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Animal Physiology > Exam 2: Ch 6 Notes > Flashcards

Exam 2: Ch 6 Notes Flashcards

1
Q

graded potential

A

size changes

curent decays over distance

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2
Q

how to improve loss of current

A

decrease resistance of cytoplasm (squid giant axons have large diameters for this)

increase membrane resistance (glial cells myelinate axons)

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3
Q

current decay w/ distance

A

length constant (measure of distance you move along axon when current is 37% of original)

record voltage change

indicator of how well current moves along axon/how badly it leaks out

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4
Q

what affects length constant

A

glial cells myleinate axons to inc length constant

squid giant axons inc diameter to inc length constant

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5
Q

what does it mean for an AP to be regenerative

A

current does not decrease w/ distance

voltage-gated channels drive the AP all along the axon

moves in 1 direction (cell body –> periphery)

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6
Q

if you artificially stimulate an axon in the middle…

A

AP goes both directions

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7
Q

cooling blocks the _____ of AP

A

conductance

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8
Q

speed of AP propagation

A

stimulate nerve at S1 and S2… measure time to contraction

speed differs in different neurons

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9
Q

cardiac AP

A

Na

voltage-gated Ca channels open (much longer inactivation)

delayed rectifier K channels

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10
Q

myelin sheath limits…

A

ions available on the extracellular side

solution: nodes of ranvier (tons of ion channels)

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11
Q

early symptoms of MS

A

blurred/double vision

clumsiness

thinking problems

loss of balance

numbness/tingling

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12
Q

2 types of synapses

A

electrical: direct coupling… very fast
chemical: indirect NT release, diffusion, bind receptors

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13
Q

modulation of 2 types of synapses?

A

electrical: not much
chemical: lots of scope

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14
Q

where are the biggest electrical synapses?

A

escape response

ex. crayfish escape response

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15
Q

glial cells have __ gap junctions

A

1/2

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16
Q

electrical synapses are…

A

specialized areas with lots of gap junctions

electrical connections, small ions and 2nd messengers

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17
Q

transmission of current has ______

A

resistance

reduced depol in post-syn cell… must be bidirectional

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18
Q

properties of electrical synapses

A

some have polarization

rectifying synapse works better in 1 direction than the other

AP in A drives AP in B, but AP in B does not drive AP in A

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19
Q

Charcot-Marie-Tooth disease (CMT)

A

slow progressive weakness/atrophy in distal leg muscles

> 400 mutations in gene coding for GJ protein connexin 32

GJs in peripheral and central myelinating cells play an important role in homeostasis of myelinated axons

stoke b/c glial cells can’t soak up excess nt

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20
Q

molecular biology techniques are used to study connexin roles

A

diff connexins have diff functions, if gene knocked out, different effects result

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21
Q

1st step in chemical synapses

A

AP in pre-syn cell reaches the terminal causing depol –> voltage-gated Na, K, and Ca channel open

Na moves in

Ca moves in

K moves out

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22
Q

2nd step chemical synapses

A

NT release (tightly regulated exocytosis) diffusion

if Ca removed extracellularly, no NT release

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23
Q

Conotoxin blocks…

A

Ca channels… no NT release

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24
Q

step 3 of chemical synapses

A

NT binds to post-syn receptor proteins; ion channels open

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25
Q

spte 4 of chemical synapses

A

NT removed from synaptic cleft (ex. ACh broken down by AChesterase), fused membrane is recycled

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26
Q

fast chemical transmission

A

vesicles are docked at active zones waiting for Ca inflow

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27
Q

slow chemical transmission

A

bigger vesicles/peptides

non-active zone release

G protein coupled receptor –> messengers

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28
Q

SNARES (proteins)

A

V-SNARE (vesicle) and T-SNARE (terminal active zone) are for docking

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29
Q

synaptotagmin

A

changes shape in presence of Ca

molecular handbrake

w/o Ca, vesicles docked

w/ Ca, vesicles touch membrane and release product

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30
Q

why did we study specialized synapses of the NMJ

A

extended and large synapses (easily accessible)

mitochondria - needs lots of energy

active zones –> multiple vesicles (pre-syn)

post-syn –> invaginations increase surface area for many receptors

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31
Q

why are the synapses of the NMJ specialized

A

1 pre-syn AP produces 1 AP in muscle

if measure close, theres a hump b4 AP

if measure further along, normal looking AP

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32
Q

synapse depol @ NMJ

A

ACh is released to nACh receptor

Na and K go through ACh receptor

toxin curare blocks ACh function

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33
Q

how to clamp voltage and measure current (muscle)

A

hold muscle membranes at set voltage initially by injecting current (control resting pot)

stimulate synapse

record changes in muscle voltage

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34
Q

reversal potential

A

the resting potential at which you get no change in voltage in the post-syn cell

no net driving force on ions so no net charge movement

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35
Q

reversal potential example

A

if channel is only permeable to Na and Na Eq pot = 65mV

if set resting pot is at 65 mV then when you stim the neuon, there is NT release and channels open but no change in muscle voltage

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36
Q

for 1 ion, _____ potential equals the reversal potential, for more than 1 ion it depends on…

A

Nernst

depends on [ ]s, and permeabilities of each ion

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37
Q

how can the same NT have a different effect on different cells

A

different receptors

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38
Q

nACh R @ NMJ vs. mACh R in the heart

A

nACh NMJ: excitatory, Na in K out, rest -70mV… depol

mACh heart: G-protein coupled, opens K channels, hyperpol, slow HR

39
Q

in post-syn neuron, excitation vs inhibition

A

excitation: depol, Na and Ca
inhibition: hyperpol, K and Cl-; GABA –> influx of Cl- causes hyperpol
inhibition: depol w/ low Erev

40
Q

do NT gated channels have specificity?

A

yes

41
Q

epilepsy (seizures)

A

depol spreads to neighboring cells (focuses activity)

GABA meds stop spread to neighboring cells in adults

in kids: siezures got worse b/c meds drive depol (Cl- balance is opposite)

42
Q

Cl- balance in adults vs kids

A

adults: low Cl- in cells
kids: high Cl- in cells

43
Q

the ____, not ______ dictate excitation vs. inhibition

A

ions, channels

44
Q

pre-syn inhibition

A

inhibiting neuron inhibits pre-syn neuron @ synapse (less nt release)

45
Q

how much nt is released when no stimulation

A

tiny depols (mini endplate potentials)

caused by single vesicles losing control and releasing nt –> 0.1mV

46
Q

tracking chemical synapses

A

Ca sensitive dye

voltage gated Ca channels –> synaptotagmin –> vesicle release

very fast change in [Ca]

47
Q

CNS development has a different physiology than ____ CNS

A

mature

Retina: spontaneous Ca “waves” involved in establishing synapse connectivity

slow change in [Ca], spread via gap junctions

48
Q

nt agonists

A

activate channels

49
Q

nt antagonists

A

block/inhibit channels

50
Q

vesicles have pumps in membrane to take in ___

A

ACh

51
Q

what in addition to Sarin gas (nerve gas) can inhibit AChesterase

A

pesticides

52
Q

NorEpi

A

reuptake pre-syn

broken down by MAO

recycled along w/ vesicles

53
Q

why are NT recycled?

A

prevent rundown of available nt

membrane recycled

54
Q

nACh R structure

A

5 subunits (2 alpha, beta, gamma, Y)

central pore w/ ACh sensitive open/close gating activity

neg charges inside channel, Na/K ions can pass

55
Q

movement of Na/K through nACh R

A

Na in and K out

more Na moves b/c larger driving force –> depol cell

56
Q

Beta subunit of nACh

A

4 transmembrane regions M1-M4

M2 lines the pore and imparts selectivity

57
Q

where do you get enough ACh receptors to study?

A

torpedo electric ray

electroplaque

58
Q

to open an ACh channel…

A

2 molecules of ACh needed b/c binds the 2 alpha subunits

change in conformation

59
Q

patch clamp of ACh single channels

A

ACh inside electrode placed in denervated muscle fiber

denervation allows channels to inset along the whole muscle fiber

ACh binds –> channel opens –> inward current

60
Q

ionotrophic glutamate receptor

A

M2 subunit doesn’t span membrane, but lines pore

provides selectivity

61
Q

not all ACh receptors are ______

A

channels

62
Q

mACh R

A

not a channel, G-protein coupled receptor

nt binds receptor and affects G-protein complex

G-protein affects the channel (voltage) and 2nd messengers and other cell functions

63
Q

change in voltage for nACh vs. mACh

A

nACh: fast

mACh: slower

64
Q

a G-protein can either do what to a channel

A

open or close a channel

65
Q

ACh + leg muscle (nACh R)

A

depol

66
Q

ACh + heart muscle (mACh R)

A

G-protein opens K channels –> hyperpol and slow HR

67
Q

stimulating frog B cells pre-syn nerve gives multiple effects

A

1) fast EPSP when ACh binds nACh R (40ms)
2) slow EPSP with more stim when ACh binds mACh R (40s)
3) late, slow EPSP w/ diff receptor –> GnRH like peptide

68
Q

slow EPSP

A

slow b/c G-protein is activated for longer

69
Q

late, slow EPSP

A

late b/c NT comes from a nearby synapse and takes time to diffuse

slow b/c G-protein coupled

70
Q

how does GnRH-like peptide cause depol

A

K channels normally open

G-prot mACh R + GnRH like receptors close channel

slow Na leak causes the depol

71
Q

slow EPSP doesn’t drive AP, but…

A

makes more sensitive to input

depol 4mV so closer to threshold

shifts “resting” pot closer to theshold

72
Q

key factors for multiple inputs on any dendrite

A

spread of depol from input PSP

density of receptors and channels

distance from spike initiating zone

1 more see PP

73
Q

NMJ has what ratio input to AP

A

1:1

74
Q

CNS APs

A

multiple small inputs sum to AP

depol or hyperpol (inhibit)

75
Q

spatial summation

A

2+ inputs stimulated simultaneously onto same cell

adds together could be excitatory or inhibitory

76
Q

temporal summation

A

same input –> multiple stim close in time occurs before 1st response has decayed

77
Q

EPSP vs. AP

A

EPSP: change in voltage has a graded size

AP: threshold –> constant voltage

78
Q

increasing stimulus size has what effect on the frequency of APs

A

increased frequency of AP

79
Q

2 types of synaptic modulation

A

short term

long term

80
Q

why is post-syn depol greater than summation? (EPSP)

A

b/c curare

Ca in nerve terminal after 1st stim

81
Q

there is post-syn _______ and _______ after a short burst of high frequency stimulus

A

depression, potentiation

82
Q

if normal stim + record (baseline) –> short tetanic stimulus –> normal stim + record………… what do you see?

A

depression followed by potentiation

83
Q

in normal Ca… tetanic stim

A

depression b/c many vesicles released, which depletes vesicle store

pre-syn buildup of Ca (to release many vesicles) that the cell cannot buffer

84
Q

in normal Ca….. delay tetanus

A

potentiation b/c excess Ca

85
Q

in low Ca… tetanic stim

A

no depression

reduced vesicle release b/c low Ca, so no vesicle depletion

86
Q

in low Ca…. delay tetanus

A

short potentiation

cell buffers Ca faster b/c low Ca

87
Q

to test role of Ca in pre-syn nerve….

A

use a no Ca bath

88
Q

heterosynaptic modulation

A

sensitization

one synapse alters function of a 2nd synapse by synapsing onto terminal

alters nt release by changing properties of 1st synapse

ex. serotonin alters channel kinetics of K channel

89
Q

5HT receptor

A

G-protein coupled –> change in cAMP in 2nd synapse –> some K channels close (wider AP, lower depol, longer Ca influx, longer Ca release)

90
Q

long term potentiation (LTP) / long term depression (LTD)

A

hippocampus

synapse strength –> nt glutamate

91
Q

receptor types

A

AMPA: allows Na through, opens when glu binds

NMDA: allows Na + Ca through, opens when glu binds AND cell must also be depol

92
Q

why does NMDA need depol?

A

Mg plug at resting pot, only removed by depol

93
Q

how does Ca influx change synaptic strength?

A

increase AMPA # / decrease # AMPA receptors in post-syn neuron

94
Q

LTP stimulates pre and post syn activity… how detect stimulus activity pre + post of single synapse?

A

pre: nt release; post: depol –> NMDA receptor –> molecular detector –> readout: change in Ca post-syn

changes AMPA receptor #

Animal Physiology (26 decks)

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