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Titolo:
Common effects of chronically administered antipanic drugs on brainstem GABA(A) receptor subunit gene expression
Autore:
Tanay, VM; Greenshaw, AJ; Baker, GB; Bateson, AN;
Indirizzi:
Univ Alberta, Fac Med, Dept Pharmacol, Edmonton, AB T6G 2H7, Canada Univ Alberta Edmonton AB Canada T6G 2H7 col, Edmonton, AB T6G 2H7, Canada Univ Alberta, Fac Med, Dept Psychiat, Edmonton, AB T6G 2H7, Canada Univ Alberta Edmonton AB Canada T6G 2H7 iat, Edmonton, AB T6G 2H7, Canada Univ Alberta, Fac Med, Div Neurosci, Edmonton, AB T6G 2H7, Canada Univ Alberta Edmonton AB Canada T6G 2H7 sci, Edmonton, AB T6G 2H7, Canada
Titolo Testata:
MOLECULAR PSYCHIATRY
fascicolo: 4, volume: 6, anno: 2001,
pagine: 404 - 412
SICI:
1359-4184(200107)6:4<404:CEOCAA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-AMINOBUTYRIC-ACID; MESSENGER-RNA LEVELS; PANIC DISORDER; RAT-BRAIN; A-RECEPTOR; BENZODIAZEPINE SENSITIVITY; ALPRAZOLAM TREATMENT; IOMAZENIL-SPECT; LOCUS-COERULEUS; PLASMA GABA;
Keywords:
GABA(A) receptors; subunit; gene expression; antidepressants; panic disorder; pons medulla;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Bateson, AN Univ Alberta, Fac Med, Dept Pharmacol, 9-70 MSB, Edmonton, AB T6G 2H7, Canada Univ Alberta 9-70 MSB Edmonton AB Canada T6G 2H7 G 2H7, Canada
Citazione:
V.M. Tanay et al., "Common effects of chronically administered antipanic drugs on brainstem GABA(A) receptor subunit gene expression", MOL PSYCHI, 6(4), 2001, pp. 404-412

Abstract

Panic disorder is an anxiety disorder that can be treated by long-term administration of tricyclic antidepressants such as imipramine, monoamine oxidase inhibitors such as phenelzine, or the selective serotonin reuptake inhibitor (SSRI) antidepressants. Clinical data also indicate that some benzodiazepines, such as alprazolam, are effective antipanic agents, and that their therapeutic onset is faster than that of antidepressants. Benzodiazepinesare well known for their action at GABA(A) receptors, and preclinical dataindicate that imipramine and phenelzine also interfere with the GABAergic system. In addition some clinical data lend support to decreased benzodiazepine-sensitive receptor function in panic disorder patients. Using imipramine, phenelzine and alprazolam, we investigated, in rats, the possibility that the therapeutic efficacy of antipanic agents stems from the remodeling of GABAergic transmission in the pons-medulla region. Of the 12 GABA(A) receptor subunit (alpha1-6, beta1-3, gamma1-3) steady-state mRNA levels investigated, we observed an increase in the levels of the alpha3-, beta1- and gamma2-subunit transcripts with all three antipanic agents tested. The effectsof imipramine and phenelzine on these subunits occurred after 21 days of treatment, while alprazolam effects were observed after 3 days of administration. Histochemical data suggest that the alpha3 beta1 gamma2 subunits comprise a receptor subtype in the pons-medulla region. Therefore, we conclude that these molecular events parallel the therapeutic profile of the drugs examined. We further propose that these events may correspond to a remodeling of the GABA(A) receptor population, and may be useful markers for investigation of the antipanic properties of drugs.

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Documento generato il 17/09/19 alle ore 22:37:05