Ca2+- INDUCED Ca2+ RELEASE MEDIATES A SLOW POST-SPIKE HYPERPOLARIZATION IN
RABBIT VAGAL AFFERENT NEURONS.
Kimberly A. Moore, Akiva S. Cohen, Joseph P.Y. Kao, Daniel Weinreich.
University of Maryland, School of Medicine, Department of Pharmacology and
Experimental Therapeutics, Medical Biotechnology Center and Department of
Physiology, 685 West Baltimore Street, Baltimore, Maryland, USA 21201-
1559.
APStracts 4:288N, 1997.
ABSTRACT
The relation between Ca2+-induced Ca2+ release (CICR) elicited by action
potentials (APs) and a Ca2+-dependent slow post-spike hyperpolarization
(AHPslow) in acutely dissociated adult rabbit nodose neurons was studied using
microfluorimetric calcium measurements in conjunction with standard
intracellular current- and voltage-clamp recording techniques. The magnitude
of the AP-induced transient increase in [Ca2+]i (_Cat) was used to monitor
CICR. There was a close correlation between the magnitude of the _Cat and the
AHPslow current over the range of 1 - 16 action potentials (r=0.985).
Functional CICR blockers, ryanodine (10 æM), thapsigargin (100 nM), 2,5-di(t-
butyl)hydroquinone (10 æM) or cyclopiazonic acid (10 æM), selectively reduced
the peak amplitude of the AHPslow ò 91%. In five neurons, simultaneous
recordings of the _Cat and the AHPslow revealed that both responses were
blocked in parallel. These findings indicate that CICR is necessary for the
generation of the AHPslow in rabbit nodose neurons. The _Cat rises and decays
significantly faster than the AHPslow. This temporal disparity suggests that
activation of the AHPslow by Ca2+ may require additional signal transduction
steps.
Received 11 August 1997; accepted in final form 10 October 1997.
APS Manuscript Number J658-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 29 October 1997