Drugs online research references
Int J Neurosci. 1998 Jul;95(1-2):115-32.
Excitatory amino acids and serotonin uptake blockers reveal two physiologically distinct serotonin systems in the retina of the skate, Raja erinacea.
Schuette E, Chappell RL.
Hunter College and the Graduate School of the City University of New York, Department of Biological Sciences, NY 10021, USA.
The retina of the skate (Raja erinacea) contains at least 2 types of cell (amacrines and bipolars) that can be visualized with an antiserum against serotonin. We have employed serotonin immunocytochemistry in combination with pharmacological manipulation of retinal tissue to analyze physiological properties of serotonergic amacrine cells and serotonin-accumulating bipolar cells. Excitatory amino acids (NMDA, aspartate) had no detectable effects on serotonin-immunoreactivity in bipolar cells but decreased staining in amacrine cells. High K+ Ringer increased staining in bipolar cell somata, however, it depleted the inner plexiform layer of the retina of serotonin. Zimelidine, a serotonin uptake inhibitor, completely blocked serotonin accumulation by bipolar cells but had no effect on amacrine cells, whereas incubation of the retinas in fluoxetine (Prozac), a different inhibitor of serotonin uptake, did not block serotonin accumulation into bipolar cells which was actually enhanced in some cases. We conclude that amacrine and bipolar cells of the skate retina employ two different serotonin uptake carrier systems, thus generating two distinct pharmacological components that are capable of interacting with each other as they compete for extracellular serotonin. Similar mechanisms may exist in the vertebrate CNS and further examination of the interaction of these systems could provide important insights into the action and possible side effects of serotonin-related drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9845022&dopt=Abstract
note: kwd match prozac online literature
Pharmacotherapy. 1998 Nov-Dec;18(6):1298-303.
Concomitant therapy with anxiolytics or hypnotics and maintenance of initial SSRI therapy.
Shields SA, Gregor KJ, Young CH, James SP.
Outcomes Research, PCS Health Systems, Inc., Scottsdale, Arizona, USA.
We conducted a retrospective analysis to evaluate the relationship between anxiolytic or hypnotic therapy and maintenance of therapy with selective serotonin reuptake inhibitors (SSRIs). Subjects were 654 patients who received anxiolytics or hypnotics early in SSRI therapy (study group ) and 15,172 patients who did not (controls). Maintenance of SSRI therapy was evaluated during the 6 months after start of therapy and included days of initial SSRI therapy and rates of discontinuation, defined as a break of more than 30 days. Rates of discontinuation in study and control groups (84% and 77%, p=0.001) and average days of initial SSRI therapy (77 and 94 days, p<0.0001) were statistically different. Thus patients receiving anxiolytic or hypnotics in the first 60 days of therapy were less likely to continue initial SSRI therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9855330&dopt=Abstract
note: kwd match prozac online literature
J Investig Med. 1998 Dec;46(9):470-4.
Antidepressants inhibit the glucocorticoid stimulation of thyrotropin releasing hormone expression in cultured hypothalamic neurons.
Jackson IM, Luo LG.
Division of Endocrinology, Rhode Island Hospital, Brown University School of Medicine, Providence 02903, USA.
BACKGROUND: The pituitary thyroid axis is frequently effected in human depression possibly due to alteration in hypothalamic thyrotropin releasing hormone (TRH) secretion. Since clinical recovery is associated with normalization of thyroid function, the direct effect of antidepressants on TRH expression in a well established fetal rat hypothalamic neuronal culture system was investigated. METHODS: Fetal rat hypothalamic neurons (day 17) in culture were treated with different concentrations of antidepressants with or without glucocorticoids for 7 days following which TRH content was measured by radioimmunoassay (RIA). RESULTS: The results showed that Imipramine (IMIP), a tricyclic antidepressant (TCA), decreased the TRH content in a dose-dependent manner (from 80.7 +/- 4.9, at 10(-9) mol/L, to 14.1 +/- 0.6, at 10(-5) mol/L, fmol/well; P < 0.05). Desipramine (DESI), another tricyclic antidepressant, also decreased the TRH content (from 63.6 +/- 2.5, at 10(-9) mol/L, to 12.6 +/- 0.4, at 10(-5) mol/L, fmol/well; P < 0.05). Sertraline (SERT) and Fluoxetine (FLUO), serotonin selective reuptake inhibitors (SSRI), also decreased TRH content in a dose dependent manner (from 83.9 +/- 7.9, at 10(-10) mol/L, to 7.6 +/- 0.4, at 10(-5) mol/L, and from 41.66 +/- 2.5, at 10(-8) mol/L, to 17.54 +/- 0.92, at 10(-6) mol/L, fmol/well, respectively; both P < 0.05). We then tested the effect of these antidepressants on the Dex stimulation of TRH content. IMIP, DESIP and FLUO at 10(-6) mol/L reduced the TRH response to glucocorticoid stimulation (36.4 +/- 4.0, 56.6 +/- 2.4, 23.75 +/- 4.0, respectively vs 107 +/- 7.5 fmol/well; P < 0.05). CONCLUSION: This raises the possibility that the enhanced thyroid function in depression, which we postulate, may result in part from glucocorticoid stimulation of TRH gene expression, can be reversed by antidepressants through a direct effect on the TRH neuron. However, other mechanisms may need to be invoked in addition since basal TRH content was also reduced.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9861783&dopt=Abstract
note: kwd match prozac online literature
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