Brainscape's Knowledge GenomeTM

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


See full index

NSC 4352 Cellular Neuroscience > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

how do we test the proposed functions of domains of channel proteins?

A

sequence homologies– determine which portions of primary sequences of ion channels are same/very similar (we look at the same channel from several different species, and what is conserved must be important)

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

sequence homologies in the ACh gated channel

A

ACh receptor portion of the channel is highly conserved

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

sequence homologies in Vg channels

A

they all have a membrane spanning region with charged amino acids at each third position; the voltage sensor is found only in voltage gated channels

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

structure of voltage gated channels

A

six transmembrane motifs, voltage sensor on S4, pore between S5 and S6; it takes four motifs to make a functional channel

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

what amino acid is highly common in voltage sensors

A

arginine

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

each ion has a different

A

radius, number of water molecules, and diameter of first hydration shield

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

carbonyls

A

replace shell of hydration in K+ but not Na+ in the K+ channel

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

procedure to transplant neurotransmitter receptors from brain to oocytes

A

injecting cell membranes or brain mrna

homogenize brain sample, centrifuge, collect and inject vesicles into oocyte
you can also homogenize then separate polyA+ RNA, inject it and wait 6 days to record

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

advantages of xenopus oocytes for studying ion channels

A

big cells so easy to do electrophysiology, will express large amounts of channel of interest, can introduce exogenous channel from native sources or recombinant DNA

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

patch clamp technique

A

record a small portion of the cell and current in that cell: can be cell-attached, whole-cell, or outside-out recording

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

patch clamp can be used to study

A

currents through individual ion channels

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

Na and K+ channels ______ by depolarization

A

are opened

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

VgNA+C at depolarization

A

quickly open, inactivate, returned to closed state

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

VgK+C at depolarization

A

don’t inactivate, delayed/slower opening

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

alpha subunits

A

are the pore forming subunits

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

K+ channels are a

A

family of voltage gated channels with greatest diversity

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

function of K channels

A

regulating excitability in many tissues, in axons and somatodendritic compartments; also help set resting potential

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

protein name format for voltage gated channels

A

ion, subscript family name (v for voltage), family number, position or individual number of protein
Nav1.7

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

Kv2.1

A

don’t inactivate, contribute to the falling phase of the AP, called delayed rectifiers

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

Kv4

A

an A type channel that rapidly inactivates, regulating AP frequency in areas like the hippocampus

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

HERG channels (Kv11.1)

A

delayed current after depolarization, contribute to duration of hyperpolarization after depolarization

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

Inward rectifying channels

A

more active at hyperpolarized potentials, increasing threshold for AP and including KATP to produce K+ when ATP is low

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

Kca

A

protect neurons from excess depolarization when Ca2+ is high (more conductance with more Ca2=)

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

2-p family

A

K+ leak channels that set resting potential

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

functions of K+ channels

A

resting membrane potential
mediate AP downstroke
regulate length of hyperpolarization after AP
regulate excitability in dendrites
decrease excitability during metabolic stress like high ca and low atp intracellularly

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

channelopathies

A

diseases caused by ion channel dysfunction, can be caused by genetic mutation or can be acquired via an autoimmune attack, can have developmental or episodic manifestations and affects many tissues,

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

episodic disorders

A

affect excitable tissues like brain, muscles, heart, characterized by attacks

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

causes of episodic disorders

A

mutations to channels or to excitability, autoimmune diseases, brain lesions/tumors

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

what triggers an attack?

A

ion imbalance, chemical triggers, stress, etc

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

seizure

A

abnornal/excessive excitation or synchronization of a population of neurons

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

epilepsy

A

spontaneous recurrent seizures unprovoked by any systemic or acute neurologic insults

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

epileptogenesis

A

sequence of events that converts a normal neuronal network into an epileptic network

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

epilepsies

A

many but not all caused by channelopathies with excess Na/Ca currents or reduced K/Cl currents
caused by periodic excess excitation in brain, GOF in depolarizing, loss of function in hyperpolarizing

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

hyper and hypokalemic periodic paralysis

A

muscle weakness triggered by exercise or stress, causing loss of muscle tone; categorized by levels of potassium associated with attacks and caused by mutations in ion channels in skeletal muscle
(hypo: low serum K_

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

in hypokalemia, low serum K+ is accompanied by

A

prolonged inactivation/reduced function of VgNaCs

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

prolonged inactivation/reduced function of VgNaCs means that

A

muscle excitability is insufficient to complete movements

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

migraines and seizures occur after

A

excess excitation in the brain; GOF in depolarizing or LOF in hyperpolarizing

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

familial hemiplegic migraine

A

disorder characterized by headaches and weakeness on one side of the body, many known genetic causes including more activity of Cav2.1

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

GEFS

A

generalized epilepsy with febrile seizure, seizures accompanied by high body temp, mutations cause slowed inactivation of VgNAcs, so excess depolarization when AP is triggered

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

list some diseases caused by altered ion channels

A

gefs, myotonia, paralysis

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

episodic ataxia type 1

A

uncoordinated movement provoked by stress, startle, exercise caused by LOF mutations in K channels in cerebellum, causing inadequate repolarization

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

Nav1.7

A

mediator of aps in nociceptive neurons

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

congenital insensitivity to pain

A

lack of pain perception, characterized often by injury or loss of extremities; loss function of Nav1.7 causing less output by DRG neurons

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

paroxysmal extreme pain disorder

A

more activity of Nav1.7, reduced inactivation, episodes of extreme pain in jaw, eyes, rectum

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

Nav1.7 associated with

A

congenital insensitivity to pain and paroxysmal extreme pain disorder

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

myotonia

A

delayed relaxation of muscle after contraction/movement due to loss of hyperpolarizing Cl- current in muscle prolonging contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

function of electrical synapses

A

synchronization of electrical activity of large neuron populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

why is synchronization in electrical synapses important

A

important for functions requiring fast responses like reflexes and pacemakers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

electrical vs chemical synapses

A

chemical involves neurotransmitter across a membrane, electrical involves direct connection via gap junctions where ions flow directly between cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

distance between membranes in gap junctions

A

wider part is 20 nm, closer part is 3.5 nm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

connexin

A

a subunit of connexonm 6 connexins make a connexon in pre or post synaptic membrane, and two hemi channels come together to make one gap junction channel

52
Q

connexin topology and structure

A

4 alpha helices connected by extracellular loops

53
Q

how large are connexon pores

A

large enough to pass ions and small molecules, size cutoff is 500 Da for vertebrates and 1000 for invertebrates

54
Q

do connexons have a negatively charged path

A

yes, in the edges of the membrane facing cytoplasm

55
Q

function of gap junctions

A

rapid signalling between neurons due to coupling, so postsynaptic response is a fraction of a millisecond after presynaptic

56
Q

gap junctions in the brain

A

allow for synchronous activity in hippocampus, thalamus
in hypothalamus, neurons secreting peptide hormones are connected by gap junctions, allowing for a burst of hormone

57
Q

majority of synapses in our nervous system are

A

chemical synapses, which are slower but more diverse in signalling

58
Q

characteristics of chemical synapses

A
  • slower than electrical, diverse in signaling
  • fast, local (msec, tens of nm)
  • postsynaptic cell contains receptors for neurotransmitter
59
Q

presynaptic terminals are distinguished by

A

synaptic vesicles

60
Q

postsynaptic side is distinguished by

A

postsynaptic density

61
Q

how long is the response delayed at the postsynaptic terminal

A

1 msec

62
Q

vesicular neurotransmitter release is

A

quantized, meaning the vesicles empty their entire contents and discrete amounts of NT are released (as seen in mini postsynaptic potentials)

63
Q

spontaneous miniature EPPs

A

occur in postsynaptic cell even without presynaptic stimulation

64
Q

vesicles vary in appearance based on

A

neurotransmitter they contain

65
Q

what contributes to differential release probability?

A

differential positioning of vesicle types

66
Q

vesicles close to active zone

A

readily releasable, high release probability, moderate Ca influx

67
Q

vesicles far from active zone

A

lower release probability, larger sustained Ca influx

68
Q

low frequency stimulation

A

preferential release of small-molecule nt

69
Q

high frequency stimulation

A

release of both types of nt

70
Q

vesicular NT release can be altered

A

to change synaptic strength

71
Q

axo-axonic synapses

A

promote of prevent neurotransmitter release

72
Q

release probability

A

intrinsic likelihood a vesicle will fuse with plasma membrane

73
Q

when release probability is high

A

presynaptic terminal releases more nt

74
Q

low release probability

A

less nt is released

75
Q

can the presynaptic release probability be altered

A

yes, changes synaptic strength; brief increase in release after high frequency APs (tetanus)

76
Q

post tetanic potentiation

A

brief increase in release probability following high frequency short train of action potentials, partially due to higher calcium levels in cell after tetanus

77
Q

post tetanic depression

A

longer term decrease in release probability following medium frequency longer train of action potentials (tetanus), usually due to depletion of NT vesicles

78
Q

NMJ is useful for study

A

due to accessibility, importance in function

79
Q

electrically excitable tissues

A

neurons, cardiac, skeletal

80
Q

process of muscle contraction

A

muscle cell plasma membrane depolarizes, travels down T tubules, which interact with ER, causing Ca release into cytoplasm, myosin moves against actin, causing contraction

81
Q

acetylcholine binds

A

nicotinic ach receptors (cation channels, so permeable to na and K)

82
Q

sufficient depolarization triggers muscle cell

A

action potential, which requires Na+ channels in muscle cell membrane (sarcolemma)

83
Q

nAch receptor is made of

A

5 subunits

84
Q

one nach4 binds ___ to open

A

2 Ach molecules

85
Q

the reversal potential for nAchRs is

A

0 mV, reflecting equal permeability to Na and K

86
Q

reversal potential for an ion channel

A

membrane potential at which there is no net current, so electrochemical forces balance out

87
Q

gaba lets in what ion

A

Cl-

88
Q

reversal potential for GABA receptor

A

-50 to 60 mv, same as equilibrium for Cl

89
Q

how does lower external Na affect reversal potential

A

shifts it to the left

90
Q

how does higher external K+ affect reversal potential

A

shifts it to the right

91
Q

what determines current amplitude?

A

drive/size of electrochemical gradient: closer membrane is to equilibrium potential, smaller net current

92
Q

ion channels are not binary (T/F)

A

F

93
Q

if reversal potential is more positive than threshold

A

excitation occurs

94
Q

reversal potential more negative than threshold

A

inhibition occurs

95
Q

IPSPs can depolarize the postsynaptic cell if

A

reversal potential is between resting and action potential threshold

96
Q

synaptic contact can occur

A

on cell body, dendrites, or axon

97
Q

spatial summation

A

synaptic potentials summed from multiple synapses across neuron

98
Q

temporal symmation

A

one synapse elicits psps that are summed

99
Q

AP frequency is shaped by

A

inhibitory input

100
Q

synapses near where will have the greatest weight in summation?

A

axon hillock

101
Q

threshold is lower for AP where

A

at hillock, enriched with NaCs, allowing distal dendritic potentials to elicit an AP

102
Q

formal criteria for neurotransmitter

A
  • chemical must be synthesized in neuron or otherwise present in it
  • when the neuron is active, the chemical must be released and produce a response in some target
  • the same response must be obtained when the chemical is experimentally placed on the target
  • a mechanism must exist for removing the chemical from its site of activation after its work is done
103
Q

what is a neurotransmitter?

A

molecules that
- carry messages between neurons via influence on postsynaptic membrane
- have little or no effect on membrane voltage but have a common carrying function like changing synapse structure
- communicate by sending reverse-direction messages that have an impact on the release or reuptake of transmitters (retrograde signaling)

104
Q

nearly ubiquitous NT

A

glutamate (excitatory)
GABA/glycine (inhibitory)

105
Q

neurotransmitters associated with specific neural circuits/functions

A
  • ach
  • dopamine
  • norepinephrine
  • serotonin
  • peptide NT
  • atypical NT
106
Q

small molecule neurotransmitters

A

ach, amino acid neurotransmitters, amine neurotransmitters, purines

107
Q

acetylcholine

A

excitatory via nicotinic ach receptors (ionotropic)

excitatory or inhibitory via muscarinic ach receptors (metabotropic)

108
Q

amino acid NTs

A

glutamate, aspartate, GABA, glycine

109
Q

glutamate

A

major excitatory nt of cns (ionotropic; metabotropic may be excitatory or inhibitory)

110
Q

gaba/glycine

A

inhibitory cns, metabotropic gaba are inhibitory

111
Q

amine nt

A

gpcr signalling (metabotropic), dopamine, norepinephrine, epinephrine, serotonin, histamine

112
Q

small molecule nt

A

ATP usually copackaged with another small molecule transmitter

113
Q

peptide hormones

A

also act as neurotransmitters, examples are enkephalins

114
Q

how are nt made

A

cannnot cross bbb, so made locally from precursors, packaged into vesicles, signal terminated by degradation or reuptake

115
Q

peptide nt synthesis

A

translation of protein in RER, precursor peptide copackaged with enzymes to make mature peptide transmitter, vesicle transported to axon terminal via active transport, after release, nt signal terminated by diffusion away from the cleft

116
Q

proteolytic processing of pre-propeptides

A

pre-propeptide has signal sequence cleaved off to become a propeptide, becomes active peptides

117
Q

neuronal signalling depends on

A

type of nt, neuron, brain region, receptor

118
Q

ionotropic receptor diversity

A

within one receptor, subunit variants like in nAchRs, families of receptors may pass different ions, like glutamate ampa vs nmda- calcium

119
Q

structure of gaba

A

pentameric cl channels

120
Q

ampa type glutamate receptor

A

4 subunits

121
Q

ioniotropic nt receptors

A

same endogenous ligand, different agonists, pass na, k, ca, cl, may be desensitized or voltage gated

122
Q

ampa receptors

A

large current, quick desensitization

123
Q

kainate and nmda

A

smaller peak current, slower desensitization

124
Q

nmda type glutamate receptors

A

ligand and voltage gated so mg blocks at negative potentials, but at higher potentials mg is kicked out

125
Q
A

NSC 4352 Cellular Neuroscience (3 decks)

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