Drugs online research references
Life Sci. 1991;48(20):1977-83.
Ethanol intake and 3H-serotonin uptake. II: A study in alcoholic patients using platelets 3H-paroxetine binding.
Daoust M, Lhuintre JP, Ernouf D, Legrand E, Breton P, Boucly P.
Pharmacochimie-U.F.R. de Medecine et Pharmacie, Saint Etienne du Rouvray, France.
The kinetic parameters of 3H-paroxetine binding and 3H-serotonin uptake were studied in platelets of alcoholic patients. There was no difference between alcoholic and non alcoholic subjects in 3H-paroxetine binding. When binding and 3H-serotonin uptake were studied, in the same plasma of the same subjects, the Vmax of serotonin uptake was increased in alcoholics. The data confirm the involvement of serotonin uptake system in alcohol dependence and suggest that serotonin uptake and paroxetine binding sites may be regulated independently in this pathology.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1827171&dopt=Abstract
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Biochem Soc Trans. 1991 Feb;19(1):99-102.
Characterization and purification of the neuronal sodium-ion-coupled 5-hydroxytryptamine transporter.
Graham D, Esnaud H, Langer SZ.
Department of Biology, Synthelabo Recherche (L.E.R.S.), Paris, France.
The selective 5-hydroxytryptamine (5-HT) uptake inhibitor, [3H]paroxetine, has been used as a specific probe in a series of experiments aimed at characterizing the substrate and 5-HT uptake inhibitor binding domains on the neuronal sodium-ion-coupled 5-HT transporter. In addition, an affinity-chromatographic protocol which provided a greater than 3000-fold purification of this neuronal transporter protein is outlined.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1828051&dopt=Abstract
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Pharmacol Biochem Behav. 1991 Mar;38(3):505-12.
3,4-Methylenedioxyamphetamine (MDA) analogues exhibit differential effects on synaptosomal release of 3H-dopamine and 3H-5-hydroxytryptamine.
McKenna DJ, Guan XM, Shulgin AT.
Department of Neurology & Neurological Sciences, Stanford University Medical Center, CA 94305.
The effect of various analogues of the neurotoxic amphetamine derivative, MDA (3,4-methylenedioxyamphetamine) on carrier-mediated, calcium-independent release of 3H-5-HT and 3H-DA from rat brain synaptosomes was investigated. Both enantiomers of the neurotoxic analogues MDA and MDMA (3,4-methylenedioxymethamphetamine) induce synaptosomal release of 3H-5-HT and 3H-DA in vitro. The release of 3H-5-HT induced by MDMA is partially blocked by 10(-6) M fluoxetine. The (+) enantiomers of both MDA and MDMA are more potent than the (-) enantiomers as releasers of both 3H-5-HT and 3H-DA. Eleven analogues, differing from MDA with respect to the nature and number of ring and/or side chain substituents, also show some activity in the release experiments, and are more potent as releasers of 3H-5-HT than of 3H-DA. The amphetamine derivatives (+/-)fenfluramine, (+/-)norfenfluramine, (+/-)MDE, (+/-)PCA, and d-methamphetamine are all potent releasers of 3H-5-HT and show varying degrees of activity as 3H-DA releasers. The hallucinogen DOM does not cause significant release of either 3H-monoamine. Possible long-term serotonergic neurotoxicity was assessed by quantifying the density of 5-HT uptake sites in rats treated with multiple doses of selected analogues using 3H-paroxetine to label 5-HT uptake sites. In the neurotoxicity study of the compounds investigated, only (+)MDA caused a significant loss of 5-HT uptake sites in comparison to saline-treated controls. These results are discussed in terms of the apparent structure-activity properties affecting 3H-monoamine release and their possible relevance to neurotoxicity in this series of MDA congeners.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1829838&dopt=Abstract
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