Week 3: More Neurophysiology Flashcards
Action Potential
- Large depolarizing wave
- Actively propagates itself down the axon
- Does not lose amplitude
Potential Sensitive Channel
Begin at the axon hillock
Open and close in response to the value of VM
Potential sensitive Na+ channels
Potential sensitive K+ channels
- both open to depolarization
Voltage Clamp
- Measures the VM
- Changes the VM to any determined value
- Adds current to either side of the membrane to maintain the given VM
Tetrodotoxin (TTX)
Binds to and clogs Na+ potential sensitive channels (Not passive Na+ channels).
This allows for the study of K+ potential sensitive channels
Tetraethylammonium (TEA)
Binds to and clogs K+ potential sensitive channels (not passive K+ channels).
This allows for the study of Na+ potential sensitive channels.
Similarities between K+ and Na+ Channels
- Both open to depolarization
2. Both have a greater (population) response the greater the depolarization
Dissimilarities between K+ and Na+ Channels
- Na+ channels open more rapidly then K+ channels open
- If the depolarization persists, Na+ channels close, K+ do not
- Na+ channels are faster to close/K+ channels are slower to close
g
Conductance: flow of ions
3 States on Na+ Potential Sensitive Channels
- Closed (ready to open)
- Open
- Closed (refractory)
Refractory
The brief period that follows an action potential where the neuron cannot fire again
Due to the closed state of the Na+ channels
Absolute Refractory
immediately following an action potential during which the neuron cannot be fired because the Na+ channels are all locked closed
Relative Refractory
Right after the absolute refractory period when an action potential can be fired only if the stimulus is stronger than usual
May be due to the fact that Na+ channels become ready have different thresholds
Accomodation
When a slow depolarization raises the VM well past a normally observed threshold before the neuron will generate an action potential
Types of K+ Potential Sensitive (Voltage gated) Channels
- Slowly activated (delayed rectifier)
- Ca++ activated K+ channel
- A-Type - fast, transient activated by depolarization
- M-type - activated by depolarization, but inactivated by ACh (acetylcholine)
General effects of Ca++ Influx
- Contributes directly to the depolarization of the action potential
- Contirubutes to hyperpolarization of the neuron
2 Factors Ca++ Hyperpolarization is due to
- Ca++ will activate K+ channels causing K+ efflux (leaving)
- Ca++ will decrease it’s own influx by blocking channels
Hyperpolarization can lead to
- a decrease in sensitivity to depolarization
OR - an increase in sensitivity to depolarization (i.e., Ca2+ channels being open again)
Plasticity
Being able to vary the outcome of processing information
What types of potential sensitive channels do NG2+ glia have?
Na+
Ca2+
K+
Where are NG2+ located?
Hippocampus
Cerebral cortex
Cerebellum
After Potential
The period of hyperpolarization following the action potential
Due to the slow closing of the K+ potential sensitive channels
Threshold (VT)
The value of VM when the net ionic current changes from outward to inward
What is mediating the Action Potential?
Not Na+ or K+
Ca2+ AT THE AXON TERMINAL is the critical factor
Ca2+ Potential Sensitive Channels
Only populate the axon terminal
Open to (slight) depolarization
Types of Ca2+ Potential Sensitive Channels
L Type - not in the active zone, but still in the terminal
N Type - in the active zone
L Type Ca2+ Potential Sensitive Channels
Slow, not located where the NT is released
N Type Ca2+ Potential Sensitive Channels
Fast, associated with the release on NT
End Plate
Post synaptic Surface
End Plate Potential
the PSP
Miniature End Plate Potentials
Very small end plate potentials that occur randomly in the absence of an action potential
~.5mV
Appear to be the result of one vesicle releasing into the synapse
Quantal Hypothesis
- under normal conditions, the end plate potential of about 70mV is due to about 150 vesicles dumping into the synapse
- variations in end plate potentials are the result of varying amounts of vesicles dumping
Dense Bar
Thickening on the inner surface of the presynaptic membrane with Ca2+ channels lining either side
Located directly opposite the postsynaptic receptor sites
Vesicles collect in rows along the top sides on the dense bars
Active Zone
Dense bars and the vesicles
Essentially where the NT release occurs
Exocytosis
The process whereby the synaptic vesicles in the axon terminal release their molecule NT’s into the synapse
Endocytosis
The recycling process where the vesicles are recaptured
Clathrin
Mark vesicle membranes for recapturing
Kiss and Run
The vesicle briefly touches and opens to the synapse releasing some on its NT
Process of Exocytosis
- restraining the vesicles to the area above the active zone
- herding the available vesicles to the active zone
- docking the vesicles
- mediating exocytosis
- endocytosis
Synapsins
Keep vesicles attached to filaments
Synaptobrevin - in vesicle
Synaptotagmin - in vesicle
Syntaxin - on membrane
SNAP-25 - on membrane
Rab
Proteins that bring vesicles into the active zone
Synaptobrevin
Binds to Syntaxin and SNAP-25
On the vesicle
Serves a receptor for clathrin
Synaptic Plasticity
the process whereby neurotransmission can change its effectiveness
How the resulting PSP can vary (via Ca2+)
Intrinsic synaptic plasticity
Potentiation?
Potentiation?
Facilitation
the increase in size of a PSP resulting from the tetanus/tetanic stimulation
Tetanus/tetanic stimulation
the high frequency firing of a neuron
Post-tetanic potentiation
potentiation that persists after the tetenic stimulation
May last for hours or days
Likely due to accumulation Ca2+ in the terminal
