Week 3-Action Potentials Flashcards
(42 cards)
1
Q
Action Potential
A
- large depolarizing wave
- actively propagates down axon
- & does not lose amplitude
2
Q
potential sensitive channels (voltage gated)
A
open and close in response to Vm
3
Q
Depolarization
A
opens V-Na+
- ->Na+ rushes into cell
- ->MORE depolarization
4
Q
hyperpolarization
A
V-K+ open
- ->K+ rushes out of cell
- ->hyperpolarization
5
Q
Voltage clamp
A
- measures Vm
- changes Vm to any determined value
- adds current to either side of membrane to this Vm
–>breaks feed forward process of V-gated channels
(Na+ doesn’t cause more depolarization)
6
Q
Threshold (Vt)
A
value of Vm when net ionic current changes from outward to inward
7
Q
Tetrodotoxin (TTX)
A
binds/clogs V-Na+
-only V-K+ functional
8
Q
Tetrathylammonium (TEA)
A
binds/clogs V-K+
-only V-Na+ functional
9
Q
V-gates similarities
A
- both open to depolarization
- both have a greater response to greater depolarization
- have inactivation protein to close channels
10
Q
V-gates differences
A
- Na+ open more rapidly than K+
- If depolarization persists, Na+ close, K+ do not
- Na+ channels faster to close than K+
* individual gates have different thresholds
11
Q
V-Na+ channels states
A
- closed-ready for opening
- open
- closed-refractory
12
Q
Refractory period
A
brief period following AP
- cannot fire again
- closed state of Na+ channels
13
Q
Absolute refractory
A
immediately following AP
-neuron cannot fire b/c all Na+ channels locked/closed
14
Q
Relative refractory
A
right after absolute refractory
- AP can be fired only if stimulus is stronger than usual
- Na+ channels that become ready have different thresholds
15
Q
Accomodation
A
- does not happen in nature
- when slow depolarization raises Vm well passed normally observed threshold before generating AP
- due to hyperpolarization of K+ channels keeping up with slow depolarization of Na+ channels
16
Q
Direction of AP
A
axon hillock–>axon terminal
- axon hillock: lowest threshold to fire over any part of an axon
- refractory period of Na+ channels
17
Q
After potential
A
AP followed by hyperpolarization
–>slowness of V-K+ channels to close after activation
18
Q
4 types of V-K+ channels
A
- slowly activated
- Ca++ activated K+ channel opens to depolarization by voltage sensitivity depends on intracellular Ca++
- A-type: fast, transient activated by depolarization
- M-type: activated by depolarization but inactivated by ACh
19
Q
V-Ca++
A
at rest-Ca++ intracellular concentrations very low
- Ca++ pump: buffering system (very slow)
- Ca++ comes in after 1 AP can exceed capacities and begins to accumulate - Series of AP–> increase Ca++ in cell
- increase probability of opening Ca+ activated K+ channels
- hyperpolarization - some Ca++ channels sensitive to intraneuronal Ca++
- binds to internal surface of channels to close them
20
Q
Ca++ influx
A
- contribute directly to depolarization of AP
- contributes to hyperpolarization of AP
- Ca++ influx activates K+ channels
- Ca++ decrease own influx by blocking own channels
21
Q
Ca++ & PSP
A
- decrease extracellular Ca++ will block PSP
- increase extracellular Ca++ increases PSP
- more Ca++ = greater PSP
22
Q
location of V-Ca++ channels
A
only at axon terminal–>opens with depolarization
23
Q
V-Ca++ channel types
A
- L-type
- P/Q type
- N type
- R type
- T type
24
Q
N-type V-Ca++
A
FAST
associated with exocytosis & release of NT
25
L-type V-Ca++
SLOW
not localized in areas of NTs
involved in neuropeptide release & vesicle mobilization
26
Miniature end plate potentials
result of vesicles dumping NT contents into synapse
27
del Castillo/Katz hypothesis
1. normal conditions: end plate potential of ~70 mV
- due to about 150 vesicles dumping into synapse
2. variations of end plate potentials = results of varying amounts of vesicles dumping
28
Dense bars
located directly opposite post synaptic receptor sites
-vesicles collect in rows along dense bar
dense bars + vesicles = ACTIVE ZONE
29
Active zone
dense bars + vesicles
| where NT release occurs
30
Exocytosis
process whereby vesicles release NT into synapse
- pore on vesicle matches axon terminal membrane pore
* N-type Ca++ channels
31
endocytosis
opposite of exocytosis
| recycling/recapturing of vesicles
32
clatherin
identifies vesicle membrane
- pulls off vesicle from membrane
- clatherin degrades & NT loaded
33
Kiss & run exocytosis
short lived pores not open long enough to release vesicles entire NT contents
*does not need clatherin
34
exocytosis mechanism
1. SYNAPSINS keep vesicles attached to filaments restrain vesicles to area above active zone
- L type Ca++ channels free vesicle from synapsins-->mobilization of vesicles
2. RAB PROTEINS move vesicles to active zone
- during exocytosis Rab proteins release
3. Docking: SYNAPTOBREVIN & SYNAPTOTAGMIN on vesicle binds to SYNTAXIN & SNAP-25 on membrane
5. endocytosis-SYNAPTOTAGMIN binds to Clatherin
35
SNAP-25
synaptosomal associated protein
36
VAMP
vesicle associated membrane protein (synaptobrevin/synaptotagmin)
37
TVAMP
target membrane associated membrane protein
| SNAP-25, syntaxin
38
Synaptic plasticity
process whereby NT can change effectiveness, or how PSP can vary
-mediated by altering amount of Ca++ entering terminal (determines how many vesicles dump)
39
intrinsic factors of synaptic plasticity
Slow Ca++ pump-->long term potentiation
| -->accumulation of Ca++ in terminal
40
Extrinsic factors of synaptic plasticity
axon branches that terminate on terminal of another neuron (axo-axonic)
- influence Vm at terminal
- ->control amount of Ca++ in terminal
- ->control PSP
- ->depolarization or hyperpolarization
41
pre-synaptic inhibition
process whereby axo-axonic synapse reduces amount of NT released
mediated by:
1. simultaneous closing of Ca++ channels & opening of K+ channels (hyperpolarization
2. increase Cl- conductance
3. direct inhibition of NT release independent of Ca++
42
Pre-synapti facilitation
mediated by enhanced Ca++ influx
