Drugs online research references
Am J Psychiatry. 1994 Nov;151(11):1642-5.
Antidepressant-associated mania: a controlled comparison with spontaneous mania.
Stoll AL, Mayer PV, Kolbrener M, Goldstein E, Suplit B, Lucier J, Cohen BM, Tohen M.
Bipolar and Psychotic Disorders Program, Mailman Research Center, McLean Hospital, Belmont, Mass.
OBJECTIVE: Antidepressants have been associated with the induction of mania and rapid cycling. This study examined whether antidepressant-associated manic states differ in any way from spontaneous mania. METHOD: Forty-nine consecutive inpatients with antidepressant-associated manic states were compared with 49 matched inpatients with spontaneous mania in a blind, retrospective chart review. RESULTS: Across virtually every clinical measure examined, the patients with antidepressant-associated manic states experienced milder and more time-limited manic episodes than the patients with spontaneous mania. The patients with antidepressant-associated manic states were subject to frequent checking by nurses and hall restriction for a significantly shorter period of time than the patients with spontaneous mania. The patients with antidepressant-associated manic states also had significantly less severe levels of delusions, hallucinations, psychomotor agitation, and bizarre behavior, according to a standard rating instrument, than the patients with spontaneous mania. For further study the patients with antidepressant-associated mania were divided into subgroups taking four individual classes of antidepressant drugs: tricyclics (N = 19), fluoxetine (N = 13), monoamine oxidase inhibitors (MAOIs) (N = 8), and bupropion (N = 6); three patients taking combinations of drugs were not included in these analyses. The patients with MAOI- and bupropion-associated mania had a slightly lower overall rating of severity of psychopathology at admission than the subgroups with fluoxetine- and tricyclic-associated mania. CONCLUSIONS: Antidepressant-associated mania appears to be a milder and more time-limited syndrome than spontaneous mania and may represent a distinct clinical entity. MAOIs and bupropion may be associated with milder manic states than either tricyclic drugs or fluoxetine.
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Depress Anxiety. 1998;7(2):73-5.
Use of bupropion with SRIs and venlafaxine.
Spier SA.
University of Maryland School of Medicine, Baltimore 21202-2165, USA.
Because of reported efficacy of combining classes of antidepressants, 25 patients were treated with bupropion in combination with SRI's and venlafaxine. Fifteen patients inadequately responsive to monotherapy received combination treatment; ten patients without residual symptoms received adjunctive bupropion to treat SRI- or venlafaxine-induced side effects. Fourteen subjects (56%) responded, 11 (44%) did not. Twelve of 15 subjects receiving combination treatment to boost the effects of monotherapy responded, while only 2 of 10 subjects receiving combination treatment for side effects responded. Combination therapy was well tolerated even by geriatric and "medically frail" patients.
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J Neurosci Res. 1994 Sep 1;39(1):11-22.
Dopamine transporter mediated release of dopamine: role of chloride.
Sitges M, Reyes A, Chiu LM.
Division de Investigaciones Clinicas, Instituto Mexicano de Psiquiatria, SSA, Mexico.
Using a rapid (0.5 ml/min) flow rate superfusion system, the dopamine (DA) transporter mediated release of DA is further explored, and compared to the depolarization evoked release of DA in rat striatal synaptosomes preloaded with radioactive DA (3H-DA). In this system external DA in the low microM range efficaciously releases the preloaded transmitter, the maximal response being reached at 3 microM DA. The external DA stimulated release is Ca(2+)-independent, Cl(-)-dependent, and blocked by both bupropion and nomifensine. The atypical antidepressant bupropion inhibits 3H-DA accumulation to rat striatal synaptosomes with a calculated IC50 of 1.3 x 10(-6) M. Among DA uptake blockers some are known to act as DA releasing agents. Here we found that the DA uptake blocker nomifensine (30 microM) is unable to modify the baseline release of 3H-DA, whereas bupropion (10 microM) clearly elevates the baseline release of 3H-DA in a Ca(2+)-independent and Cl(-)-dependent manner. The non releasing agent nomifensine blocks the release of 3H-DA induced by bupropion. The Ca(2+)-dependent, high K+ depolarization evoked release of 3H-DA is not modified by nomifensine and does not depend on the external Cl- concentration. When the depolarizing medium contains DA the carrier mediated release of 3H-DA induced by the external DA is additive to the high K+ induced response. A drastic drop in the external Cl- concentration induces 3H-DA release. This release of 3H-DA induced by low external Cl- levels is completely blocked by nomifensine, which only slightly diminished the release of 3H-DA induced by the absence of external Na+. On the basis of these results, it is concluded that: 1) Rapid perfusion flow rates eliminate DA reuptake. 2) DA uptake inhibitors either with or without DA releasing capabilities block the release of DA induced by microM levels of external DA. 3) By preventing translocation of the DA transporter mobile moiety, nomifensine may inhibit the release of DA induced by external DA or bupropion and by drastic drops in the external Cl- concentration. 4) In the absence of nomifensine, the DA transporter works under both resting and depolarized conditions, but in contrast to the GABA transporter (Sitges et al.: Neurochem Res 18:1081-1087, 1993), the DA transporter does not contribute to the amount of the DA released by depolarization. 5) Reversal of the DA uptake carrier is favored by conditions increasing the internal DA levels. 6) Cl- rather than Na+ is a major determinant in 3H-DA movements through the DA transporter.
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