

Seizures occur due to abnormal, synchronized firing of hyperexcitable neurons in the brain

97
Q

RER contains calcium. How it participates in vesicles fusion in neuron?

A

It doesn’t play any role. Calcium that is in RER and is released, is more important for skeletal muscle contraction

98
Q

What 4 changes are collectively known as action potential?

A

depolarization, repolarization, hyperpolarization and resting potential

99
Q

The action potential occurs due to changes in the membrane permeability to …………………. (2) ions.

A

Na+ and K+ ions

100
Q

Resting potential is maintained at -70mV bys high permeability to …….. and low permeability to ………….

A

potassium and sodium

101
Q

While at the resting potential, the inner side of the membrane is ………………. charged with respect to the outer surface of the membrane

A

negatively

102
Q

K efflux at resting potential occurs via …………………. channels.

A

non-gated K+ channels (leak channels)

103
Q

is there potassium efflux or influx at resting potential?

A

efflux

104
Q

Depolarization occurs due to opening of ……………….. channels with rapid influx of …………into the cell.

A

voltage-gated Na+ channels with rapid influx of Na+ into the cell.

105
Q

The large influx of Na+ leads to an ………………….. charge inside the membrane known as depolarization.

A

increased positive

106
Q

What is the maximum value of action potential?

A

+35mV

107
Q

Repolarization results from closure …………. channels and simultaneous opening of ………….. channels

A

Na+; K+

108
Q

What process is responsible for returning the membrane potential back to the resting potential?

A

Potassium efflux during repolarization

109
Q

Why occurs hyperpolarization?

A

Because the VOLTAGE-gated K+ channels remain open for a short time after repolarization is completed.

110
Q

What is mV when hyperpolarization?

A

-85mV

111
Q

What channels cause maintains hyperpolarization and what maintains resting potential?

A

hyper - voltage gated;
when they close - hyperpolarized MP returns to normal resting MP - and is maintained by NON-GATED POTASSIUM CHANNELS (leak channels)

112
Q

K+ ion permeance is highest during the ……………….. phase of the action potential.

A

repolarization

113
Q

What is overshoot in MP?

A

voltage above 0. eg maximum MP is around +35mv. So overshoot is from 0 to 35.

1 STEP UWorld neuro+psycho (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions