Modulation of nicotinic AChR channels by Prostaglandin E2 in chick
sympathetic ganglion neurons.
Wen Tan, Chuang Du, Steven A. Siegelbaun and Lorna Role.
Center for Neurobiology and Behavior, Departments of Anatomy and Cell
Biology, Pharmacology, Howard Hughes Medical Institute, Columbia University,
722 W. 168 St. New York, NY 10032.
APStracts 4:299N, 1997.
ABSTRACT
1. The effects of prostaglandin E2 (PGE2), an important metabolite of
arachidonic acid, were studied on the activity of nicotinic AChR channels in
cultured chick sympathetic ganglion neurons. 2. In whole-cell recordings, PGE2
(25 nM) inhibited significantly, the ACh-evoked macroscopic current. 3. In
cell-attached patch recordings, PGE2 significantly inhibited single AChR
channel currents as a result of a decrease in the frequency of channel opening
with no change in open time and conductance. 4. PGE2 did not alter the extent
or rate of agonist- induced desensitization of the AChR channels. 5. These
effects are specific since the related compound PGD2 had no effect on AChR
channel function. 6. Since there is an abundant endogenous production of PGE2
within sympathetic ganglia in response to certain stimuli, the inhibition of
AChR channel function by PGE2 could serve an important role to modulate
synaptic transmission in the sympathetic nervous system.
Received 16 October 1996; accepted in final form 23 October 1997.
APS Manuscript Number J830-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 14 November 1997