Pp1 inhibitors depolarize hermissenda photoreceptors and title: pp1 inhibitors
depolarize hermissenda photoreceptors and reduce k+currentsreduce k+ currents.
Huang, Haojiang, and Joseph Farley.
Neural Science, Indiana University, Bloomington, IN 47405-7007
APStracts 8:0239J, 2001.
Previous research indicates that activation of protein kinase C (PKC) plays a critical role
in the induction and maintenance of memory-related changes in neural excitability of
Type B photoreceptors in the eyes of nudibranch mollusc Hermissenda crassicornis
(H.c.). The enhanced excitability of B cells is due in part to PKC-mediated reduction in
somatic K+ currents. Here, we examined the effects of protein phosphatase inhibitors
upon Type B photoreceptor excitability and K+ currents to determine the role(s) of
protein phosphatases upon memory formation in Hermissenda. Using
electrophysiological and pharmacological methods, we found that the PP1 inhibitors
calyculin A and inhibitor-2 depolarized Type B photoreceptors by 20-30 mV. A broad-
spectrum kinase inhibitor, H7, blocked this effect. The depolarization induced by PP1
inhibition occluded that produced by an in vitro associative conditioning procedure.
Calyculin and inhibitor-2 reduced the same B cell K+ currents (IA and Idelayed) that are
reduced by in vitro and behavioral conditioning. H7 blocked the reductions. Cantharidic
acid (PP2A inhibitor) and cyclosporin (PP2B inhibitor) had negligible effects on B cell
resting membrane potential, K+ currents, and in vitro conditioning-produced cumulative
depolarization of B cells. These results suggest that the functional activity of K+ channels
in B cells is sustained by basal activity of PP1. Inhibiting PP1 appears to allow one or
more constitutively active kinase(s) to reduce K+ channel activity and thus mimic the
effects of conditioning. Our results suggest that PP1 may oppose and/or constrain the
extent of learning-produced changes in B cell excitability.
Received 13 October 2000; accepted in final form 30 May 2001
APS Manuscript Number J749-0.
Article publication pending Am J Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 31 July 2001