Action Potential II

Question 1

1. Describe how action potential propagation relies on voltage-gated sodium channels acting like molecular “booster stations.”

Answer 1

With the AP, the voltage signal is regenerated at several points along the axon (by the voltage-gated channels), so it doesn’t degrade with distance

Without the voltage-gated ion channels (i.e., without APs), the voltage signal decays over short distances: neurons could not communicate over long distances without APs.

Essentially they let Na into the cell, depolarize it,

Furthermroe, at gaps in the myelin (nodes of Ranvier), voltage-gated ion channels regenerate the AP.

Question 2

2. Discuss why action potential propagation is much slower than the velocity of light.

Answer 2

1) What’s moving in a copper wire are photons. For all intents and purposes, photons don’t weigh anything. What’s actually moving in a nerve fiber are sodium ions. A sodium ion would have 11-12 neutrons and protons.
2) Secondly, electrons are moving through a copper wire. The sodium ions are moving through cytoplasm.

Question 3

3. Describe how myelination increases action potential conduction velocity.

Answer 3

• Myelin insulates the membrane, increasing rm.
• rm: resistance to current flow through the membrane
• increasing rm increases conduction velocity

Question 4

4. Describe refractoriness, and explain how it prevents an action potential from reversing its direction of propagation.

Answer 4

The piece of axon “behind” the active locus (back towards soma) is refractory: prevents AP from propagating “back” in that direction. In refractory period an AP wont fire again (absolute) and if it does, (relative), much harder to do so.

the h gates behind the wave are closed, your not gonna let sodium in; there is a wake of refractory period.

Question 5

5. Describe the effect of extracellular calcium ions on action potential threshold.

Answer 5

calcium outside makes it more positive, so there is a bigger difference trying to get to threshold, harder to excite

Question 6

6. Discuss the effect of axon diameter on conduction velocity, threshold to extracellular stimulation, safety factor of conduction, and likelihood of being myelinated.

Answer 6

Myelin increases conductance velocity by increasing membrane resistance (Rm) and increasing the length constant while decreasing Cm. It allows for saltatory conduction because AP can jump longer distances from node to node; longer length of membrane gets depolarized. Myelin also decreases the leakiness of the node by acting as an electrical insulator. Increases resistance between axoplasm and the ECF. Myelination + axon diameter can affect conduction velocity. Axons carrying more time-sensitive info are large and heavily myelinated (temp/pain receptors and skin mechanoreception).
Axons with very small diameters aren’t really myelinated.
Demyelination can be bad because it makes an AP go slower and travel less smaller distances, which isn’t very effective.
-MS  damages myelin in the CNS, many complications.
-Guillain-Barre syndrome = immune response against myelin in innervating muscles
-demyelination may also play role in chronic pain

bigger diameter = faster conduction, more likely to be myelinated
safety factor= 5-10x more VG na channels; becuase of
branching and super busy cells

Question 7

7. Hyperkalemia: Put it all together. Describe two causes, the mechanism of cardiac arrhythmias, the mechanism of action of calcium ion administration, two treatments to increase cell uptake of potassium ions from the ECF, and two treatments to remove potassium from the body. Identify what CBIGK means.

Answer 7

Hyperkalemia:

• elevated blood [K+], leading to elevated [K+] in ECF
• Elevated [K+] in ECF slightly depolarizes neurons (raise K+ reversal potential)
• Long-lasting depolarization causes accomodation, which can interfere with AP generation in cardiac pacemaker cells, causing arhythmias
• Caused by crush, burn, or other trauma that allows the cell to essentially break releasing K+ into the ECF

Treatment:
C BIG K Di
C: intravenous calcium
B: Bicarbonate or beta2 agonist
I: Insulin and
G: Glucose
K: Kayexalate
Di: Dieretics or Dialysis

treatments to increase K uptake:
bicarb stimulates na/k pump and insulin glucose also stimulates na/k pump

Intravenous calcium stabilizes the heart allowing for contractions to happen normally. High levels of K+ actually depolarize cardiac cells; thus fucking the normal cell contraction rhythm.

Ca2t for same reason.
more k outside cell makes it difficult for k to leave cell, k stays in cell which means you are more positive, more depolarized, easier excitable, leading to arymias