Question

In the experiment by Otto Loewi, stimulation of the vagus nerve caused an isolated frog's heart to slow its beating (an effect called bradycardia). This effect was ultimately shown by others to be due to the release of acetylcholine (ACh) from vagus axon terminals at synapses with cardiac muscle. However, Loewi also showed that the solution bathing this heart, rich with ACh released from the stimulated nerve axons, could be used to cause bradycardia in a 2nd heart, without direct vagus nerve stimulation. Indeed, we can replicate this by spritzing ACh directly onto a beating heart, again without vagus nerve stimulation.

So, how is it possible for a neurotransmitter like ACh to exert its effects on a target without being released presynaptically at a particular synapse? What does this say about the contribution of neurotransmitter degradation/reuptake to the precision and integrity of neurotransmission?

Answer 1

Vagus nerve is the Xth cranial nerve and forms a part of the involuntary nervous system. One of the functions of the vagus nerve is to keep the heart rate constant.

When the heart rate increases by sympathetic nervous system under the influence of adrenalin during emergency situation, the heart rate will be brought back to normalcy by parasympathetic nervous system which is influenced by acetylcholine, a neurotransmitter.

The right vagus innervates the SAN / pacemaker. When the vagus nerve is stimulated through parasympathetic ganglia , acetylcholine is released in the SA node of heart , slowing the heart rate.

In the given experiment by Loewi when the heart is bathed by acetylcholine solution the heart rate decreased because acetylcholine is a chemical which decreases the pacemaker rate by increasing the potassium and decreasing the calcium and sodium movement. As the pacemaker slows, the heart rate decreases. Acetylcholine controls the contraction of the cardiac muscles.