Vasoactive intestinal polypeptide (VIP) as a cholinergic co-transmitter: Some recent results

Vp, Whittaker

doi:10.1016/0309-1651(89)90018-0

Cited by 27 publications

(9 citation statements)

References 16 publications

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“…A previous study demonstrated VIP-like immunoreactivity colocalized with ACh in presynaptic terminals of pigeon ciliary ganglia (Reiner, 1987). In addition, there is good evidence that VIP and ACh are co-released from presynaptic terminals by depolarizing stimuli (reviewed by Whittaker, 1989), suggesting the peptide normally acts as a cholinergic cotransmitter (e.g., Willard, 1990). The co-release of ACh and VIP from cholinergic terminals in salivary gland and myenteric plexus is approximately equal at the low stimulation frequencies (about 10 Hz; Agoston, 1988;Lundberg, 1981) associated with efficient cholinergic transmission in the chick ciliary ganglion (Landmesser and Pilar, 1972;Dryer and Chiappenelli, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, CGRP immunoreactivity is present in motoneurons (Fontaine et al, 1986;New and Mudge, 1986) and in motor endplate terminals (Takami et al, 1985;Matteoli et al, 1988) and postsynaptically by increasing the excitability of myenteric neurons (Willard, 1990). VIP-like immunoreactivity is observed in nerve terminals distributed throughout the nervous system (Power et al, 1988;Sundler et al, 1988; reviewed by Gozes and Brenneman, 1989) and is often colocalized with ACh Eckenstein and Baughman, 1984;Whittaker, 1989), as occurs in preganglionic terminals of the avian ciliary ganglion (Reiner, 1987). The colocalization with ACh suggests that a VIPlike peptide may act as a cholinergic cotransmitter (Said, 1986; Willard, 1990) since VIP is known to be released from presynaptic terminals by depolarization (Giachetti et al, 1977;reviewed by Whittaker, 1989).…”

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confidence: 99%

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VIP modulates neuronal nicotinic acetylcholine receptor function by a cyclic AMP-dependent mechanism

et al. 1994

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Neuronal nicotinic ACh receptors (AChRs) mediate synaptic transmission throughout the nervous system, and are regulated by cellular processes and interactions that include second messenger signaling pathways. In the case of chick ciliary ganglion neurons, activation of the cAMP-dependent signaling pathway with cAMP analogs enhances ACh sensitivity in a manner consistent with an increase in the number of functional nicotinic receptors. We have now identified vasoactive intestinal peptide (VIP) as a neuromodulator or "first messenger" in the cAMP-mediated pathway that regulates neuronal AChRs. Using cAMP imaging and biochemical detection assays, we find that bath application of VIP elevates intracellular cAMP in freshly isolated ciliary ganglion neurons within minutes. The VIP treatment also enhances neuronal ACh sensitivity assessed with whole-cell recording. The enhanced ACh sensitivity produced by VIP appears with a short latency, similar to that associated with the increase in cAMP, and is not additive with the enhanced ACh sensitivity produced by bath application of a cAMP analog. In contrast, calcitonin gene-related peptide (CGRP), known to regulate muscle nicotinic AChRs via a cAMP-dependent pathway, has no detectable effect on levels of either cAMP or ACh sensitivity in the neurons. The results indicate that VIP enhances the ACh sensitivity of ciliary ganglion neurons via a cAMP-dependent signaling pathway, presumably by interaction with a specific receptor. Since VIP-like immunoreactivity is present in the presynaptic nerve terminals of avian ciliary ganglia, a VIP-like peptide could modulate AChRs in vivo.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

VIP modulates neuronal nicotinic acetylcholine receptor function by a cyclic AMP-dependent mechanism

et al. 1994

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“…Consequently, VIP acts as an inhibition factor of gastric emptying and reduced gastric acid secretion. Simultaneously, VIP is involved in the regulation of blood flow in the submucosal layer[ 16 ]. It is also essential that this substance has an effective neuroprotective function.…”

Section: Introductionmentioning

confidence: 99%

Changes in expression of inhibitory substances in the intramural neurons of the stomach following streptozotocin- induced diabetes in the pig

Bulc

Palus

Zielonka

et al. 2017

WJG

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AIMInfluence of chronic hyperglycemia on chemical coding of enteric neurons in stomach using pig as a model for human diabetic complications.METHODSTen pigs were divided into two groups: diabetic (D group, n = 5) and control (C group, n = 5). Pigs constituting the experimental group were given streptozotocin (150 mg/kg). Animals were euthanized six weeks after the induction of diabetes. The samples of stomach were collected from animals of both groups. The cryostat sections were processed for double immunofluorescence staining using primary antisera directed towards pan-neuronal marker (Hu C/D) proteins and/or neuronal isoform of nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and galanin (GAL).RESULTSIn the control group in the myenteric ganglia (MG) of the corpus we have noted 22.28% ± 1.19% of nNOS positive neurons, while in diabetic group we have found 40.74% ± 2.22% of nNOS immunoreactive perikarya (increase by 82.85 %). In turn in the pylorus we have observed 15.91% ± 0.58% nNOS containing neurons in control animals and 35.38% ± 1.54% in the diabetes group (increase by 122.37%). In the MG of the antrum and submucosal ganglion (SG) in the corpus hyperglycemia did not cause statistically significant changes. With regard to VIP-positive cell bodies in the antrum MG in the control animals we have noted 18.38 ± 1.39% and 40.74% ± 1.77% in the experimental group (increase by 121.65%). While in the corpus we have observed 23.20% ± 0.23% in the control and 30.93% ± 0.86% in the diabetes group (increase by 33.31%). In turn in the pylorus VIP positive cells bodies constituted 23.64% ± 1.56% in the control group and 31.20% ± 1.10% in the experimental group (increase by 31.97%). In the submucosal ganglion in the corpus we have noted 43.61% ± 1.06% in the control animals and 37.00% ± 1.77% in the experimental group (decrease by 15.15%). Expression of GAL-positive perikarya showed statistically significant changes only in the MG of the antrum and pylorus. In the antrum GAL positive perykarya constituted 26.53% ± 1.52% in the control and 36.67% ± 1.02% in the experimental animals (increase by 38.22%). While in the pylorus GAL positive neurons in the control group constituted 16.32% ± 0.92% and 17.99% ± 0.38% in the experimental animals (increase by 10.23%).CONCLUSIONOur results support the hypothesis that in the course of diabetes, long term episodes of high glucose serum level may influence the chemical phenotyping of enteric neurons.

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“…However, the function of VIP in the alimentary tract is less variable. The most important role seems to be an inhibitory action [54]. This inhibitory action includes smooth muscle relaxation and a decrease in gastric acid and intestinal fluid secretion [51].…”

Section: Discussionmentioning

confidence: 99%

Effect of Streptozotocin-Inducted Diabetes on the Pathophysiology of Enteric Neurons in the Small Intestine Based on the Porcine Diabetes Model

Bulc

Całka

Palus

2020

IJMS

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Hyperglycemia is one of the main causes of diabetes complications. Gastrointestinal (GI) disturbances are one of the most frequent complications during diabetes. The porcine digestive tract possesses physiological and pathological similarities to the human digestive tract. This also applies to the innervation of the gastrointestinal tract. In this study, the influence of experimentally-inducted hyperglycemia was examined on the expression of vesicular acetylcholine transporter (VAChT), cocaine- and amphetamine-regulated transcript (CART), galanin (GAL), vasoactive intestinal polypeptide (VIP), and calcitonin gene-related peptide (CGRP) in the enteric nervous system (ENS) neurons in the small intestine of the pig. During the current study, an increased number of neurons containing CART, VIP, GAL, and CGRP under streptozotocin injection were observed. The augmentation of expression included all enteric plexuses present in the small intestine. The same results were obtained in the case of VAChT; namely, chronic hyperglycemia led to an increase in the number of neurons utilizing VAChT in all investigated plexuses. The obtained results suggested that the function of neuropeptides studied in this experiment depended on their localization in the ENS structures, as well as part of the GI tract. Diabetes led to alterations in the neurochemical phenotype of small intestine enteric neurons.

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Vasoactive intestinal polypeptide (VIP) as a cholinergic co-transmitter: Some recent results

Cited by 27 publications

References 16 publications

VIP modulates neuronal nicotinic acetylcholine receptor function by a cyclic AMP-dependent mechanism

VIP modulates neuronal nicotinic acetylcholine receptor function by a cyclic AMP-dependent mechanism

Changes in expression of inhibitory substances in the intramural neurons of the stomach following streptozotocin- induced diabetes in the pig

Effect of Streptozotocin-Inducted Diabetes on the Pathophysiology of Enteric Neurons in the Small Intestine Based on the Porcine Diabetes Model

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