Acetylcholine receptors in rat cardiac neurones

• Published in: Journal of the autonomic nervous system Vol. 40; no. 1; pp. 33 - 47
• Main Authors: Selyanko, A.A., Skok, V.I.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.08.1992; Elsevier Science
• Subjects: Acetylcholine; Animals; Autonomic ganglia; Biological and medical sciences; Bungarotoxins - pharmacology; Cardiac neurone; Electrophysiology; Fundamental and applied biological sciences. Psychology; Ganglion-blocking agents; Ganglionic Blockers - pharmacology; Heart Conduction System - cytology; Heart Conduction System - metabolism; Heart Conduction System - physiology; Muscarine; Muscarine - antagonists & inhibitors; Muscarine - pharmacology; Neurons - metabolism; Neurons - physiology; Nicotine - antagonists & inhibitors; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Rats; Receptors, Cholinergic - metabolism; Vertebrates: nervous system and sense organs; Autonomic ganglia; Muscarine; Acetylcholine; Cardiac neurone; Ganglion-blocking agents; Cardiac ganglion; Peripheral nervous system; Vertebrata; Cholinergic receptor; Mammalia; Rat; Autonomic nervous system; Rodentia; Electrophysiology; Muscarinic receptor; Nicotinic receptor
• ISSN: 0165-1838; 1872-7476
• DOI: 10.1016/0165-1838(92)90223-4

Membrane potential changes produced by acetylcholine (ACh), and their underlying mechanisms, were studied in neurones of isolated cardiac ganglia of the rat by means of intracellular microelectrodes. Five components of membrane potential change could be detected in cardiac neurones following 1–5 s micro-application of ACh; (i) fast depolarization resulting from an activation of nonselective cationic conductance; (ii) slow depolarization associated with a decreased membrane conductance, presumably for potassium ions; slow hyperpolarization which consisted of (iii) early and (iv) late parts resulting from an activation of calcium-sensitive potassium current and from inhibition of steady-state inward current, respectively; and (v) delayed slow hyperpolarization associated with an increased conductance, most likely for potassium ions. Components (i), (iii) and (iv) persisted in the presence of atropine and were inhibited by nicotinic antagonists. Thus they were due to activation of nicotinic ACh receptors. However, the sensitivity of component (i) to ganglion-blocking agents appeared to be rather low: IC 50s for inhibiting (i) were 226 ± 34.2 μM, 31.2 ± 4.31 μM and 15.3 ± 3.27 μM for hexamethonium, d-tubocurarine, and trimetaphan, respectively. Components (ii) and (v) were abolished by atropine (1 μM) and mimicked by muscarine (component (ii) also persisted in d-tubocurarine), hence they resulted from activation of muscarinic ACh receptors. It is concluded that cardiac neurones are endowed with both nicotinic and muscarinic ACh receptors. Their activation leads to membrane depolarization and discharges followed by hyperpolarization and inhibition of discharges.