Drugs online research references
Biochim Biophys Acta. 1996 Aug 16;1302(3):241-8.
Liposomes bearing platelet proteins: a model for surface functions studies.
Dalencon F, Rosilio V, Puisieux F, Baszkin A, Wautier JL.
Physico-Chimie des Surfaces et Innovation en Pharmacotechnie, URA CNRS 1218. Universite Paris-Sud. Chatenay-Malabry, France.
An improved procedure for the direct transfer of membrane proteins from human platelets to liposomes involving the treatment of platelets with linolenic acid was developed. The transfer of platelet proteins to liposomes prepared from the mixture of L-alpha-dimyristoyl-phosphatidylcholine/sphingomyelin in the molar ratio 80/20 appeared to be significantly enhanced compared with liposomes prepared from the same components mixed in other ratios. A wide range of platelet proteins was transferred, the most important being GPIb (170 kDa), GPIIb/IIIa (135 and 110 kDa). GPIV (90 kDa), GPIX (24 kDa) and the serotonin transporter (68 kDa). The recognition interactions between these proteoliposomes and specific protein antibodies clearly indicate that the non-invasive procedure used in this study ensured the reproducible transfer of platelet proteins without essentially altering their original conformation. The obtained results reveal also that the affinity of proteoliposomes to bind paroxetin was virtually the same as that of the native serotonin transporter. These results provide an indication of the possible use of such proteoliposomes as models to study at the molecular level the interaction of these proteins with their ligands.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8765146&dopt=Abstract
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Behav Brain Res. 1996;73(1-2):169-75.
Serotonin2 receptors and the serotonin transporter in the schizophrenic brain.
Dean B, Hayes W, Opeskin K, Naylor L, Pavey G, Hill C, Keks N, Copolov DL.
Rebecca L. Cooper Laboratories, Mental Health Research Institute of Victoria, Parkville, Australia.
The binding of [3H]paroxetine and [3H]ketanserin to particulate membranes from frontal cortex of subjects who had or did not have schizophrenia was measured as was [3H]paroxetine binding to particulate membranes from the hippocampus and caudate nucleus. There was no change in either the affinity or density of [3H]ketanserin binding to membranes from the frontal cortex of subjects who had schizophrenia. Similarly, there was no difference in the density of [3H]paroxetine binding to membranes from subjects who had or did not have schizophrenia. The affinity of [3H]paroxetine binding in the frontal cortex and putamen did not differ in subjects who had schizophrenia. By contrast, there was a significant decrease in the affinity of [3H]paroxetine binding to the hippocampal membrane from subjects who had schizophrenia (0.40 +/- 0.06 nM vs 0.26 +/- 0.02 nM; p < 0.05). Furthermore, this difference was more apparent in the subjects who had schizophrenia and committed suicide (0.49 +/- 0.09 nM) than it was in those who had schizophrenia but did not commit suicide (0.32 +/- 0.09 nM). As [3H]ketanserin binds to the serotonin2 receptor our data suggest that this receptor is not changed in the Brodmann's area 9 of the frontal cortex. By contrast, [3H]paroxetine binds to the serotonin transporter and therefore our data suggest that the serotonin transporter is altered in the hippocampus of subjects with schizophrenia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8788497&dopt=Abstract
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Behav Brain Res. 1996;73(1-2):281-3.
5-HT1A autoreceptors and the mode of action of selective serotonin reuptake inhibitors (SSRI).
Hjorth S, Auerbach SB.
Department of Pharmacology, University of Goteborg, Sweden.
The clinical efficacy of antidepressant drugs that block serotonin (5-HT) reuptake may be restrained in the short term by the indirect activation of autoreceptors. In vivo microdialysis in rat hippocampus was used to study the putative release-inhibitory properties of the SSRI citalopram and paroxetine. With 5-HT reuptake first blocked by local 'reverse-dialysis' infusion of citalopram (1 microM) into the hippocampus, acute systemic administration of citalopram or paroxetine resulted in a marked decrease in hippocampal 5-HT overflow. This presumably reflected the inhibition of 5-HT neuronal discharge and release, subsequent to reuptake blockade in the raphe nuclei and thus, activation of somatodendritic autoreceptors. In support of this hypothesis, pretreatment with (+/-)-pindolol or (+)-WAY100135, to block 5-HT1A autoreceptors, abolished the decrease in extracellular 5-HT produced by acute systemic injection of the reuptake blockers. The results suggest that the clinical efficacy of antidepressants that block 5-HT reuptake could be enhanced by co-administration of a 5-HT1A autoreceptor antagonist.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8788519&dopt=Abstract
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