Detail of "102577-25-3"

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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. .

Differential effects of haloperidol and clozapine on neurotensin gene transcription in rat neostriatum

Differential effects of haloperidol and clozapine on neurotensin gene transcription in rat neostriatum. Merchant, Kalpana M.; Dobner, Paul R.; Dorsa, Daniel M.Several substances are used for example 39379-15-2 and 102577-25-3 which are their cas registry numbers. (Dep. Pharmacol., Univ. Washington, Seattle, WA 98195, USA). J. Neurosci., 12(2), 652-63 (English) 1992. CODEN: JNRSDS. ISSN: 0270-6474. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) A single dose of typical neuroleptic, haloperidol, has been demonstrated to increase the expression of neurotensin/neuromedin N (NT/N) mRNA in the dorsolateral striatum within 1 h of its administration (Merchant et al., 1991). The present study further investigated neuroleptic-induced regulation of NT/N gene transcription. Levels of NT/N mRNA were examd. at various times following a single dose of haloperidol (1 mg/kg, i.p.) or the atypical antipsychotic clozapine (20, 30, or 40 mg/kg, i.p.) by in situ hybridization histochem. and quant. soln. hybridization. In the dorsolateral striatum, the two drugs had strikingly different effects; haloperidol rapidly (within 30 min) increased the expression of mature NT/N mRNA while virtually no increase was obsd. in response to nontoxic doses of clozapine at any of the time points examd. Following haloperidol, maximal induction occurred at 7 h, at which time NT/N mRNA levels were an order of magnitude higher than basal levels. By 20 h after haloperidol, there was a decline in striatal NT/N mRNA levels. In situ hybridization anal. using an intron-derived probe revealed that haloperidol-induced increases in mature NT/N mRNA levels in the striatum were preceded by a transient increase in intron-contg. NT/N gene transcripts. These data strongly indicate that acute haloperidol treatment results in transient transcriptional activation of NT/N gene, although a concomitant effect on the stability of NT/N primary transcripts cannot be ruled out. In contrast to their differential effects in the dorsolateral striatum, a single dose of both haloperidol and clozapine induced a small but significant increase in NT/N mRNA expression in the shell sector of the nucleus accumbens. These results raise the possibility that NT neurons in the nucleus accumbens may, at least in part, mediate the antipsychotic effects of classical neuroleptics, whereas NT cells in the dorsolateral region of the striatum may be involved in mediating other effects of typical neuroleptics such as extrapyramidal motor symptoms. .