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J Neurophysiol 79: 870-878, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 79 No. 2 February 1998, pp. 870-878
Copyright ©1998 The American Physiological Society

Modulation of Nicotinic AChR Channels by Prostaglandin E2 in Chick Sympathetic Ganglion Neurons

Wen Tan1, Chuang Du1, Steven A. Siegelbaum2, and Lorna W. Role1

1 Department of Anatomy and Cell Biology and 2 Department of Pharmacology, Center for Neurobiology and Behavior, Howard Hughes Medical Institute, Columbia University, New York, New York 10032

Tan, Wen, Chuang Du, Steven A. Siegelbaum, and Lorna W. Role. Modulation of nicotinic AChR channels by prostaglandin E2 in chick sympathetic ganglion neurons. J. Neurophysiol. 79: 870-879, 1998. 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. In whole cell recordings, PGE2 (25 nM) inhibited significantly the ACh-evoked macroscopic current. 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. PGE2 did not alter the extent or rate of agonist-induced desensitization of the AChR channels. These effects are specific since the related compound PGD2 had no effect on AChR channel function. Because 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.




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