In the experiment by Otto Loewi, stimulation of the vagus nervecaused an isolated frog's heart to slow its beating (an effectcalled bradycardia). This effect was ultimately shown by others tobe due to the release of acetylcholine (ACh) from vagus axonterminals at synapses with cardiac muscle. However, Loewi alsoshowed that the solution bathing this heart, rich with ACh releasedfrom the stimulated nerve axons, could be used to cause bradycardiain a 2nd heart, without direct vagus nerve stimulation. Indeed, wecan 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 exertits effects on a target without being released presynaptically at aparticular synapse? What does this say about the contribution ofneurotransmitter degradation/reuptake to the precision andintegrity of neurotransmission?
