INNERVATION OF THE GALLBLADDER - STRUCTURE, NEUROCHEMICAL CODING, ANDPHYSIOLOGICAL-PROPERTIES OF GUINEA-PIG GALLBLADDER GANGLIA

The muscle and epithelial tissues of the gallbladder are regulated by a ganglionated plexus that lies within the wall of the organ. Although these ganglia are derived from the same set of precursor neural crest cells that colonize the gut, they exhibit structural, neurochemical a nd physiological characteristics that are distinct from the myenteric and submucous plexuses of the enteric nervous system. Structurally, th e ganglionated plexus of the guinea pig gallbladder is comprised of sm all clusters of neurons that are located in the outer wall of the orga n, between the basal lamina, and are devoid of collagen. Gallbladder n eurons are rather simple in structure, consisting of a soma, a few sho rt dendritic processes and one or two long axons. Results reported her e indicate that all gallbladder neurons are probably cholinergic since they all express immunoreactivity for choline acetyltransferase. The majority of these neurons also express substance P, neuropeptide Y, an d somatostatin, and a small remaining population of neurons express va soactive intestinal peptide (VIP) immunoreactivity and NADPH-diaphoras e enzymatic activity. We report here that NADPH-diaphorase activity, n itric oxide synthase immunoreactivity, and VIP immunoreactivity are ex pressed by the same neurons in the gallbladder. Physiological studies indicate that the ganglia of the gallbladder are the site of action of the following neurohumoral inputs: 1) all neurons receive nicotinic i nput from vagal preganglionic fibers; 2) norepinephrine released from sympathetic postganglionic fibers acts presynaptically on vagal termin als within gallbladder ganglia to decrease the release of acetylcholin e from vagal terminals; 3) substance P and calcitonin gene-related pep tide, which are co-expressed in sensory fibers, cause prolonged depola rizations of gallbladder neurons that resemble slow EPSPs; and 4) chol ecystokinin (CCK) acts presynaptically within gallbladder ganglia to i ncrease the release of acetylcholine from vagal terminals. Results rep orted here indicate that hormonal CCK can readily access gallbladder g anglia, since there is no evidence for a blood-ganglionic barrier in t he gallbladder. Taken together, these results indicate that gallbladde r ganglia are not simple relay stations, but rather sites of complex m odulatory interactions that ultimately influence the functions of musc le and epithelial cells in the organ. (C) 1997 Wiley-Liss, Inc.