Action Potential II Flashcards
Local anesthetic
Blocks Na channels, has greatest effect on small axons (low safety factor). Channels must open for lidocaine entry.
safety factor
Need enough density of Na channels to supply enough current for depolarization.
Axons have more than enough Na channels (safety factor of transmission is 5-10x minimum required for propagation).
Why safety factor?
Excess of Na channels because axons branch (at each branch point the safety factor for transmission is reduced), ring of membrane before branch has to deliver enough current to depolarize both branches
Also because more Nav means # of open Nav (inactivation gate open) is reached sooner
So increased frequency and velocity (more current) of AP’s.
Factors in conduction velocity
- ) Time to depolarize mem. ahead of it to threshold
- ) Length of axon membrane it can depolarize (Depends on diameter only). Small diameter polarizes shorter length of mem. ahead of the active locus (Slower, so we have large axons for survival).
Myelin fx.
Decreases leaky cable properties. It increases the effective resistance b/w axoplasm and extracellular fluid.
Myelination greatly increases conduction velocity.
Makes up 1/3 of axon diameter
Node of Ranvier
Without myelin. Has Na channels and node becomes active locus, current then spreads ahead to next node and depolarizes it.
Little current lost b/w nodes.
AP “jumps”. Saltatory conduction.
Myelination and velocity
It changes the relationship so it is directly proportional (doubling diameter doubles the conduction velocity!).
Why aren’t all axons big?
You must balance detail vs. speed. you can have more fibers or 1 big axon. More fibers gives you more info.
Neurotoxins
Block Na channels, stop AP’s.
Tetrodotoxin, saxitoxin. Batrochotoxin (frongs).
Hyperkalemia causes
K escapes from cells and Kidney can’t do its job of keeping K outside below 5mM.
Acute issue is dealing with EKG abnormalities.
The heart
Backup system, all cells in cardiac conduction system depolarize spontaneously (just that ones in SA node depolarize fastest and get to threshold first).
Backups make trouble in hyperkalemia.
The heart in hyperkalemia
Increased K, depolarization moves Vm closer to threshold and makes it easier to get an AP, but also inactivates some Na channels.... get maverick pacemakers as a result. (H/K exchanger, K is leaving H is coming in, so Ca is being pumped out to compensate). Repolarization is blocked. (it brings Vm to be more positive, and thus closer to an AP). Latter case (block of conduction) cells distal to block keep having AP's. Heart muscle fibers not contracting synchronously. Can become refractory.
Ca ions and the heart
Ca bind and trick Na channels into seeing hyperpolarization, so you get increased threshold for AP.
It helps govern the threshold for AP.
Ca and AP threshold
Local Vm (neg) only detected basically on the membrane. Ca ions screens naked fixed negative charges, hyperpolarizing the local Vm (more difficult for cells to fire an AP...). So they increase threshold. (hyperkalemia makes the resting mem more positive, Ca makes the threshold potential more positive so there is a greater/restored difference b/w AP generation and resting potential. Otherwise interval is too small and AP's get generated frequently). Get heart to recover.