Detail of "74853-69-3"

Reference

Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice

Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. Erwin, V. Gene; Korte, A.; Marty, M. (Sch. Pharm., Univ. Colorado, Boulder, CO 80309-0297, USA). Brain Res., 400(1), 80-90 (English) 1987. CODEN: BRREAP. ISSN: 0006-8993. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Neurotensin (NT) [39379-15-2] differentially altered EtOH [64-17-5]-induced anesthesia as measured by duration of loss of righting response or by blood EtOH levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to EtOH. At doses of 5-500 ng injected intracerebroventricularly, NT increased EtOH sensitivity in SS mice, but not in LS mice, as measured by blood EtOH concns. at loss of righting response. At higher doses, 0.5-10 mg, NT enhanced the sensitivity of both SS and LS mice to EtOH-induced anesthesia. The hypothermic effect of EtOH detd. at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced EtOH-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for EtOH in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogs N-acetyl-NT8-13 [74853-69-3] and [D-Trp11]-NT [73634-68-1] but not NT1-8 [80887-44-1] enhanced the anesthetic action of EtOH in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin, and corticotropin-releasing hormone (CRF) were not effective in enhancing EtOH-induced anesthesia in LS or SS mice. CRF appeared to decrease EtOH sensitivity in LS but not in SS mice. b-Endorphin [60617-12-1] markedly increased the EtOH sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g., 0.5-1.0 mg. Thus, differences in brain sensitivity of LS and SS mice to EtOH may be mediated by genetic differences in NT systems. Likewise, NT, and probably b-endorphin, may interact with other neurochem. processes that are involved in the mechanism of EtOH-induced anesthesia and that differ genetically in LS and SS mice.

Comparison of the stimulation of inositol phospholipid hydrolysis and of cyclic GMP formation by neurotensin, some of its analogs, and neuromedin N in neuroblastoma clone N1E-115

Comparison of the stimulation of inositol phospholipid hydrolysis and of cyclic GMP formation by neurotensin, some of its analogs, and neuromedin N in neuroblastoma clone N1E-115. Kanba, Kiyoko S.; Richelson, Elliott (Dep. Psychiatry Pharmacol., Mayo Clin. Found.Chemical with cas number 61445-54-3 also plays role., Rochester, MN 55905, USA). Biochem. Pharmacol., 36(6), 869-74 (English) 1987. CODEN: BCPCA6. ISSN: 0006-2952. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Neurotensin [39379-15-2], some of its analogs, and neuromedin N [102577-25-3] were examd. for comparison of their potencies at stimulating inositol phospholipid hydrolysis and cGMP [7665-99-8] synthesis in intact murine neuroblastoma cells (clone N1E-115). Neurotensin(8-13) [60482-95-3] and acetylneurotensin 8-13) [74853-69-3] had the highest potencies for the stimulation of the hydrolysis of inositol phospholipid, which were ~3-fold as potent as neurotensin (50% ED = 0.9 nM). On the other hand, fragments of the N-terminal portion of neurotensin, such as neurotensin(1-6) [87620-09-5], neurotensin(1-8) [80887-44-1], and neurotensin(1-11) [74032-89-6], showed no ability to stimulate this hydrolysis. Neuromedin N, which is similar in structure to neurotensin(8-13) and which has been previously demonstrated to stimulate cGMP formation, had50% ED values of 2.5 and 4.5 nM for the release of [3H]inositol phosphates and stimulation of [3H]cGMP, resp. A strong correlation was obtained between the 50% ED values for neurotensin and several analogs in the stimulation of the release of inositol phosphates and the 50% ED values for these peptides in the stimulation of cGMP formation in neuroblastoma clone N1E-115 cells under similar exptl. conditions. Thus, these 2 different biochem. effects of neurotensin and its analogs appear to be mediated by the same receptor site, which may also have been the site of action of neuromedin N in these cells. .