Chemical coding and electrophysiology of enteric neurons expressing neurofilament 145 in guinea pig gastrointestinal tract

2001 ◽  
Vol 442 (3) ◽  
pp. 189-203 ◽  
Author(s):  
Hong-Zhen Hu ◽  
Na Gao ◽  
Zhong Lin ◽  
Chuanyun Gao ◽  
Sumei Liu ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Guinea Pig ◽  
Enteric Neurons ◽  
Chemical Coding

scholarly journals The Influence of a Hyperglycemic Condition on the Population of Somatostatin Enteric Neurons in the Porcine Gastrointestinal Tract

Animals ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 142
Author(s):  
Michał Bulc ◽  
Katarzyna Palus ◽  
Jarosław Całka
Keyword(s):  
Gastrointestinal Tract ◽  
Glucose Level ◽  
Neuronal Response ◽  
Physiological State ◽  
Enteric Neurons ◽  
Gi Tract ◽  
Chemical Coding ◽  
Elevated Glucose ◽  
High Glucose Level

Somatostatin (SOM) is the most common agent in the gastrointestinal (GI) tract that is involved in the regulation of several gastric functions, as well as in gastric disorders. Hyperglycemia, which develops as a consequence of improperly treated diabetes, can cause numerous disturbances in the appropriate functioning of the gastrointestinal tract. High glucose level is toxic to neurons. One of the lines of defense of neurons against this glucotoxicity are changes in their chemical coding. To better understood the role of SOM secreted by enteric neurons in neuronal response on elevated glucose level, pancreatic β cells were destroyed using streptozotocin. Due to the close similarity of the pig to humans, especially the GI tract, the current study used pigs as an animal model. The results revealed that the number of enteric neurons immunoreactive to SOM (SOM-IR) in a physiological state clearly depend on the part of the GI tract studied. In turn, experimentally induced diabetes caused changes in the number of SOM-IR neurons. The least visible changes were observed in the stomach, where an increase in SOM-IR neurons was observed, only in the submucosal plexus in the corpus. However, diabetes led to an increase in the population of myenteric and submucosal neurons immunoreactive to SOM in all segments of the small intestine. The opposite situation occurred in the descending colon, where a decrease in the number of SOM-IR neurons was visible. This study underlines the significant role of SOM expressed in enteric nervous system neurons during diabetes.

PKC δ-isoform translocation and enhancement of tonic contractions of gastrointestinal smooth muscle

2007 ◽  
Vol 292 (3) ◽  
pp. G887-G898 ◽  
Author(s):  
Daniel P. Poole ◽  
John B. Furness
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscles ◽  
Specific Inhibitor ◽  
Smooth Muscle Contraction ◽  
Enteric Neurons ◽  
Guinea Pig Ileum ◽  
Tonic Component ◽  
Gastrointestinal Smooth Muscle ◽  
Immunohistochemical Evidence

PKC is involved in mediating the tonic component of gastrointestinal smooth muscle contraction in response to stimulation by agonists for G protein-coupled receptors. Here, we present pharmacological and immunohistochemical evidence indicating that a member of the novel PKC isoforms, PKC-δ, is involved in maintaining muscarinic receptor-coupled tonic contractions of the guinea pig ileum. The tonic component of carbachol-evoked contractions was enhanced by an activator of conventional and novel PKCs, phorbol 12,13-dibutyrate (PDBu; 200 nM or 1 μM), and by an activator of novel PKCs, ingenol 3,20-dibenzoate (IDB; 100 or 500 nM). Enhancement was unaffected by concentrations of bisindolylmaleimide I (BIM-I; 22 nM) that block conventional PKCs or by a PKC-ε-specific inhibitor peptide but was attenuated by higher doses of BIM-I (2.2 μM). Relevant proteins were localized at a cellular and subcellular level using confocal analysis. Immunohistochemical staining of the ileum showed that PKC-δ was exclusively expressed in smooth muscles distributed throughout the layers of the gut wall. PKC-ε immunoreactivity was prominent in enteric neurons but was largely absent from smooth muscle of the muscularis externa. Treatment with PDBu, IDB, or carbachol resulted in a time- and concentration-dependent translocation of PKC-δ from the cytoplasm to filamentous structures within smooth muscle cells. These were parallel to, but distinct from, actin filaments. The translocation of PKC-δ in response to carbachol was significantly reduced by scopolamine or calphostin C. The present study indicates that the tonic carbachol-induced contraction of the guinea pig ileum is mediated through a novel PKC, probably PKC-δ.

Neurochemical identification of enteric neurons expressing P2X3 receptors in the guinea-pig ileum

2002 ◽  
Vol 118 (3) ◽  
pp. 193-203 ◽  
Author(s):  
Luc Nassauw ◽  
Inge Brouns ◽  
Dirk Adriaensen ◽  
Geoffrey Burnstock ◽  
Jean-Pierre Timmermans
Keyword(s):  
Guinea Pig ◽  
Enteric Neurons ◽  
Guinea Pig Ileum ◽  
P2x3 Receptors

Effects of neurotransmitter release on mucosal transport in guinea pig ileum

1983 ◽  
Vol 245 (6) ◽  
pp. G745-G750 ◽  
Author(s):  
H. J. Cooke ◽  
K. Shonnard ◽  
G. Highison ◽  
J. D. Wood
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Neurotransmitter Release ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Scorpion Venom ◽  
Enteric Neurons ◽  
Sodium Absorption ◽  
Guinea Pig Ileum ◽  
Ileal Mucosa

Scorpion venom (Leiurus quinquestriatus), a substance that evokes neurotransmitter release by depolarizing neurons, was used to activate enteric neurons in short-circuited guinea pig ileum. Scorpion venom increased transmural potential difference and short-circuit current, and this response was similar to the increase that occurred after electrical stimulation of enteric neurons. The stimulus- or venom-evoked response in short-circuit current was abolished by tetrodotoxin. Atropine reduced by 47% the increments in short-circuit current produced by either electrical stimulation or venom. Scorpion venom increased active chloride secretion in short-circuited guinea pig ileal mucosa but had no significant effect on active sodium absorption, residual flux, or total tissue conductance. No morphological changes in transmission electron micrographs of ileal mucosa treated with scorpion venom were evident compared with controls. Alanine caused an increase in short-circuit current in venom-treated tissue that was similar to control values. These results show that scorpion venom mimics the mucosal effects of electrical activation of enteric neurons. These results suggest that a significant component of both scorpion venom action and the response to electrical field stimulation is mediated by neural release of acetylcholine, which activates epithelial muscarinic receptors.

Neurochemical coding of enteric neurons in the guinea pig stomach

1995 ◽  
Vol 353 (2) ◽  
pp. 161-178 ◽  
Author(s):  
Michael Schemann ◽  
Cornelia Schaaf ◽  
Michael Mäder
Keyword(s):  
Guinea Pig ◽  
Enteric Neurons ◽  
Neurochemical Coding ◽  
Guinea Pig Stomach
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