MODULATION OF NICOTINIC ACHR CHANNELS BY PROSTAGLANDIN E-2 IN CHICK SYMPATHETIC-GANGLION NEURONS

The effects of prostaglandin E-2 (PGE(2)), an important metabolite of arachidonic acid, werts studied on the activity of nicotinic AChR chan nels in cultured chick sympathetic ganglion neurons. In whole cell rec ordings, PGE(2) (25 nM) inhibited significantly the ACh-evoked macrosc opic current. Tn cell-attached patch recordings, PGE(2) significantly inhibited single AChR channel currents as a result of a decrease in th e frequency of channel opening, with no change in open time and conduc tance. PGE(2) did not alter the extent or rate of agonist-induced dese nsitization of the AChR channels. These effects are specific since the related compound PGD(2) had no effect on AChR channel function. Becau se there is an abundant endogenous production of PGE(2) within sympath etic ganglia in response to certain stimuli, the inhibition of AChR ch annel function by PGE(2) could serve an important role to modulate syn aptic transmission in the sympathetic nervous system.