Regulation of the M current: transduction mechanism and role in ganglionic transmission

• Published in: Canadian journal of physiology and pharmacology Vol. 70 Suppl; p. S12
• Main Authors: Smith, P A, Chen, H, Kurenny, D E, Selyanko, A A, Zidichouski, J A
• Format: Journal Article
• Language: English
• Published: Canada 01.01.1992
• Subjects: Animals; Ganglia, Sympathetic - physiology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Potassium Channels - drug effects; Potassium Channels - physiology; Rana catesbeiana; Rana pipiens; Signal Transduction - physiology; Synaptic Transmission - physiology
• ISSN: 0008-4212
• DOI: 10.1139/y92-238

Slow excitatory postsynaptic potentials in sympathetic ganglia often involve suppression of a voltage-dependent potassium current termed the M current. This current is suppressed by the muscarinic action of acetylcholine, by peptides such as luteinizing hormone releasing hormone, and sometimes by alpha-adrenoceptor agonists. Activation of beta-adrenoceptors sometimes produces weak potentiation. The voltage dependence of the M current is such that its suppression increases the excitability of ganglionic neurones. Since this sometimes leads to spontaneous discharge, activation of the slow excitatory postsynaptic potential mechanism (or modulation of M current) within a sympathetic ganglion produces effects that manifest in the autonomic outflow to the target organ. In frogs, M currents are present in the neurones of both paravertebral sympathetic ganglia and cardiac parasympathetic ganglia. Since the M current is suppressed by adrenaline in the parasympathetic ganglia and these ganglia often receive adrenergic fibres from sympathetic ganglia, this might reflect an important means of interaction between the two branches of the autonomic system. At the cellular level, M-current suppression is little affected by drugs that interfere with membrane phosphorylation--dephosphorylation processes. This observation is discussed in relationship to the current understanding of the transduction mechanism for agonist-induced M-current suppression.