Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 6164459

[Palatal myoclonus associated with a decrease in 5-hydroxy-indole acetic acid in cerebrospinal fluid and responding to clonazepam].

S Gauthier·S N Young·D W Baxter
View original source ↗Export metadata ↓

Abstract

A patient representing with palatal myoclonus was diagnosed as suffering from possible multiple sclerosis. A reduction of cerebrospinal 5-hydroxy-indole-acetic acid suggested a decreased central serotonergic turnover. A therapeutic trial with clonazepam, a serotonergic agonist, improved the myoclonus symptomatically. The possible involvement of serotonergic inhibitory systems in the expression of palatal myoclonus is discussed.

Explore related subjects

BenzodiazepinonesClonazepamFemaleHumansHydroxyindoleacetic AcidMiddle AgedMultiple SclerosisMusclesMyoclonusPalatal MusclesTryptophanCase ReportsEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Gauthier, S N Young, D W Baxter. 1981. [Palatal myoclonus associated with a decrease in 5-hydroxy-indole acetic acid in cerebrospinal fluid and responding to clonazepam].. https://pubmed.ncbi.nlm.nih.gov/6164459/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1995

Cholecystokinin effect on human lymphocyte ionized calcium and mitogenesis.

Cholecystokinin (CCK) is a peptide present in large amounts in gut, brain, and neurons innervating lymphatic tissues. Plasma CCK levels increase in enterally alimented patients. Enteral alimentation is also associated with enhanced immune function. The effects of CCK and a CCK antagonist were studied on human peripheral blood mononuclear cells (H-PBMC), lymphocyte intracellular ionized calcium ([Ca2+]i), and lymphocyte mitogenesis. CCK receptors transduce their signal via the release of [Ca2+]i. CCK octapeptide caused a specific increase in [Ca2+]i measured by Fura-2 fluorometry in H-PBMC and human T helper lymphocytes. Neither gastrin-17 nor pentagastrin produced a signal. While the highly specific CCK antagonist MK329 blocked the CCK [Ca2+]i signal, it had no effect on the PHA-mediated signal. At high dosages (10(-7)-10(-8) M), CCK was a comitogen with "complete" lymphocyte mitogens such as anti-CD3 monoclonal antibody (mAb) or low-dose PHA, but not for "partial" mitogens such as phorbol esters. CCK comitogenic effect occurred even in the presence of cyclosporine. CCK radioimmunoassay demonstrated that H-PBMC contained CCK and that anti-CD3 mAb- or PHA-mediated H-PBMC mitogenesis caused release of CCK. MK329 blocked PHA and anti-CD3 mAb mitogenesis and CCK comitogenic effects. We conclude that CCK octapeptide may be a coregulator of lymphocyte Ca2+ activation signals. The immunologically beneficial effect of enteral nutrition may, in part, be mediated by increased levels of CCK.

Benzodiazepinones↗
PubMed1995

Differential effects of 4'-chlorodiazepam on expressed human GABAA receptors.

The interactions of the atypical benzodiazepine 4'-chlorodiazepam (Ro 5-4864) with functionally expressed human GABAA receptor cDNAs were determined. Cotransfection of human alpha 2, beta 1, and gamma 2 subunits was capable of reconstituting a 4'-chlorodiazepam recognition site as revealed by a dose-dependent potentiation of t-[35S]butylbicyclophosphorothionate ([35S]-TBPS) binding to the GABA-activated chloride channel. This site is found on GABAA receptor complexes containing sites for GABA agonist-like benzodiazepines and neuroactive steroids. The importance of the alpha subunit was further demonstrated as substitution of either alpha 1 or alpha 3 for the alpha 2 subunit did not reconstitute a 4'-chlorodiazepam recognition site that was capable of modulating [35S]TBPS binding under the same experimental conditions. The 4'-chlorodiazepam modulatory site was shown to be distinct from the benzodiazepine site, but the phenylquinolines PK 8165 and PK 9084 produced effects similar to 4'-chlorodiazepam, consistent with the previous analysis of the 4'-chlorodiazepam site in brain homogenates. Further analysis of the subunit requirements revealed that coexpression of alpha 2 and beta 1 alone reconstituted a 4'-chlorodiazepam recognition site. It is interesting, however, that the 4'-chlorodiazepam site was found to inhibit [35S]TBPS binding to the GABA-activated chloride channel. Thus, the 4'-chlorodiazepam site may be reconstituted with only the alpha and beta polypeptides.

Benzodiazepinones↗