Disease relevance of NTS

• These data demonstrate the presence in chicken liver of large amounts of high-affinity NT receptor(s) coupled to pertussis toxin-sensitive G-protein(s) [1].
• Neurotensin (NT), given intravenously at 10-50 pmol/kg per min to anesthetized female chickens equipped with a bile duct fistula, dose-dependently elevated hepatic bile flow and bile acid output but only when the enterohepatic circulation was maintained by returning the bile to the intestinal lumen [2].

High impact information on NTS

• Substance P (SP), neurotensin (NT), bombesin (BB), serotonin (5HT), and carbamylcholine (CCH) transiently increase electrogenic anion secretion in chinchilla and chicken ileum [3].
• Loperamide (LP) inhibits the short-circuit current responses caused by SP, NT, and BB, but not those caused by CCH, 5HT, Ca ionophore, or cyclic nucleotides [3].
• Hence pancreatic mesenchyme did not materially affect the proportions of these three cell types in experimental grafts, induced no specific pancreatic (insulin) cell type and allowed the differentiation of the characteristic proventricular endocrine cell types, neurotensin and bombesin/GRP cells [4].
• Distribution of neurotensin-containing neurons in the central nervous system of the pigeon and the chicken [5].
• Our observations suggest the presence of a very wide network of neurotensin-containing neurons in the avian brain and spinal cord, which is also the case in mammals [5].

Biological context of NTS

• Membrane potential and current responses to neurotensin in the longitudinal muscle of the rectum of the fowl [6].
• 5. The apparent Kd (approximately 91 pM) for this single class of binding sites was similar to Kds reported for the high-affinity components of NT binding to mammalian brain and intestinal membranes [1].
• Neurotensin produced a contractile response in ileal muscle strips pretreated with apamin (50 nM) and in isolated chick rectums and both contractile effects were inhibited by SR 48692 with IC50 of 31.6+/-9.5 nM and Kh of 3.2+/-0.9 nM (n = 6) and with IC50 of 28.9+/-6.9 nM and Kb of 5.4+/-1.0 nM (n = 7), respectively [7].
• Neurotensin decreases pepsin output and gastrointestinal motility in chickens [8].
• The amino acid sequence of a smooth muscle-contracting peptide from chicken rectum. Identity to chicken neurotensin [9].

Anatomical context of NTS

• The ontogeny and distribution of nerve cell bodies and fibres which contain vasoactive intestinal polypeptide-, substance P-, enkephalin- and neurotensin-like immunoreactivity have been studied in the chicken gastrointestinal tract, using immunocytochemistry [10].
• 1. The effects of neurotensin (NT) on membrane potential and membrane current of the longitudinal smooth muscle of chicken rectum were investigated by intracellular recording and whole-cell voltage clamp [6].
• Neurotensin is widely located in neurons of the central and peripheral nervous systems among mammalian species [5].
• 5. In single muscle cells enzymatically isolated from the muscle and dialyzed under voltage clamp at -50 mV with a CsCl-rich solution, NT (5 or 10 microM) produced an inward current [6].
• Extremely dense networks of neurotensin-containing fibers were found in the pallial commissure, the lateral septal nucleus, the preoptic area, the periventricular gray around the third ventricle, the dorsalis hypothalamic area, the hypothalamic nuclei, the parabrachial nucleus, the locus ceruleus, and the dorsal vagal complex [5].

Associations of NTS with chemical compounds

• NT-induced inward currents were obtained with inclusion of 10 mM EGTA in the pipette solution and their reversal potential was around 0 mV [6].
• Using immunofluorescence, immunoperoxidase, and autoradiographic techniques, we found a subpopulation of amacrine cells in the chicken retina exhibited enkephalin- and neurotensin-like immunoreactivity and high-affinity uptake of glycine [11].
• This happened with antisera detecting gastrin- and neurotensin-like cells, with secretin, vasoactive intestinal polypeptide, glucagon and substance P [12].
• In contrast, acrylamide treatment causes major increases of retinal Met-enkephalin and neurotensin concentrations [13].
• Quantitative studies of enkephalin's coexistence with gamma-aminobutyric acid, glycine and neurotensin in amacrine cells of the chicken retina [14].

Other interactions of NTS

• Kainic acid causes a sharp reduction in Met-enkephalin and somatostatin while neurotensin levels are unchanged [13].
• They always remained moderate in number and co-stored mainly serotonin, gastrin/CCK and neurotensin [15].
• Density and intensity were always much higher for galanin and neurotensin than for neuropeptide Y and bombesin [16].
• Nervous elements immunoreactive for galanin first appeared from days 6 to 7, for neurotensin from days 7 to 8, for neuropeptide Y from 13 to 15 and for bombesin from 15 to 18 [16].
• The distribution of vasoactive intestinal polypeptide (VIP)- and neurotensin (NT)-like immunoreactivities in the chicken retina was investigated by immunohistochemistry [17].

Analytical, diagnostic and therapeutic context of NTS

• A 17 kDa protein was identified by Western blotting as a potential precursor to NT and LANT6 [18].
• Peripheral intravenous infusion of physiological levels of neurotensin inhibited pepsin output from the proventriculus, but had no effect on the volume or pH of gastric secretions [8].
• The development of the enkephalin-, neurotensin- and somatostatin-like immunoreactive (ENSLI) amacrine cells in the chicken retina has been investigated by radioimmunoassay (RIA) and immunocytochemistry (ICC) [19].
• In addition, infusion of NT at 40 pmol/kg min gave a plasma level of iNT (approximately/= 88 pM) which was within the range of those observed during duodenal perfusion with lipid (54-300 pM) and near to that measured in hepatic portal blood from fed animals (52 +/- 5 pM) [2].

References