Drugs online research references
J Neurosci Res. 2000 Jul 1;61(1):82-7.
Antidepressant-induced regulation of 5-HT(1b) mRNA in rat dorsal raphe nucleus reverses rapidly after drug discontinuation.
Anthony JP, Sexton TJ, Neumaier JF.
Department of Psychiatry and Behavioral Sciences and Harborview Medical Center, University of Washington, Seattle 98104-2499, USA.
Serotonin release from dorsal raphe projections in the forebrain is regulated by terminal 5-HT(1B) autoreceptors; dysregulation of these receptors may be involved in the pathophysiology of clinical depression. Using in situ hybridization, we have previously reported that fluoxetine reduces 5-HT(1B) mRNA in rat dorsal raphe nucleus (DRN) in a time-dependent and reversible manner. In this study we examined longer term treatment (8 weeks) with several different serotonin-selective reuptake inhibitors (SSRIs) or a tricyclic antidepressant on 5-HT(1B) mRNA regulation in DRN and hippocampus, and evaluated the stability of these drugs' effects after drug discontinuation. Fluoxetine (5 mg/kg/d), paroxetine (5 mg/kg/d), sertraline (10 mg/kg/d) or nortriptyline (10 mg/kg/d) was administered to rats via subcutaneous osmotic minipumps. Paroxetine and fluoxetine reduced DRN 5-HT(1B) mRNA by 36% and 27%, respectively whereas sertraline had a no significant effect. After 3-14 days of drug washout, DRN 5-HT(1B) mRNA levels in SSRI treated rats were no longer different from control. 5-HT(1B) mRNA levels in hippocampus were not affected by SSRI drugs at any timepoint. Nortriptyline had no significant effect on 5-HT(1B) mRNA in either DRN or hippocampus. These results confirm that SSRI antidepressants reduce presynaptic 5-HT(1B) mRNA selectively, and that this effect is maintained for at least 8 weeks of antidepressant treatment but reverses rapidly after discontinuation. Furthermore, it is possible that washout after chronic antidepressant treatment, that is routinely used in functional assays of autoreceptor action in animal models, may lead to more rapid reversal of biological effects than has previously been thought. Copyright 2000 Wiley-Liss, Inc.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10861803&dopt=Abstract
Neuropsychopharmacology. 2000 Jul;23(1):13-9.
Effects of antidepressants on weight and on the plasma levels of leptin, TNF-alpha and soluble TNF receptors: A longitudinal study in patients treated with amitriptyline or paroxetine.
Hinze-Selch D, Schuld A, Kraus T, Kuhn M, Uhr M, Haack M, Pollmacher T.
Max Planck Institute of Psychiatry, Munich, Germany.
Leptin, tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptors are involved in weight regulation. Antipsychotic agents, such as clozapine, induce weight gain and increase circulating levels of these cytokines. To assess whether obesity-inducing antidepressants have a similar effect, we measured plasma cytokine levels in depressive inpatients during the first six weeks of treatment with tricyclic agents (amitriptyline or nortriptyline, n = 12), with paroxetine (n = 10), or without medication (n = 14). There was an increase in the body mass index at week 6 of treatment with the tricyclics, which was preceded by a significant increase in soluble TNF receptor p75 plasma levels. Circulating levels of leptin were not affected. Paroxetine and drug-free treatment did not affect any of these parameters. We conclude that weight gain induced by psychotropic agents may occur without increased circulating levels of leptin. However, activation of the TNF-alpha system might be an early and sensitive marker of ensuing weight gain.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10869882&dopt=Abstract
J Anal Toxicol. 2000 May-Jun;24(4):271-4.
Blood concentrations of amitriptyline and its metabolite in rats after acute oral administration of amitriptyline.
Baeck SK, Lim MA, Park SY, Lee JS, Lee HS, Koo KS.
Forensic Science Department, National Institute of Scientific Investigation, Seoul, Korea.
Amitriptyline (AMT), a tricyclic antidepressant that is a dibenzocycloheptadine derivative, is frequently used. However, the case reports of AMT-related fatalities are increased, nowadays, due to the low levels of toxic and fatal concentration in blood. So, this study was carried out to determine the concentrations of AMT and its demethylated metabolite, nortriptyline (NTR), after acute single oral administration of AMT in rats. Blood samples were collected five times from the ophthalmic venous plexus at 0, 1, 2, 4, and 8 h after acute single oral administration of AMT in toxic doses of 10 (Group I) or 20 mg/kg (Group II), and the concentrations of AMT and NTR and the mean ratios of AMT to NTR (AMT/NTR) in the blood were periodically determined at designated times. The blood concentrations of AMT and NTR were identified and quantitated by gas chromatography with thermionic specific detection and gas chromatography-mass spectrometry after solid-phase extraction with a Clean Screen DAU column. The peak blood concentrations of AMT and NTR in Group I were 0.34 and 0.28 microg/mL, respectively, and those of AMT and NTR in Group II were 0.59 and 0.43 microg/mL, respectively, and were reached at 1 h after single oral administration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10872574&dopt=Abstract
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