ONTOGENESIS OF ADRENERGIC AND CHOLINERGIC NEUROEFFECTOR TRANSMISSION IN CHICK EMBRYO HEART

¹ Department of Pharmacology, University of Connecticut Health Center, Farmington, Connecticut

Simultaneous stimulation of extrinsic vagal and sympathetic nerves to hearts isolated from chicks after hatching (21st incubation day) elicited atropine-sensitive cardioinhibition followed by propranolol-sensitive cardioacceleration. Field stimuli applied to the sinoatrial pacemaker region in such hearts also evoked a biphasic chronotropic effect by initiating tetrodotoxin-sensitive impulses that released autonomic transmitter from intracardiac postganglionic autonomic nerves. Atropine-sensitive cholinergic neuroeffector transmission was observed for the first time in ontogenesis on the 12th incubation day. Physostigmine predisposed the appearance of cholinergic neuroeffector transmission to the 10th incubation day presumably by inhibiting cholinesterase and thereby allowing the small amount of acetylcholine released to reach pacemaker cells and cause inhibition. Propranolol-sensitive adrenergic neuroeffector transmission appeared initially on the 21st incubation day and was not observed earlier in ontogenesis, even when cholinergic neuroeffector transmission had been blocked by atropine. Cholinergic and adrenergic neuroeffector transmission appeared several days after ingrowth of autonomic nerves of the heart had occurred. The delay between morphologic and functional innervation can be attributed to the time required to synthesize sufficient amounts of transmitter available for release as well as to an increase in pacemaker cell sensitivity to exogenously applied acetylcholine and catecholamines.

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