Drugs online research references
cbb.ivic.ve
1. Serotonin is a neurotransmitter in the central nervous system which has been implicated in the aetiology and pathogenesis of affective disorders. The serononergic system also plays several roles in the immune system through the expression of a number of its receptor subtypes in the immune cells. 2. Following release serotonin is inactivated by reuptake into neurons and other cells by a specific serotonin sodium and chloride-dependent transporter molecule, whose structure has been elucidated. 3. Measurement [3H]paroxetine binding showed that human lymphocytes contain a high-affinity serotonin transporter. 4. To assess the serotonin function in major depression, we investigated serotonin transporter density in blood lymphocytes from patients with this disorder and selected according to the interview of the American Psychiatric Association. 5. Patients were divided into two groups and treated with two different antidepressant drugs, one group receiving fluoxetine, a selective serotonin reuptake inhibitor, and another mirtazapine, an antagonist of alpha2-adrenergic auto and heteroreceptors, for a period of 6 weeks. 6. Blood samples were obtained before and after the treatment, lymphocytes were isolated by Ficoll/Hypaque gradient, subjected to differential adhesion to plastic, and cell membranes were prepared for binding assay of [3H]paroxetine. 7. Lymphocytes serotonin transporter number was significantly reduced, while the affinity was unchanged, in patients with major depression disorder as compare to controls. 8. In addition, there was a partial recovery in lymphocytes serotonin (5HT) transporter number in the period posterior to the antidepressants administration, accompanied with clinical and depression rating scales improvement. Serotonin was determined in platelet-poor plasma and in lymphocytes before and after drugs administration, showing a significant decrease in the patients treated compared to untreated and controls. 9. These results are evidence of the potential interaction between the nervous and immune systems. The mechanisms underlying this interaction are under study, and might be related to modifications in the expression or function of the serotonin transporters in lymphocytes of depressed patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12585696&dopt=Abstract
note: kwd match prozac online literature
Brain Behav Immun. 2002 Apr;16(2):87-103.
Role of central 5-HT(2) receptors in fluoxetine-induced decreases in T lymphocyte activity.
Pellegrino TC, Bayer BM.
Department of Pharmacology, Georgetown University Medical Center, 3900 Reservoir Road, Washington, DC 20007, USA.
Previous studies have demonstrated that fluoxetine administration decreases mitogen-induced T lymphocyte proliferation. The present studies were carried out to determine which receptor subtype(s) was involved and whether these effects on lymphocyte responses were centrally or peripherally mediated. Two hours following administration of the 5-HT(1A) agonist 8-OH-DPAT (1 mg/kg), there was no change in lymphocyte proliferation responses, whereas the 5-HT(2) agonist DOI (2.5 mg/kg) significantly decreased (80%) proliferation. Similarly, pretreatment with the 5-HT(2) antagonists ritanserin (5 mg/kg, 30 min) or ketanserin (5 mg/kg, 1 h) was found to completely antagonize the effects of fluoxetine on lymphocyte proliferation. Consistent with central 5-HT(2) receptor involvement, microinjection of DOI (50 microg) resulted in a decrease in lymphocyte proliferation similar to that observed following systemic administration. Furthermore, central administration of ketanserin (20 microg) prevented the suppressive effects of systemic fluoxetine. Collectively, these results suggest that decreases in mitogen-induced lymphocyte proliferation following acute fluoxetine administration was due to indirect effects of fluoxetine following the activation of central 5-HT(2) receptors. Copyright 2001 Elsevier Science (USA).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11908920&dopt=Abstract
note: kwd match prozac online literature
unisi.it
Depression is a mood disorder characterized by complex alterations of neurotransmitters such as serotonin, norepinephrine, and dopamine. In particular, there is substantial evidence of abnormalities in serotonin neurotransmission. Peripheral parameters of serotoninergic transmission, such as the 5-hydroxytryptamine content of plasma and platelets, have been used to identify biochemical alterations related to depression. In recent years, these parameters have also been used to examine the mechanism of action of antidepressive drugs such as the selective serotonin reuptake inhibitors.This study investigated the interaction between the plasma and platelet levels of fluoxetine and serotonin after fluoxetine administration to depressed patients. Twelve patients affected by major depression (according to the DSM-IV criteria) received a single oral dose of fluoxetine in the morning: 5 mg in the first 5 days, 10 mg from day 6 to day 10, and 20 mg from day 11 to day 40. Blood samples were collected at 0, 7, 10, and 24 hours after drug administration on the day 1 of fluoxetine 5 mg and on the 1st and the 30th day of fluoxetine 20 mg (days 11 and 40 of treatment, respectively).Plasma fluoxetine and serotonin levels increased after drug administration, reaching the highest levels on the 30th day of fluoxetine 20 mg. Fluoxetine levels were also detectable in platelets, with a time variation similar to plasma values. Platelet serotonin levels decreased after drug administration, and the lowest values were observed on the 30th day of fluoxetine 20 mg.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11910257&dopt=Abstract
note: kwd match prozac online literature
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Antibiotics and prescription medications online literature ||