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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
spte 4 of chemical synapses
NT removed from synaptic cleft (ex. ACh broken down by AChesterase), fused membrane is recycled
26
fast chemical transmission
vesicles are docked at active zones waiting for Ca inflow
27
slow chemical transmission
bigger vesicles/peptides non-active zone release G protein coupled receptor --> messengers
28
SNARES (proteins)
V-SNARE (vesicle) and T-SNARE (terminal active zone) are for docking
29
synaptotagmin
changes shape in presence of Ca molecular handbrake w/o Ca, vesicles docked w/ Ca, vesicles touch membrane and release product
30
why did we study specialized synapses of the NMJ
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
31
why are the synapses of the NMJ specialized
1 pre-syn AP produces 1 AP in muscle if measure close, theres a hump b4 AP if measure further along, normal looking AP
32
synapse depol @ NMJ
ACh is released to nACh receptor Na and K go through ACh receptor toxin curare blocks ACh function
33
how to clamp voltage and measure current (muscle)
hold muscle membranes at set voltage initially by injecting current (control resting pot) stimulate synapse record changes in muscle voltage
34
reversal potential
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
35
reversal potential example
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
36
for 1 ion, _____ potential equals the reversal potential, for more than 1 ion it depends on...
Nernst depends on [ ]s, and permeabilities of each ion
37
how can the same NT have a different effect on different cells
different receptors
38
nACh R @ NMJ vs. mACh R in the heart
nACh NMJ: excitatory, Na in K out, rest -70mV... depol mACh heart: G-protein coupled, opens K channels, hyperpol, slow HR
39
in post-syn neuron, excitation vs inhibition
excitation: depol, Na and Ca inhibition: hyperpol, K and Cl-; GABA --> influx of Cl- causes hyperpol inhibition: depol w/ low Erev
40
do NT gated channels have specificity?
yes
41
epilepsy (seizures)
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
Cl- balance in adults vs kids
adults: low Cl- in cells kids: high Cl- in cells
43
the ____, not ______ dictate excitation vs. inhibition
ions, channels
44
pre-syn inhibition
inhibiting neuron inhibits pre-syn neuron @ synapse (less nt release)
45
how much nt is released when no stimulation
tiny depols (mini endplate potentials) caused by single vesicles losing control and releasing nt --> 0.1mV
46
tracking chemical synapses
Ca sensitive dye voltage gated Ca channels --> synaptotagmin --> vesicle release very fast change in [Ca]
47
CNS development has a different physiology than ____ CNS
mature Retina: spontaneous Ca "waves" involved in establishing synapse connectivity slow change in [Ca], spread via gap junctions
48
nt agonists
activate channels
49
nt antagonists
block/inhibit channels
50
vesicles have pumps in membrane to take in ___
ACh
51
what in addition to Sarin gas (nerve gas) can inhibit AChesterase
pesticides
52
NorEpi
reuptake pre-syn broken down by MAO recycled along w/ vesicles
53
why are NT recycled?
prevent rundown of available nt membrane recycled
54
nACh R structure
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
movement of Na/K through nACh R
Na in and K out more Na moves b/c larger driving force --> depol cell
56
Beta subunit of nACh
4 transmembrane regions M1-M4 M2 lines the pore and imparts selectivity
57
where do you get enough ACh receptors to study?
torpedo electric ray electroplaque
58
to open an ACh channel...
2 molecules of ACh needed b/c binds the 2 alpha subunits change in conformation
59
patch clamp of ACh single channels
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
ionotrophic glutamate receptor
M2 subunit doesn't span membrane, but lines pore provides selectivity
61
not all ACh receptors are ______
channels
62
mACh R
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
change in voltage for nACh vs. mACh
nACh: fast mACh: slower
64
a G-protein can either do what to a channel
open or close a channel
65
ACh + leg muscle (nACh R)
depol
66
ACh + heart muscle (mACh R)
G-protein opens K channels --> hyperpol and slow HR
67
stimulating frog B cells pre-syn nerve gives multiple effects
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
slow EPSP
slow b/c G-protein is activated for longer
69
late, slow EPSP
late b/c NT comes from a nearby synapse and takes time to diffuse slow b/c G-protein coupled
70
how does GnRH-like peptide cause depol
K channels normally open G-prot mACh R + GnRH like receptors close channel slow Na leak causes the depol
71
slow EPSP doesn't drive AP, but...
makes more sensitive to input depol 4mV so closer to threshold shifts "resting" pot closer to theshold
72
key factors for multiple inputs on any dendrite
spread of depol from input PSP density of receptors and channels distance from spike initiating zone 1 more see PP
73
NMJ has what ratio input to AP
1:1
74
CNS APs
multiple small inputs sum to AP depol or hyperpol (inhibit)
75
spatial summation
2+ inputs stimulated simultaneously onto same cell adds together could be excitatory or inhibitory
76
temporal summation
same input --> multiple stim close in time occurs before 1st response has decayed
77
EPSP vs. AP
EPSP: change in voltage has a graded size AP: threshold --> constant voltage
78
increasing stimulus size has what effect on the frequency of APs
increased frequency of AP
79
2 types of synaptic modulation
short term long term
80
why is post-syn depol greater than summation? (EPSP)
b/c curare Ca in nerve terminal after 1st stim
81
there is post-syn _______ and _______ after a short burst of high frequency stimulus
depression, potentiation
82
if normal stim + record (baseline) --> short tetanic stimulus --> normal stim + record............ what do you see?
depression followed by potentiation
83
in normal Ca... tetanic stim
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
in normal Ca..... delay tetanus
potentiation b/c excess Ca
85
in low Ca... tetanic stim
no depression reduced vesicle release b/c low Ca, so no vesicle depletion
86
in low Ca.... delay tetanus
short potentiation cell buffers Ca faster b/c low Ca
87
to test role of Ca in pre-syn nerve....
use a no Ca bath
88
heterosynaptic modulation
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
5HT receptor
G-protein coupled --> change in cAMP in 2nd synapse --> some K channels close (wider AP, lower depol, longer Ca influx, longer Ca release)
90
long term potentiation (LTP) / long term depression (LTD)
hippocampus synapse strength --> nt glutamate
91
receptor types
AMPA: allows Na through, opens when glu binds NMDA: allows Na + Ca through, opens when glu binds AND cell must also be depol
92
why does NMDA need depol?
Mg plug at resting pot, only removed by depol
93
how does Ca influx change synaptic strength?
increase AMPA # / decrease # AMPA receptors in post-syn neuron
94
LTP stimulates pre and post syn activity... how detect stimulus activity pre + post of single synapse?
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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