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Titolo:
Neutrophil beta(2)-adrenoceptor function in major depression: G(s) coupling, effects of imipramine and relationship to treatment outcome
Autore:
Gurguis, GNM; Vo, SP; Griffith, JM; Rush, AJ;
Indirizzi:
Dept Vet Affairs Med Ctr, Dallas, TX USA Dept Vet Affairs Med Ctr Dallas TX USA t Affairs Med Ctr, Dallas, TX USA Univ Texas, SW Med Sch, Dallas, TX 75230 USA Univ Texas Dallas TX USA 75230 iv Texas, SW Med Sch, Dallas, TX 75230 USA
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 2-3, volume: 386, anno: 1999,
pagine: 135 - 144
SICI:
0014-2999(199912)386:2-3<135:NBFIMD>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA-ADRENERGIC-RECEPTOR; 5-HYDROXYTRYPTAMINE UPTAKE INHIBITOR; INTACT HUMAN-LYMPHOCYTES; PROTEIN-KINASE ACTIVITY; RAT CEREBRAL-CORTEX; SUICIDE VICTIMS; CYCLIC-AMP; MONONUCLEAR LEUKOCYTES; FRONTAL-CORTEX; MESSENGER-RNA;
Keywords:
beta(2)-adrenoceptor; G(s) protein, coupling; neutrophil; depression, major; anxiety; antidepressant, tricyclic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Gurguis, GNM VA N Texas Hlth Care Syst, Lab Clin Neurosci, Dallas, TX 75216 USA VA N Texas Hlth Care Syst Dallas TX USA 75216 , TX 75216 USA
Citazione:
G.N.M. Gurguis et al., "Neutrophil beta(2)-adrenoceptor function in major depression: G(s) coupling, effects of imipramine and relationship to treatment outcome", EUR J PHARM, 386(2-3), 1999, pp. 135-144

Abstract

Abnormal beta(2)-adrenoceptor density and beta(2)-adrenoceptor-mediated cyclic adenosine monophosphate (cAMP) responses were inconsistently reported in major depressive disorder. Tricyclic antidepressants downregulate beta-adrenoceptor density and decrease coupling to G(s) protein. Abnormal beta-adrenoceptor coupling may exist in major depressive disorder and may relate to treatment response. We investigated beta(2)-adrenoceptor coupling to G(s)protein in 25 controls, 23 major depressive disorder drug-free patients and 16 major depressive disorder patients after chronic imipramine treatment using agonist displacement experiments. Pretreatment beta(2)-adrenoceptor coupling and density were normal in patients as a whole. Chronic imipramine induced beta(2)-adrenoceptor uncoupling. This effect was observed in treatment responders who had increased beta(2)-adrenoceptor density in the high-conformational state and supercoupling prior to treatment. beta(2)-adrenoceptor density decreased after imipramine treatment. Treatment non-responders had seemingly normal pretreatment beta(2)-adrenoceptor function, which was not changed by imipramine. Differences in beta(2)-adrenoceptor regulation in major depressive disorder may underlie treatment response. The results indirectly implicate abnormal agonist-mediated beta(2)-adrenoceptor gene expression, protein kinase A, and protein kinase C in major depressive disorder. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:48:57