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Issue 1070 coverVIP, PACAP, AND RELATED PEPTIDES: FROM GENE TO THERAPY Volume 1070 published July 2006
Ann. N.Y. Acad. Sci. 1070: 317–321 (2006). doi: 10.1196/annals.1317.036
Copyright © 2006 by the New York Academy of Sciences
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Articles by HARDWICK, J. C.
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Calcium Influx through Channels Other than Voltage-Dependent Calcium Channels Is Critical to the Pituitary Adenylate Cyclase-Activating Polypeptide-Induced Increase in Excitability in Guinea Pig Cardiac Neurons

JEAN C. HARDWICKa, JOHN D. TOMPKINSb, SARAH A. LOCKNARb, LAURA A. MERRIAMb, BETH A. YOUNGb AND RODNEY L. PARSONSb

a Department of Biology, Ithaca College, Ithaca, New York 14850, USA b Department of Anatomy and Neurobiology, University of Vermont, Burlington, Vermont 05405, USA

Key Words: PACAP • calcium influx • intracellular calcium release • action potential generation • voltage-dependent calcium channels

Address for correspondence: Rodney L. Parsons, Ph.D., University of Vermont College of Medicine, Department of Anatomy and Neurobiology, 89 Beaumont Ave., Given C427, Burlington, VT 05405. Voice: 802-656-2230; fax: 802-656-8704. e-mail: Rodney.Parsons{at}uvm.edu

Pituitary adenylate cyclase-activating polypeptide (PACAP) effects on intracellular calcium ([Ca2+]i) and excitability have been studied in adult guinea pig intracardiac neurons. PACAP increased excitability, but did not elicit Ca2+ release from intracellular stores. Exposure to a Ca2+-deficient solution did not deplete [Ca2+]i stores but did eliminate the PACAP-induced increase in excitability. We postulate that Ca2+ influx is required for the PACAP-induced increase in excitability.






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