PGE1-Induced cAMP Biosynthesis in the Superior Cervical Ganglion of Different Animal Species
Some years ago Greengard and coworkers (5–7) put forward a comprehensive hypothesis to explain the genesis of the slow synaptic potentials observed in curarized mammalian sympathetic ganglia after tetanization of preganglionic fibers. Following this hypothesis the slow synaptic potentials were due to an increase of cyclic nucleotides levels brought about by the interaction of either acetylcholine (ACh)(slow EPSP) or dopamine (DA)(slow IPSP) with specific receptors located on ganglion neuron membranes. In particular, according to Greengard’s hypothesis, prostaglandin E1 (PGE1) would act as a DA antagonist reducing the amplitude of the slow IPSP extracellularly recorded from isolated ganglion preparations. Since DA was supposed to increase cAMP levels via activation of adenylate cyclase, PGE1 would exert an inhibitory action on this enzyme.
KeywordsAdenylate Cyclase cAMP Level Superior Cervical Ganglion Increase cAMP Level Ganglion Inter
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