THE EFFECTS OF AXOTOMY AND PREGANGLIONIC DENERVATION ON THE EXPRESSION OF PITUITARY ADENYLATE-CYCLASE ACTIVATING PEPTIDE (PACAP), GALANIN AND PACAP TYPE-1 RECEPTORS IN THE RAT SUPERIOR CERVICAL-GANGLION

The effects of axotomy, chemical sympathectomy and preganglionic dener vation on the expression of the neuropeptides, pituitary adenylate cyc lase-activating peptide (PACAP), galanin (GAL), and the PACAP type I r eceptor in the rat superior cervical ganglion (SCG) were investigated by immunocytochemistry, in situ hybridization and receptor autoradiogr aphy. An antibody recognizing the rat vesicular acetylcholine transpor ter (VAChT) was used for the detection of preganglionic cholinergic fi bers. In the normal SCG, PACAP-immunoreactivity (-IR) was present in n umerous, basket-forming, preganglionic nerve fibers, while very few SC G neurons expressed PACAP. GAL-IR was restricted to occasional neurons , and a few nerve fibers, most of which were, in addition, PACAP-IR. P ACAP type 1 receptors were expressed in all nerve cell bodies. Axotomy resulted in a rapid and prominent upregulation of PACAP in a large nu mber of nerve cell bodies. There was a large increase also in GAL expr ession in many nerve cell bodies. In contrast, there was marked declin e in PACAP type 1 receptor expression. Chemical sympathectomy by admin istration of the catcholaminergic neurotoxin, 6-hydroxydopamine (6-OHD A), gave rise to similar changes. Preganglionic denervation led to the disappearance of PACAP- and VAChT-IR baskets and to the upregulation of PACAP and GAL expression in neurons located close to the entrance o f the sympathetic chain, whereas PACAP type 1 receptor expression was not affected. PACAP and GAL were coexpressed in most neurons after axo tomy and chemical sympathectomy. Taken together, these results indicat e that disruption of target contact and/or the infliction of an injury to the axons of the sympathetic neurons, rather than the preganglioni c output, regulates the expression of PACAP, GAL and the PACAP type 1 receptor. (C) 1997 Elsevier Science B.V.