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Gene Review

NMS  -  neuromedin S

Homo sapiens

Synonyms: Neuromedin-S
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Disease relevance of NMS


Psychiatry related information on NMS


High impact information on NMS

  • After short preincubations with N-[(3)H]methylscopolamine ([(3)H]NMS) or R(-)-[(3)H]quinuclidinyl benzilate ([(3)H]QNB), radioligand dissociation from muscarinic M(1) receptors in Chinese hamster ovary cell membranes was fast, monoexponential, and independent of the concentration of unlabeled NMS or QNB added to reveal dissociation [8].
  • The effect of the synthetic toxins on the atropine-induced [3H]N-methylscopolamine (NMS) dissociation confirms that sMT7 targets the allosteric site on the M1 receptor, whereas sMT1 seems interact on the orthosteric one [9].
  • We have studied the interactions of five indolocarbazoles with N-[methyl-(3)H]scopolamine (NMS) and unlabeled acetylcholine at M(1)-M(4) muscarinic receptors, using equilibrium and nonequilibrium radioligand binding studies [10].
  • In human embryonic lung fibroblasts, transforming growth factor-beta 1 (TGF-beta 1) induced a time-dependent down-regulation of M2 muscarinic receptor binding sites as measured with the nonselective hydrophilic ligand [3H]N-methylscopolamine (NMS) [11].
  • m1-Toxin was found to slow the dissociation of [3H]N-methyl-scopolamine (NMS) and [3H]pirenzepine from m1 muscarinic receptors expressed in the membranes of Chinese hamster ovary cells [12].

Chemical compound and disease context of NMS


Biological context of NMS

  • Central expression of NMS appears restricted to the suprachiasmatic nucleus, and NMS has been involved in the regulation of dark-light rhythms and suppression of food intake [16].
  • Our data are the first to disclose the potential implication of NMS in the regulation of gonadotropic axis, a function that may contribute to the integration of circadian rhythms, energy balance, and reproduction [16].
  • Central administration of NMS evoked modest LH secretory responses in pubertal and cyclic females at diestrus, whereas exaggerated LH secretory bursts were elicited by NMS at estrus and after short-term fasting [16].
  • In adult females, hypothalamic expression of NMS (which was confined to suprachiasmatic nucleus) and NMU2R significantly varied during the estrous cycle (maximum at proestrus) and was lowered after ovariectomy and enhanced after progesterone supplementation [16].
  • MATERIALS AND METHODS: Competitive inhibitory effects of antimuscarinic agents on specific NMS [H] (PerkinElmer Life Sciences, Boston, Massachusetts) binding were examined in human tissue homogenates and in CHO-K1 cell membranes expressing human muscarinic receptor subtypes [17].

Anatomical context of NMS

  • Expression of NMS and NMU2R genes was detected at the hypothalamus along postnatal development, with significant fluctuations of their relative levels (maximum at prepubertal stage and adulthood) [16].
  • The principal findings are that (1) elevated urinary catecholamines and metabolites are a frequent but inconstant feature of NMS; (2) it is likely that sympathetic nervous system hyperactivity contributes to the picture of fulminant NMS; and (3) the role of the adrenal medulla in producing excess catecholamines during NMS is uncertain [1].
  • On the other hand, MAF was less effective in depressing antigen- and mitogen-induced proliferation of human blood cells than were NMS or human serum [18].
  • Muscarinic cholinergic receptors were assayed in frozen sections of the umbilical artery and vein by a radioligand binding assay technique, using [3H]-N-methyl scopolamine (NMS) as a ligand [19].
  • There have been cases where the authors are convinced that the "pneumonia" or "urinary tract infection" was in fact a mild case of NMS that cleared [20].

Associations of NMS with chemical compounds


Other interactions of NMS

  • We found in one patient with a history of NMS a nucleotide substitution at codon 310 (CCG-->TCG) of exon 7 of the DRD2 gene which predicts the replacement of proline to serine in the third cytoplasmic loop of the receptor, a part of the receptor that interacts with G-proteins [25].
  • Although both methods use CK-B antisera and radioiodinated CK-B, one ("M" for Mallinckrodt) uses hybridized CK-MB for calibration, while the other ("NMS" for Nuclear Medical Systems) uses CK-B [3].
  • The clinical triad of fever, movement disorder, and altered mentation known as NMS represents an infrequent yet highly lethal side effect of neuroleptic therapy [26].

Analytical, diagnostic and therapeutic context of NMS

  • A patient suffering from schizophrenia developed diabetic keto-acidosis and NMS after treatment with neuroleptics [27].
  • In this patient, treatment of NMS with bromocriptine did not start until 10 days into hospitalization [28].
  • However, insulinemia decreased more in the postoperative period in the MS group compared to the NMS group (p<0.05) [29].
  • These results indicate that the application of human/mouse chimeric antibodies in two-site immunoassays is more effective for reducing interference from heterophilic antibodies than the adding of NMS or purified mouse IgG in the assay using conventional MAbs [30].
  • Discontinuation of antipsychotics, maintenance of supportive therapy aimed at preventing dehydration, hemodynamic, and electrolyte imbalances, and pharmacotherapy are essential in the treatment of NMS [28].


  1. Sympathoadrenomedullary activity in the neuroleptic malignant syndrome. Gurrera, R.J., Romero, J.A. Biol. Psychiatry (1992) [Pubmed]
  2. A possible variant of the neuroleptic malignant syndrome. Sullivan, C.F. The British journal of psychiatry : the journal of mental science. (1987) [Pubmed]
  3. Two radioimmunoassays compared with isoenzyme electrophoresis for the detection of serum creatine kinase-MB in acute myocardial infarction. Witherspoon, L.R., Shuler, S.E., Genre, C.F., Mackenzie, F.J., Garcia, M.M. J. Nucl. Med. (1982) [Pubmed]
  4. Toxin-induced hyperthermic syndromes. Rusyniak, D.E., Sprague, J.E. Med. Clin. North Am. (2005) [Pubmed]
  5. NMS and lethal catatonia. Weller, M. The Journal of clinical psychiatry. (1992) [Pubmed]
  6. Neuroleptic malignant syndrome. Caroff, S.N., Mann, S.C. Med. Clin. North Am. (1993) [Pubmed]
  7. Effect of neuromedin S on feeding regulation in the Japanese quail. Shousha, S., Nakahara, K., Sato, M., Mori, K., Miyazato, M., Kangawa, K., Murakami, N. Neurosci. Lett. (2006) [Pubmed]
  8. Evidence for a tandem two-site model of ligand binding to muscarinic acetylcholine receptors. Jakubik, J., El-Fakahany, E.E., Tucek, S. J. Biol. Chem. (2000) [Pubmed]
  9. Chemical synthesis of MT1 and MT7 muscarinic toxins: critical role of Arg-34 in their interaction with M1 muscarinic receptor. Mourier, G., Dutertre, S., Fruchart-Gaillard, C., Ménez, A., Servent, D. Mol. Pharmacol. (2003) [Pubmed]
  10. Allosteric interactions of staurosporine and other indolocarbazoles with N-[methyl-(3)H]scopolamine and acetylcholine at muscarinic receptor subtypes: identification of a second allosteric site. Lazareno, S., Popham, A., Birdsall, N.J. Mol. Pharmacol. (2000) [Pubmed]
  11. Transforming growth factor-beta 1 induces transcriptional down-regulation of m2 muscarinic receptor gene expression. Haddad, E.B., Rousell, J., Mak, J.C., Barnes, P.J. Mol. Pharmacol. (1996) [Pubmed]
  12. Stable allosteric binding of m1-toxin to m1 muscarinic receptors. Max, S.I., Liang, J.S., Potter, L.T. Mol. Pharmacol. (1993) [Pubmed]
  13. Toxic serotonin syndrome or neuroleptic malignant syndrome? Fink, M. Pharmacopsychiatry (1996) [Pubmed]
  14. Rhabdomyolysis associated with haloperidol without evidence of NMS. Marinella, M.A. The Annals of pharmacotherapy. (1997) [Pubmed]
  15. Neuroleptic malignant syndrome. Paul, G.E., Landers, D.F., Newman, T. The Nebraska medical journal. (1990) [Pubmed]
  16. Neuromedin s as novel putative regulator of luteinizing hormone secretion. Vigo, E., Roa, J., López, M., Castellano, J.M., Fernandez-Fernandez, R., Navarro, V.M., Pineda, R., Aguilar, E., Diéguez, C., Pinilla, L., Tena-Sempere, M. Endocrinology (2007) [Pubmed]
  17. Human muscarinic receptor binding characteristics of antimuscarinic agents to treat overactive bladder. Maruyama, S., Oki, T., Otsuka, A., Shinbo, H., Ozono, S., Kageyama, S., Mikami, Y., Araki, I., Takeda, M., Masuyama, K., Yamada, S. J. Urol. (2006) [Pubmed]
  18. Immunosuppressive properties of mouse amniotic fluid. Tyan, M.L. Proc. Soc. Exp. Biol. Med. (1976) [Pubmed]
  19. Muscarinic cholinergic receptors and acetylcholinesterase activity in umbilical artery and vein in pregnancy-induced hypertension (pre-eclampsia). Tayebati, S.K., Giannella, M., Indraccolo, S.R., Pigini, M., Sabbatini, M., Zaccheo, D., Amenta, F. Clin. Exp. Hypertens. (1997) [Pubmed]
  20. Neuroleptic malignant syndrome: recognizing an unrecognized killer. Hooper, J.F., Herren, C.K., Goldwasser, H. Journal of psychosocial nursing and mental health services. (1989) [Pubmed]
  21. Crossover reaction between haloperidol and amoxapine for NMS. Otani, K., Mihara, K., Okada, M., Kaneko, S., Fukushima, Y. The British journal of psychiatry : the journal of mental science. (1991) [Pubmed]
  22. The treatment of neuroleptic malignant syndrome. Are dantrolene and bromocriptine useful adjuncts to supportive care? Rosebush, P.I., Stewart, T., Mazurek, M.F. The British journal of psychiatry : the journal of mental science. (1991) [Pubmed]
  23. Stimulation of glucagon-like peptide-1 secretion by muscarinic agonist in a murine intestinal endocrine cell line. Abello, J., Ye, F., Bosshard, A., Bernard, C., Cuber, J.C., Chayvialle, J.A. Endocrinology (1994) [Pubmed]
  24. Zuclopenthixol-induced neuroleptic malignant syndrome at rechallenge and its extrapyramidal effects. Kemperman, C.J. The British journal of psychiatry : the journal of mental science. (1989) [Pubmed]
  25. Structural change in dopamine D2 receptor gene in a patient with neuroleptic malignant syndrome. Ram, A., Cao, Q., Keck, P.E., Pope, H.G., Otani, K., Addonizio, G., McElroy, S.L., Kaneko, S., Redlichova, M., Gershon, E.S. Am. J. Med. Genet. (1995) [Pubmed]
  26. Aetiology and treatment of neuroleptic malignant syndrome. Harpe, C., Stoudemire, A. Medical toxicology. (1987) [Pubmed]
  27. Neuroleptic malignant syndrome and diabetic keto-acidosis. de Boer, C., Gaete, H.P. The British journal of psychiatry : the journal of mental science. (1992) [Pubmed]
  28. An atypical course of neuroleptic malignant syndrome. Schneiderhan, M.E., Marken, P.A. Journal of clinical pharmacology. (1994) [Pubmed]
  29. Changes in Insulin Sensitivity in Morbidly Obese Patients with or without Metabolic Syndrome after Gastric Bypass. Coppini, L.Z., Bertevello, P.L., Gama-Rodrigues, J., Waitzberg, D.L. Obesity surgery : the official journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand (2006) [Pubmed]
  30. Reducing interference from heterophilic antibodies in a two-site immunoassay for carcinoembryonic antigen (CEA) by using a human/mouse chimeric antibody to CEA as the tracer. Kuroki, M., Matsumoto, Y., Arakawa, F., Haruno, M., Murakami, M., Kuwahara, M., Ozaki, H., Senba, T., Matsuoka, Y. J. Immunol. Methods (1995) [Pubmed]
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