Role of cAMP in electrical and secretory activity of the neuroendocrine caudo-dorsal cells of Lymnaea stagnalis

Abstract

The peptidergic neuroendocrine caudo-dorsal cells (CDC) in the cerebral ganglia of the freshwater snail Lymnaea stagnalis L. produce an ovulation-stimulating neurohormone (CDCH). Release occurs by exocytosis in a calcium-dependent way from axon terminals in the periphery of the intercerebral commissure, particularly during a period of electrical activity (the ‘discharge’). An important factor in electrical and, hence, secretory activity of the CDC appears to be cyclic adenosine 3′, 5′-monophosphate (cAMP). Incubation of cerebral ganglia in snail Ringer with the cAMP-analogue 8-(4-chlorophenylthio)-cAMP (cpt-cAMP) or with the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) leads to activation of the CDC: electrophysiological, quantitative electron microscopic and bioassay studies show that incubation results in the onset of intense electrical activity, a marked reduction in the number of secretory granules in the axon terminals, an enormous increase in the number of exocytosis phenomena and a strong stimulation of CDCH-release. It is assumed that treatment with IBMX or with cpt-cAMP mimics a rise in the cytoplasmic level of cAMP when the CDC become activated by a physiological stimulus. This rise most likely effectuates a permeability change of the axolemma for ions involved in the discharge. As a consequence of the depolarization of the axolemma during the discharge, calcium ions would enter the axon terminal and induce exocytotic release of CDCH.