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At least 649 records · Page 36Linked to original sources
PubMed1978

Slowly-developing depolarization of neurones in the guinea-pig inferior mesenteric ganglion following repetitive stimulation of the preganglionic nerves.

Intracellular recordings were made from cells of the isolated guinea-pig inferior mesenteric ganglion. Stimulation of both hypogastric nerves at 30 Hz for 2 sec caused a slowly developing depolarization (SD) and fall in cell input resistance which reached a peak 10-30 sec after the end of stimulation. The amplitude of the SD was increased in a graded manner if the stimulus voltage was increased. The SD was unaffected by tubocurarine, atropine or guanethidine, but was blocked by removing external Ca. These results suggested that the SD was caused by the release of some substance from a large number of nerve terminals.

Animals↗
PubMed1981

An electron microscopic study on substance P-like immunoreactive nerve fibers in the celiac ganglion of guinea pigs.

Substance P-immunoreactive nerve fibers in the celiac ganglion of guinea pigs were revealed with the PAP procedures to contain abundant small clear vesicles mixed with a few large granular vesicles. The immunoreactive materials were localized around cytoplasmic components including vesicles and on the inside of the plasma membrane. The immunoreactive fibers directly apposed to unlabelled dendrites of postganglionic neurons and also to preganglionic axons. Morphological features of synapses could be identified at sites of apposition to unlabelled dendrites: clusters of vesicles in the immunoreactive fibers, intercellular spaces of about 20 nm, and an intermediate density on the postjunctional membrane of unlabelled dendrites. On the other hand, no distinct electron density together with accumulations of vesicles was seen underneath the apposed membrane of unlabelled axons. These findings indicate at the ultrastructural level that substance P-fibers form axo-dendritic synapses on the postganglionic neurons and also suggest the presence of the presynaptic interaction between substance P-fibers and some preganglionic axons in this ganglion.

Animals↗
PubMed1982

Gastric vagotomy inhibits drinking after hypertonic saline.

Rats with bilateral subdiaphragmatic vagotomy drank later and less in response to cellular dehydration produced by hypertonic saline. In an attempt to localize this deficit neurologically, we performed selective gastric, hepatic or coeliac vagotomies. The drinking responses of such selectively lesioned rats were compared with total bilateral vagotomized rats and sham operated rats after 0.15 M and 1 M NaCl (1% BW). Gastric vagotomy reproduced the drinking deficits that occurred after total vagotomy, but hepatic and coeliac vagotomies did not. These results demonstrate that disconnection of the gastric vagal fibers is the necessary and sufficient lesion of the abdominal vagal system for decreasing the drinking response to hypertonic saline.

Animals↗
PubMed1982

Celiac vagotomy attenuates the ingestive responses to epinephrine and hypertonic saline but not insulin, 2-deoxy-D-glucose, or polyethylene glycol.

The ingestive responses of rats given celiac vagotomy (C), combined celiac and hepatic vagotomy (CH), or low total vagotomy (removal of all tissue from around the esophagus, stomach and duodenum; LT) were compared with sham operated controls (S) in a series of regulatory challenges. The vagotomized groups responded normally to 2-deoxy-D-glucose (2DG; 125, 250, 500 mg/kg, IP), insulin (4, 8, 12 U/kg, IP), and polyethylene glycol (10 ml/kg: 30% w/v, SC), but displayed attenuated responses to epinephrine (40, 80, 120 micrograms/kg, IP) and hypertonic saline (10 ml/kg: 0.25, 0.5, 1.0 M, IP). These results can be interpreted as evidence that the celiac vagus carries a major component of hepatic afferent innervation. Additionally, when considered with other findings they suggest that whereas the anorectic activity of epinephrine is mostly confined to the liver, 2DG hyperphagia involves stimulation of a wider population of peripheral metabolic receptors.

Animals↗
PubMed1982

Gastric or coeliac vagotomy decreases drinking after peripheral angiotensin II.

After bilateral subdiaphragmatic vagotomy, rats drank later and less in response to peripherally administered angiotensin II [13]. We attempted to localize this deficit neurologically by performing selective gastric, hepatic or coeliac vagotomies. The drinking responses of such selectively lesioned rats to 0.1 and 1.0 mg X kg-1 angiotensin II (SC) were compared to those of total bilateral vagotomized rats and sham vagotomized rats. Gastric or coeliac vagotomy produced drinking deficits that were similar to those produced by total abdominal vagotomy, but hepatic vagotomy did not. These results demonstrate the importance of abdominal vagal mechanisms in the drinking response to circulating angiotensin II.

Angiotensin II↗
PubMed1993

Hepatic glucose-sensitive unit regulation of glucose-induced insulin secretion in rats.

Vagal glucose receptors, or glucose-sensitive units which modulate insulin secretion, exist in the liver. This study sought to determine the pathway of portal glucose-sensitive unit-regulated insulin secretion by measuring plasma insulin after intraperitoneal (IP) injection of glucose under unanesthetized and unrestrained conditions (Experiment 1), and by recording electrical discharge after intraportal injection of glucose (Experiment 2) in rats with hepatic and/or celiac vagotomy. In Experiment 1, plasma insulin was significantly reduced and plasma glucose elevated after IP glucose injection (1 g/kg) in the three groups of hepatic-, celiac-, and hepatic- and celiac-vagotomized rats in comparison with a sham-vagotomized group. There were no significant differences among the four groups in plasma insulin or glucose after IV glucose injection (0.5 g/kg). In Experiment 2, intraportal injection of 400 mg/dl of glucose solution, a similar concentration to that produced by 1 g/kg of IP glucose injection, caused a reduction in the discharge rate of hepatic vagal afferents and an increase in that of pancreatic vagal efferents. This increase was blocked by prior sectioning of the hepatic branch of the vagus nerve. These results suggested that hepatic glucose-sensitive units enhanced glucose-induced insulin secretion via the hepatic vagal afferents and the pancreatic vagal efferents mediated by the brain stem center in vivo. The physiological role of these hepatic glucose-sensitive units is assumed to maintain blood glucose homeostasis by enhancing glucose-induced insulin secretion.

Afferent Pathways↗
PubMedDate not supplied

Origins of nerve terminals containing nitric oxide synthase in the guinea-pig coeliac ganglion.

Nitric oxide synthase was localised immunohistochemically and by NADPH diaphorase activity in two groups of nerve terminals and in rare cell bodies in the guinea-pig coeliac ganglion. Strongly reactive varicose terminals surrounded a subgroup of principal ganglion cells, most of which were in the medial lobes of the ganglion and most of which were somatostatin immunoreactive. A second set of varicose terminals, which were less intensely reactive, were found throughout the ganglia. Nitric oxide synthase containing nerve cell bodies in the intermediolateral cell columns of the spinal cord were labelled by dye retrogradely transported from the coeliac ganglion. Lesion of nerve connections between abdominal viscera and the coeliac ganglion caused a loss of the strongly reactive fibres, while the widely distributed, less intensely reactive fibres persisted. It is concluded that nitric oxide synthase terminals in the coeliac ganglion come from two sources, sympathetic preganglionic neurons and intestinofugal neurons.

Amidines↗
PubMed1995

Chemical coding of neurons that project from different regions of intestine to the coeliac ganglion of the guinea pig.

The chemical codings of neurons that project from the small intestine, caecum, proximal colon, distal colon and rectum to the coeliac ganglion of the guinea pig were investigated. The coeliac ganglion was injected with the retrogradely transported dye Fast Blue, and each of the regions was examined 6 days later in wholemounts that had been prepared for immunohistochemical localisation of pairs of antigens. In both the small and large intestines, all intestinofugal neurons were immunoreactive (IR) for choline acetyltransferase (ChAT). In each region of the large intestine, the largest population, representing 50-60% of retrogradely labelled neurons in each region, was immunoreactive for ChAT, bombesin (BN), calbindin (Calb) and nitric oxide synthase (NOS). Most intestinofugal neurons in the small intestine contain bombesin and VIP-IR along with ChAT-IR but none contain either Calb or NOS. Thus, nerve endings of enteric origin in the coeliac ganglion that contain NOS-IR or Calb-IR come from the large intestine and those with bombesin-IR but not NOS-IR are from the small intestine. The gastric wall was injected with Fast Blue in order to label noradrenergic (NA) neurons in the coeliac ganglion and to determine, by localisation of NOS and bombesin-IR, whether they receive inputs from the small and large intestine. Some NA neurons received inputs from the large intestine (and perhaps also from the small intestine) and some received inputs exclusively from the small intestine. Most NA neurons that received intestinofugal inputs had the chemical code NA/-; some were immunoreactive for somatostatin (NA/SOM neurons), but those with IR for neuropeptide Y (NA/NPY) rarely received intestinofugal inputs.

Animals↗
PubMed1993

Effects of renal denervation and reinnervation on ganglionic gene expression of neurotransmitter proteins and c-fos in rat.

To investigate the molecular basis for reno-renal interactions, Northern blot analyses of sympathetic ganglia were used to study the changes in levels of mRNA encoding tyrosine hydroxylase (TH), neuropeptide Y (NPY), and c-fos at 4, 14, 21, and 56 days after denervation of the left kidney, and of c-fos mRNA at 1 and 4 h after denervation. Ganglia included in the study were right and left paravertebral chain ganglia (PVG, T11 to L2), celiac-mesenteric plexus (CMP), and right and left superior cervical ganglia (SCG). Levels of TH mRNA in the left PVG and CMP were decreased at 4 and 14 days compared to controls. Levels were elevated at 21 days and similar to control levels at 56 days. In the right PVG, TH mRNA levels were elevated at 4 and 14 days, diminished from this elevated level at 21 days, and similar to control levels at 56 days. No differences were found in TH mRNA levels of left or right SCG compared to controls. In long-term experiments (days), no differences in NPY or c-fos mRNA levels were found in any of the ganglia from experimental rats compared to controls. Levels of c-fos mRNA in the left PVG and CMP were decreased at 1 hour compared to control levels. By 4 h, differences in mRNA levels were no longer apparent. In the right PVG, c-fos mRNA levels were elevated at 1 hour and no longer different from control levels at 4 h. No differences were found in c-fos mRNA levels of left or right SCG compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗