Drugs online research references
neuro.mu-luebeck.de
Modulation of the dopamine (DA) transporter inhibitor GBR-12909 effect on DA release by protein kinases and protein phosphatases was studied in slices of the rat caudate nucleus measuring DA outflow in the superfusate of static chambers. Activation of protein kinase A and C markedly enhanced the effect of GBR-12909, whereas protein kinase inhibition by H7 reduced the GBR-12909 effect. Inhibition of protein phosphatases (PPP) 1 and 2A by okadaic acid did not modify basal outflow of DA. However, after the addition of okadaic acid a dramatic and biphasic effect was found when DA outflow was enhanced by GBR-12909. Inhibition of PPP 2A enhanced extracellular DA levels, while inhibition of PPP 1 and 2A completely abolished the effect of GBR-12909. In contrast to tetrodotoxin, the voltage-activated calcium channel blocker omega-conotoxin MVIIC inhibited GBR-12909 effects on DA outflow. Additionally, in aCSF devoid of calcium GBR-12909 did not increase DA liberation. These results suggest a complex and strong influence of phosphorylation on GBR-12909 effects on calcium channel-dependent DA outflow at low-affinity piperazine binding sites in slices of the rat caudate nucleus in vitro. Copyright 2002 Wiley-Liss, Inc.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12211084&dopt=Abstract
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Adverse Drug React Toxicol Rev. 2002;21(3):161-6.
Adverse drug reaction update.
[No authors listed]
Increasing numbers of articles on adverse drug reactions are published in a wide range of medical journals. To help keep you up-to-date with the latest advances worldwide on all aspects of adverse drug reactions, this section of the journal brings you information selected from the drug safety alerting service Reactions Weekly. The following reports are selected from the latest issues, summarizing the most important clinical studies, adverse reaction news, and expert opinion pieces published across a broad range of literature sources.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12298425&dopt=Abstract
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sghms.ac.uk
The thermogenic and hypophagic effects of sibutramine's metabolite (metabolite 2), a 5-hydroxytryptamine (5-HT) and noradrenaline reuptake inhibitor, were investigated in rats and compared with duloxetine and bupropion. Metabolite 2 increased colonic temperature for 2.5-4.5 h. Duloxetine was also thermogenic but was less effective than metabolite 2. Bupropion similarly increased colonic temperature and was as efficacious, but less potent, than metabolite 2. At -8 degrees C, metabolite 2, duloxetine and bupropion all decreased response to heat reinforcement and reduced colonic temperature. Metabolite 2 produced a sustained increase in oxygen consumption (VO(2)) at 29 degrees C from 90 to 240 min, whereas duloxetine was far less effective. Bupropion rapidly enhanced VO(2), but its effect was less prolonged than that of metabolite 2. Metabolite 2 markedly reduced 24-h food intake. Duloxetine decreased feeding although its effect was shorter-lived, but bupropion was without effect. Thus, sibutramine's antiobesity action is probably attributable to effects on energy intake and expenditure. Duloxetine shares these properties, but is generally less efficacious. Any potential weight-reducing effect of bupropion is probably due to thermogenesis. Copyright 2002 Elsevier Science B.V.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12323384&dopt=Abstract
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