Drugs online research references
Brain Res Dev Brain Res. 1996 May 31;93(1-2):155-61.
Programming of brainstem serotonin transporter development by prenatal glucocorticoids.
Slotkin TA, Barnes GA, McCook EC, Seidler FJ.
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710, USA.
Prenatal stress or exposure to excess glucocorticoids are known to alter central nervous system function and to result in lasting changes in reactions to stress. The potential involvement of specific elements of brainstem serotonergic neurons was examined in the current study. Pregnant rats were given 0.05, 0.2 or 0.8 mg/kg of dexamethasone on gestational days 17, 18 and 19, and the effects on development of the serotonin presynaptic transporter were assessed from birth to young adulthood by measurement of [3H]paroxetine binding to membrane preparations. Dexamethasone produced a dose-dependent retardation of body and brainstem growth but evoked a significant elevation of [3H]paroxetine binding that persisted into adulthood. Effects on [3H]paroxetine binding were robust even at the lowest dose, which did not suppress growth, indicating that the programming of this transporter is more sensitive to glucocorticoids than is general development. At the highest dose, promotional effects on serotonin transporter expression were offset by impaired growth, so that the peak effect was seen at the intermediate dose of dexamethasone. There were no comparable effects on serotonin transmitter levels, indicating selectivity toward promotion of transporter expression as distinct from simply increasing the number of serotonergic nerve terminals or all nerve terminal components. As the effect of prenatal dexamethasone treatment on the serotonin transporter is more persistent than those on other monoamine transporters, and is not shared by postnatal treatment or by treatment in adulthood, it likely represents specific programming by glucocorticoids during the prenatal period. Aberrant serotonergic transporter expression may contribute to alterations of synaptic function that ultimately produce the physiological abnormalities seen after prenatal stress or glucocorticoid treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8804702&dopt=Abstract
note: kwd match paxil online literature
Neurochem Int. 1996 Mar;28(3):299-307.
The serotonin transporter from human brain: purification and partial characterization.
Rotondo A, Giannaccini G, Betti L, Chiellini G, Marazziti D, Martin C, Lucacchini A, Cassano GB.
Institute of Psychiatry, University of Pisa, Italy.
The serotonin (5-HT) transporter from human striatum was solubilized by digitonin and purified by affinity chromatography. The native protein-detergent complex had a molecular mass of 205 kDa, as estimated by gel-exclusion chromatography of the eluates obtained from affinity chromatography. The purified 5-HT transporter migrated as a single band of 67 kDa in SDS-PAGE. To clarify the spatial relationships between the binding sites of the tricyclic antidepressants, as [3H]-imipramine, and of the selective serotonin reuptake inhibitors, as [3H]-paroxetine, on the 5'HT transporter, both radioligands were used to label it in the purification steps. [3H]-paroxetine bound with the same affinity to a single high-affinity site on both membrane and purified preparations. [3H]-imipramine labeled a high- and a low-affinity site on parent membranes, whereas it bound to a single high-affinity site on the purified extract. Tricyclic antidepressants, selective serotonin reuptake inhibitors and 5-HT itself displaced [3H]-paroxetine and [3H-]imipramine from their high-affinity binding sites on both the membrane-bound and the purified 5-HT transporter in a monophasic fashion with Hill coefficients close to unity. Furthermore, both [3H]-paroxetine and [3H]-imipramine displayed a similar maximum binding capacity on an identical protein of 205 kDa. Our results suggest overlapping binding sites for tricyclic antidepressants, selective serotonin reuptake inhibitors and 5-HT on the 5-HT transporter.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8813248&dopt=Abstract
note: kwd match paxil online literature
Brain Res. 1996 Jan 15;706(2):347-50.
[3H]WIN 35,428 binding in the human brain.
Allard P, Marcusson JO, Ross SB.
Department of Psychiatry, University of Umea, Sweden.
The binding of [3H]WIN 35,428 was studied in post-mortem human brain, including extrastriatal regions. In the putamen, dopamine almost completely inhibited the [3H]WIN 35,428 binding. Paroxetine inhibited the binding with similar affinity as cocaine, in the range 200-300 nM. In the frontal cortex, [3H]WIN 35,428 labelled cocaine- and alaproclate sensitive binding sites, of which a major fraction was of protein nature. The elucidation of the cocaine sensitive sites in the frontal cortex should be the subject of further research.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8822381&dopt=Abstract
note: kwd match paxil online literature
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Antibiotics and prescription medications online literature ||