ActionPotentials / V-gated Channels Flashcards
Four phases of an action potential (in order)
1) Rising Phase
2) Overshoot Phase
3) Falling Phase
4) Undershoot Phase
Which channel type gates faster? voltage gated Na or K?
Na+
Is there an inactivation mechanism for voltage-gated K+ channels?
No
Cause of the absolute refractory period
inactivation of voltage-gated Na+ channels
Cause of the relative refractory period
activation of voltage-gated K+ channels
Toxins which block voltage-gated Na+ channels (2)
Tetrodotoxin and Saxitoxin
Drug categories which block/inactivate Na+ channels (3)
1) local anesthetics
2) some antiarrhythmics
3) some antiepileptics
Toxin used for treating multiple sclerosis, blocking voltage-gated K+ channels
4-aminopyridine
Toxins/Drugs (3) affecting voltage-gated K+ channels. Block delayed rectifier channel pore.
1) Tetraethylammonium (TEA)
2) 4-aminopyridine
3) some ions (barium, cesium)
What is the affect of blocking voltage-gated K+ channels on action potentials.
Increases the duration of the action potential and shortens the refractory period. Enhance action potential initiation.
How are action potential conducted in unmyelinated axons?
The action potential is regenerated at each segment along the length of the axon
Name for the flow down an axon “ahead” of the action potential, depolarizing next segment to threshold
capacitive current
Structural area where voltage-gated Na+ channels are densely clustered in myelinated axons
Nodes of Ranvier
Areas of voltage-gated K+ channel concentration in myelinated axons
Juxtaparanodal region
Where are juxtaparanodal regions situated in relations to Nodes of Ranvier?
Off to the sides of the node, with the paranode sandwiched in between
How does the internodal membrane in myelinated axons affect the length constant?
Very high Rm increases the length constant.
How does the internodal membrane in myelinated axons affect the time constant?
Time constant = (resistance) x (capacitance)
Decreased capacitance due to the thick membrane balances out the increased membrane resistance. Slight decrease in time constant.
Why do demyelinating disease affect either the central OR peripheral axons?
CNS axons are myelinated by oligodendrocytes instead of Schwann cells in the PNS. So there’s a different pathology.
Demyelination has what mechanism of action
Exposes voltage-gated and leak K+ channels, decreasing the Rm and then also length constant.
What is the typical cause for acquired (as opposed to inherited) channelopathies?
Autoimmune
Main pore-forming subunit in voltage-gated ion channels
alpha subunit
Voltage-gated ion channels have how many alpha subunits (either homo or heterotetramers)
four
How many transmembrane segments are in each alpha subunit of voltage-gated ion channels?
six
Lines the pores of voltage-gated ion channels. Controls ion selectivity and permeability of channel.
Pore-loop (P-loop). In between transmembrane segments S5 and S6
The S4 segment of voltage-gated ion channels. Contains positively charged amino acids (arginine, lysine)
Voltage-sensor
Where might there be an inactivation particle on voltage-gated K+ channels?
N-terminal
When are HVA Ca2+ channels activated?
High voltage activated during action potentials.
When are HVA Ca2+ channels activated?
Low voltage activated so they activate somewhere between resting potential and action potential threshold.
Myotonia, periodic paralysis and GEFS (generalized epilepsy with febrile seizures) are examples of…
Channelopathies
Auxiliary subunits of voltage-gated ion channels
Beta, gamma, etc..
Inheritance pattern of periodic paralysis
autosomal dominant (patients will have both mutated and normal voltage-gated sodium channels)
What’s wrong with mutated voltage-gated sodium channels in periodic paralysis?
They inactivate slowly. Hyperkalemia (high blood/extracellular potassium) may play a role in this.
Target L-type HVA channels on vascular smooth muscle (used to control hypertension) specifically.
Dihydropyridine calcium channel blockers
