Question

Compare and Contrast the Neuronal Action Potential vs Cardiac Action Potential. Focus on THE STEPS of...

Compare and Contrast the Neuronal Action Potential vs Cardiac Action Potential. Focus on THE STEPS of the both action potentials and identify the difference(s).
What is the significance and involvement of Calcium ions in the cardiac action potentials? Why are Calcium ions not necessary in the neuronal action potentials, but are essential in the myocardial AP?

Homework Answers

Answer #1

Cardiac muscle acts as a functional syncytium via the gap junctions located within intercalated disks while neruonal cells acts as a single unit, Action potential propagate from cell to cell making cardiac muscle fibers to act as one functional unit this is known as functional synctium. Source of calcium for neuronal cells are sarcoplasmic reticulum, but source of calcium is different in cardiac muscles, because the sarcoplasmic reticulum is poorly developed so it cannot sequester large amount of calcium, therfore most of the calcium comes from extracellular source. In a typical nerve, the action potential duration is about 1 ms. In skeletal muscle cells, the action potential duration is approximately 2-5 ms, but however in cardiac cells the duration of action potential is around 200 to 400 ms. In a nerve cell there is no extended plateau phase, but in cardiac cells there is extended plateau phase.

In nerve cells, the depolarization phase of the action potential is caused by an opening of fast sodium channels. In non-pacemaker cells, of the cardiac cell, calcium influx prolongs the duration of the action potential and produces a characteristic plateau phase, in this extended plateau phase of cardiac cells  the membrane is held at a high voltage for a few hundred milliseconds prior to being repolarized by the potassium current, This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat known as cardiac arrythmias, This plateau is due to the action of slower calcium channels opening and holding the membrane voltage near their equilibrium potential even after the sodium channels have inactivated.

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