Substitution of the selective serotonin reuptake inhibitors fluoxetine and paroxetine for the discriminative stimulus effects of ethanol in rats. 5-HT2B receptor-mediated serotonin morphogenetic functions in mouse cranial neural crest and myocardiac cells. Managing rapid metabolizers of antidepressants. Rx drugs

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Psychopharmacology (Berl). 1997 Apr;130(4):404-6.
Substitution of the selective serotonin reuptake inhibitors fluoxetine and paroxetine for the discriminative stimulus effects of ethanol in rats.

Maurel S, Schreiber R, De Vry J.

Institute for Neurobiology, Troponwerke GmbH & Co. KG, Koln, Neurather Ring 1, Germany.

Rats trained to discriminate ethanol (EtOH, 1 g/kg IP) from saline in a two-lever procedure completely generalized to the selective serotonin reuptake inhibitors (SSRIs) fluoxetine and paroxetine. Substitution of fluoxetine was completely blocked by the selective 5-HT2A receptor antagonist MDL 100,907 and not affected by the selective 5-HT1A receptor antagonist WAY-100635. It is suggested that the previously reported effectiveness of SSRIs in reducing EtOH consumption could be based on similarities in discriminative stimulus effects of SSRIs and EtOH. Stimulation of 5-HT2A receptors may underlie these stimulus similarities and contribute to the EtOH intake-reducing effects of SSRIs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9160858&dopt=Abstract

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Development. 1997 May;124(9):1745-55.
5-HT2B receptor-mediated serotonin morphogenetic functions in mouse cranial neural crest and myocardiac cells.

Choi DS, Ward SJ, Messaddeq N, Launay JM, Maroteaux L.

Institut de Genetique et de Biologie Moleculaire et Cellulaire, Universite L. Pasteur de Strasbourg, CNRS, INSERM, Illkirch, France.

During embryogenesis, serotonin has been reported to be involved in craniofacial and cardiovascular morphogenesis. The detailed molecular mechanisms underlying these functions, however remain unknown. From mouse and human species, we have recently reported the cloning of 5-HT2B receptors which share signal transduction pathways with other 5-HT2 receptor subtypes (5-HT2A and 5-HT2C). In addition to phospholipase C stimulation, it appears that these three subtypes of receptor transduce a common serotonin-induced mitogenic activity, which could be important for cell differentiation and proliferation. We have first investigated the expression of 5-HT2 receptor mRNAs in the mouse embryo. Interestingly, a peak of 5-HT2B receptor mRNA expression was detected 8-9 days postcoitum, whereas there was only low level 5-HT2A and no 5-HT2C receptor mRNA expression at this stage. Expression of this receptor was confirmed by binding assays using a 5-HT2-specific ligand which revealed a peak of binding to membrane preparations from 9 days postcoitum embryos. In addition, whole mount in situ hybridisation and immunohistochemistry on similar stage embryos detected 5-HT2B expression in neural crest cells, heart myocardium and somites. The requirement for functional 5-HT2B receptors between 8 and 9 days postcoitum is supported by culture of embryos exposed to 5-HT2-specific ligands; 5-HT2B high-affinity antagonist such as ritanserin, induced morphological defects in the cephalic region, heart and neural tube. These antagonistic treatments interfere with cranial neural crest cell migration, induce their apoptosis, and are responsible for abnormal sarcomeric organisation of the subepicardial layer and for the absence of the trabecular cell layer in the ventricular myocardium. This report indicates for the first time that 5-HT2B receptors are actively mediating the action of serotonin on embryonic morphogenesis, probably by preventing the differentiation of cranial neural crest cells and myocardial precursor cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9165122&dopt=Abstract

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Depress Anxiety. 1996-97;4(6):320-7.
Managing rapid metabolizers of antidepressants.

Kraus RP, Diaz P, McEachran A.

Department of Psychiatry, London Health Sciences Centre, Ontario, Canada.

Depressed patients who rapidly metabolize antidepressants may be common, and may not respond to even high doses of antidepressants if subtherapeutic plasma levels are produced. Rapid metabolizers (RMs) are identifiable if patients are on tricyclic antidepressants (TCAs), and TCA plasma levels (commonly available) are monitored. Strategies to achieve therapeutic levels in RMs include: (1) megaprescribing, or (2) inhibiting the metabolism of the parent drug. Megaprescribing TCAs runs the risk of markedly elevating levels of potentially toxic hydroxy metabolites. In this study twelve depressed, non-responding RMs were identified while taking the TCA, desipramine. Fluoxetine or paroxetine, selective serotonin re-uptake inhibitors (SSRIs) known to potently inhibit cytochrome P450 2D6 (the isoenzyme responsible for desipramine metabolism), was then added to continuing desipramine. Therapeutic range desipramine levels were achieved in ten patients, and seven of the ten achieved excellent or good sustained responses. The combination SSRI and TCA therapy was well tolerated. Whether response primarily reflected the TCA at therapeutic range levels, or a synergistic serotonin-noradrenaline interaction between the respective antidepressants, requires further clarification. The results of this open study suggest the need for controlled trials of antidepressant metabolism inhibition in RMs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9166660&dopt=Abstract

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