Endocrinology, Vol 137, 2269-2277, Copyright © 1996 by Endocrine Society

ARTICLES

Corticotropin-releasing hormone stimulates Ca2+ entry through L- and P- type Ca2+ channels in rat corticotropes

YA Kuryshev, GV Childs and AK Ritchie
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555, USA.

CRH induces corticotrope membrane depolarization and facilitates action potential firing. The increase in electrical excitability causes large oscillatory increases in cytosolic Ca2+ levels. In this study on highly enriched populations of cultured rat corticotropes, inhibitors were used to determine the contribution of the Na+ channel and Ca2+ channel subtypes to membrane excitability and cytosolic Ca2+ levels. Tetrodotoxin, an inhibitor of the voltage-dependent Na+ channel, inhibited a rapid initial component of the action potential, but generally did not influence spontaneous or CRH-induced firing frequency. Tetrodotoxin also had no effect on spontaneous or CRH- induced cytosolic Ca2+ levels. The L-type Ca2+ channel inhibitor nifedipine abolished spontaneous and CRH-induced action potentials and cytosolic Ca2+ transients, but did not eliminate the CRH-induced membrane depolarization or completely restore cytosolic Ca2+ to basal levels. Inhibition of P-type Ca2+ channels with omega-agatoxin-IVA decreased action potential firing frequency and reduced the CRH-induced increase in cytosolic Ca2+. The combination of nifedipine and omega- agatoxin-IVA abolished the CRH-induced rise in Ca2+, but did not abolish the membrane depolarization. Thus, cytosolic Ca2+ is mainly increased by CRH-induced action potentials that are completely dependent on L-type Ca2+ channels and partially regulated by P-type Ca2+ channels. CRH-induced Ca2+ entry also occurs independently of action potentials and is due to P-type, and possibly L-type, Ca2+ channels activated by the CRH-induced membrane depolarization.

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