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To unravel the expression of the Shaker-related delayed rectifier potassium subunits Kv1.1 and Kv1.2 in the ileum of three murine strains. Immunofluorescence using cell type markers was performed on cryosections and whole mounts, containing the myenteric or submucous plexus, which were analysed by fluorescence and confocal microscopy. Distribution of Kv1.1 and Kv1.2 was similar in the ileum of the three murine strains. Kv1.1 was found in myenteric ganglionic S100-immunoreactive (ir) glial cells, in almost all extraganglionic S100-ir glial cells, in S100-ir glial cells of the submucosa. Kv1.1 was also detected in some GFAP-ir glial cells of the myenteric ganglia and in the GFAP-ir glial cells of the submucous internodal strands. Kv1.2 was found in intramuscular and submucous S100-ir glial cells, and in a few GFAP-ir glial cells. Kv1.1 or Kv1.2 were not found in interstitial cells of Cajal. Kv1.2 was expressed in some ganglionic nerve cell bodies. A part of these neurons was cholinergic. Kv1.1 and Kv1.2 are predominantly expressed in distinct phenotypes of the ileal enteroglial cells. Kv1.2 is also expressed on the somata of distinct enteric subpopulations. These results support the active role of enteroglial cells in intestinal motility.

Alcohol consumption interferes with gastrointestinal transit causing symptoms in alcoholic patients. Nitric oxide (NO), synthesized by neuronal nitric oxide synthase (nNOS) plays an important role in the control of gastrointestinal motility. Our aim was to investigate whether chronic alcohol intake in a murine model induces gastrointestinal motility disturbances and affects the nitrergic myenteric neurons in the stomach and jejunum. Gastric emptying, small intestinal transit and geometric centre were measured in vivo after intragastric gavage of Evans blue. Nitrergic relaxations to electrical field stimulation (EFS) and exogenous NO were recorded in jejunal muscle strips in vitro. The proportion of nNOS-immunopositive myenteric neurons was assessed using PGP9.5 and nNOS immunostaining. After chronic alcohol consumption, gastric emptying and small intestinal transit were delayed compared with control mice, and the nitrergic nerve-mediated relaxations to EFS in the jejunum were decreased, whereas relaxations to exogenous NO did not differ. The proportion of nNOS-immunoreactive neurons did not change in the stomach, whereas in the jejunum the percentage decreased from 33% to 27% (P

Patients with inflammatory bowel disease often suffer from gastrointestinal motility and sensitivity disorders. The aim of the current study was to investigate the role of transient receptor potential of the vanilloid type 1 (TRPV1) receptors in the pathophysiology of colitis-induced pelvic afferent nerve sensitization. Trinitrobenzene sulphate (TNBS) colitis (7.5 mg, 30% ethanol) was induced in Wistar rats 72 h prior to the experiment. Single-fibre recordings were made from pelvic nerve afferents in the decentralized S1 dorsal root. Fibres responding to colorectal distension (CRD) were identified in controls and rats with TNBS colitis. The effect of the TRPV1 antagonist N-(4-tertiarybutylphenyl)-4-(3-chlorophyridin-2-yl)tetrahydropyrazine-1(2H)carboxamide (BCTC; 0.25–5 mg kg−1) or its vehicle (hydroxypropyl-β-cyclodextrin) was tested on the afferent response to repetitive distensions (60 mmHg). Immunocytochemical staining of TRPV1 and NF200, a marker for A-fibre neurons, was performed in the dorsal root ganglia L6–S1. TNBS colitis significantly increased the response to colorectal distension of pelvic afferent C-fibres. BCTC did not significantly affect the C-fibre response in controls, but normalized the sensitized response in rats with colitis. TNBS colitis increased the spontaneous activity of C-fibres, an effect which was insensitive to administration of BCTC. TNBS colitis had no effect on Aδ-fibres, nor was their activity modulated by BCTC. TNBS colitis caused an immunocytochemical up-regulation of TRPV1 receptors in the cell bodies of pelvic afferent NF200 negative neurons. TRPV1 signalling mediates the colitis-induced sensitization of pelvic afferent C-fibres to CRD, while Aδ-fibres are neither sensitized by colitis nor affected by TRPV1 inhibition.

Rauber's sickle fragments from unincubated quail blastoderms, associated or not with chicken central subgerminal ooplasm, were placed on the deep side of the upper layer (UL) of the isolated anti-sickle region of unincubated chicken blastoderms and cultured in vitro. When only a Rauber's sickle fragment was placed, we observed always a pronounced thickening of the UL (pregastrulation) in the immediate neighbourhood. Some times a primitive streak (PS) developed. When the Rauber's sickle fragment was "sandwiched" between the UL and a central subgerminal ooplasmic mass [containing the nucleus of Pander (1817)], always a (pre)neural plate accompanied by endophyll developed, not or well associated with a primitive streak. In the latter case a complete miniature embryo developed. De novo formation of endophyll was observed. As it contained quail nuclei it was derived from Rauber's sickle cells which colonized the subgerminal ooplasm. Our experiments indicate that the uncommitted upper layer (UL) of the anti-sickle of unincubated blastoderms constitutes an excellent reactor tissue for inductions. The thickening induced in the UL of the anti-sickle region by Rauber's sickle initiates (pre)gastrulation and the thickening induced by endophyll initiates (pre)neurulation. In the beginning, pregastrulation and preneurulation seem to be independent phenomena. It is only later, when both become correctly linked at the right place and time, that a normal embryo will develop.

Three days old quail embryos were hypothalamectomized in ovo by the decapitation technique according to Callebaut (1993). Half of these embryos was exposed to day cyclically repeated prolonged low subnormal incubation temperatures (25 degrees C). The other half of these decapitated embryos was normally continuously incubated. As is the case for not decapitated embryos the ovaries of the first group presented a tamoxifen like effect: cortical rim atrophy with proportional hypertrophy of the medulla and a pronounced decrease in the number of oogonia and oocytes. By contrast the ovaries of the second group of decapitated embryos presented a normal aspect without sterilization of the ovigerous sex cords. It was concluded that: 1. the hypophysis, the hypothalamus or other prosencephalic tissues play no intermediary role in the establishment of a tamoxifen like effect in the ovary; 2. the early embryonic development of the quail ovary during the considered period takes place without the intervention of the hypothalamus.