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psychiatry.umsmed.edu
Increased platelet activation has been suggested as a possible reason for the increased vulnerability of depressed patients to ischemic heart disease (IHD). Translocation of P-selectin, an integral alpha-granule membrane protein, to the platelet surface is a measure of platelet activation. Herein, western blots of platelet plasma membranes containing P-selectin were quantified in patients with major depression (n=19; mean age=39 +/- 2 years) and healthy comparison subjects (n=17; mean age=36 +/- 2 years). None evidenced clinical signs of IHD, and only two patients had a lifestyle IHD risk factor (smoking). Blood was obtained from all 19 depressed patients before treatment, and 15 returned after 6-8 weeks of open-label bupropion treatment. Bupropion was chosen as the antidepressant because it did not elevate plasma norepinephrine or serotonin, endogenous agonists that can induce platelet degranulation. Western blotting revealed more P-selectin immunoreactivity (75 kD band) in depressed patients compared to healthy controls (P=0.003). After bupropion treatment, P-selectin remained high in depressed patients. beta3-Integrin, a reference plasma membrane protein that does not translocate during activation, was of equivalent density in depressed patients and healthy control subjects, and was unchanged after treatment with bupropion. P-Selectin failed to correlate with severity of illness based on the Hamilton Depression scale, or with the post-treatment plasma concentration of bupropion. The results suggest an elevation in P-selectin on platelet plasma membranes might be a trait marker for depression.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11165307&dopt=Abstract
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Neuropharmacology. 1983 Nov;22(11):1257-67.
Bupropion: a new antidepressant drug, the mechanism of action of which is not associated with down-regulation of postsynaptic beta-adrenergic, serotonergic (5-HT2), alpha 2-adrenergic, imipramine and dopaminergic receptors in brain.
Ferris RM, Beaman OJ.
The present experiments were undertaken to determine: (1) whether bupropion had any direct effects on receptors present in rat brain; (2) whether the drug could down-regulate postsynaptic beta-adrenergic, alpha 2-adrenergic, serotonergic, imipramine and dopaminergic receptors after chronic administration, as had been demonstrated for tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, electroconvulsive therapy (ECT) and "atypical" antidepressants. Bupropion was found to be weak or inactive when its affinity for 14 different receptors present in brain was assessed by binding assays. The drug failed to desensitize beta-adrenergic receptors in the cerebral cortex of the rat as determined by [3H]dihydroalprenolol binding, after being administered at 25 mg/kg (i.p.) once a day for 6 weeks, or after being administered by the intraperitoneal route to rats at doses as large as 150 mg/kg per day for 4 days. When administered at doses of 37.5, 75 and 150 mg/kg per day for 21 days, the drug had no effect on beta-adrenergic, alpha 2-adrenergic, imipramine or serotonergic (5-HT2) receptors in the brain of the rat as determined by Scatchard analysis of the binding data. These data show that the antidepressant activity of bupropion is not associated with a down-regulation of receptors in the CNS commonly implicated in the mechanism of action of antidepressant drugs. Bupropion also produced a dose-dependent tendency to decrease the activity of norepinephrine-stimulated adenylate cyclase in slices of cerebral cortex obtained from rats treated chronically with the drug. However, the decrease was highly variable, was most obvious in tissues obtained from rats receiving large, non-pharmacologically relevant doses (150 mg/kg per day) of the drug and was statistically significant at only one of three concentrations of the agonist that produced maximal stimulation of the enzyme.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6320035&dopt=Abstract
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J Pharmacol Exp Ther. 2001 Mar;296(3):789-96.
Titer-dependent antagonism of cocaine following active immunization in rhesus monkeys.
Koetzner L, Deng S, Sumpter TL, Weisslitz M, Abner RT, Landry DW, Woods JH.
Department of Pharmacology, University of Michigan, Ann Arbor, Michigan 48109-0632, USA.
Immunization may be a useful pharmacokinetic antagonist therapy for cocaine users. Three rhesus monkeys were immunized with a cocaine:bovine serum albumin conjugate in alum and later with complete and incomplete Freund's adjuvants. Monkeys developed cocaine-binding antibodies (as measured by enzyme-linked immunosorbent assay) after immunization with alum; greater antibody titers developed after immunization with Freund's adjuvants. The response rate-decreasing effect of cocaine diminished in proportion to antibody titer; there was no substantial change in the rate-decreasing effect of bupropion. Plasma cocaine concentrations increased in proportion to antibody titer. Immunizations were well tolerated and had no effect on response rates. These data suggest that the antibody response to a cocaine antigen can produce a specific pharmacokinetic shift in cocaine distribution sufficient to antagonize a behavioral effect of the drug, and can do so with minimal side effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11181908&dopt=Abstract
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