Do glucocorticoids contribute to the abnormalities in serotonin transporter expression and function seen in depression? An animal model. Effect of fluvoxamine on 5-hydroxytryptamine uptake, paroxetine binding sites and ketanserin binding sites in the Japanese monkey brain and platelets, in vivo and in vitro. Serotonin reuptake inhibitor withdrawal. Rx drugs

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Biol Psychiatry. 1996 Oct 1;40(7):576-84.
Do glucocorticoids contribute to the abnormalities in serotonin transporter expression and function seen in depression? An animal model.

Slotkin TA, McCook EC, Ritchie JC, Seidler FJ.

Department of Pharmacology, Duke University Medical Center, Durham, NC 27710, USA.

Adrenocorticosteroids and serotonergic neurons exert reciprocal regulatory actions, and both are abnormal in depression. We evaluated whether glucocorticoids influence the serotonin transporter in rat platelets and brain by infusing dexamethasone for 26 days, sufficient for replacement of the entire platelet population. Effectiveness was verified by measurement of plasma dexamethasone levels, adrenal atrophy, and growth inhibition. At the end of the infusion, we examined [3H]paroxetine binding to platelet, hippocampal, and cerebrocortical membranes, and [3H]serotonin uptake into platelets and synaptosomes. Dexamethasone slightly reduced platelet [3H]paroxetine binding (12%) and had no effect on binding in brain. Platelet [3H]serotonin uptake was unaffected, but synaptosomal uptake was significantly reduced. In neither platelets nor synaptosomes did dexamethasone alter imipramine's ability to inhibit uptake. Thus, elevated glucocorticoids are not responsible for reduced platelet serotonin transporter expression in depression, nor for resistance to imipramine's effect in platelets in elderly depression; however, reduced synaptosomal [3H]serotonin uptake indicates that glucocorticoids can affect transport efficiency, even when the number of transporter molecules is unaltered.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8886290&dopt=Abstract

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Jpn J Pharmacol. 1996 Aug;71(4):291-8.
Effect of fluvoxamine on 5-hydroxytryptamine uptake, paroxetine binding sites and ketanserin binding sites in the Japanese monkey brain and platelets, in vivo and in vitro.

Goto S, Egashira T, Wada Y, Takayama F, Yamanaka Y.

Department of Pharmacology, Oita Medical University, Japan.

We investigated the in vitro effects of fluvoxamine on 3H-paroxetine binding and 3H-monoamine uptake in monkey cerebral cortex in comparison with those of other antidepressants. Fluvoxamine selectively inhibited 3H-5-hydroxytryptamine (5-HT) uptake and 3H-paroxetine binding. However, it did not alter 3H-norepinephrine or 3H-dopamine uptake. In addition, we examined the effects of chronic treatment with fluvoxamine (5 mg/kg per day, p.o.) on 5-HT uptake sites that bind 3H-paroxetine and 5-HT2 receptors that bind 3H-ketanserin, in monkey brains and platelets. Chronic treatment with fluvoxamine affected neither the paroxetine binding sites nor the kentanserin binding sites of the brains and platelets. These results suggest that long-term treatment with fluvoxamine does not affect either the 5-HT uptake sites or 5-HT2-receptors of 5-HT neurons in monkey brain in spite of its strong inhibitory effect on 5-HT uptake in vitro.

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J Clin Psychopharmacol. 1996 Oct;16(5):356-62.
Serotonin reuptake inhibitor withdrawal.

Coupland NJ, Bell CJ, Potokar JP.

Department of Psychiatry, University of Alberta, Edmonton, Canada.

We studied reported withdrawal symptoms in a retrospective chart review of 352 patients treated in an outpatient clinic with the nonselective serotonin reuptake inhibitor clomipramine or with one of the selective serotonin reuptake inhibitors (SSRIs), fluoxetine, fluvoxamine, paroxetine, or sertraline. In 171 patients who were supervised during medication tapering and discontinuation, the most common symptoms were dizziness, lethargy, paresthesia, nausea, vivid dreams, irritability, and lowered mood. When patients with at least one qualitatively new symptom were defined as cases, these symptoms occurred significantly more frequently in patients who had been treated either with one of the shorter half-life SSRIs, fluvoxamine or paroxetine (17.2%), or with clomipramine (30.8%), than in patients taking one of the SSRIs with longer half-life metabolites, sertraline or fluoxetine (1.5%). The rate was not significantly different between the different shorter half-life treatments. Cases treated with fluvoxamine or paroxetine had received a significantly longer period of treatment (median 28 weeks) than noncases (16 weeks), but there were no significant associations with age or with diagnostic grouping. There was a trend toward an association with male sex. The majority of cases occurred despite slowly tapered withdrawal. Symptoms persisted for up to 21 days (mean = 11.8 days) after onset. These symptoms were relieved within 24 hours by restarting the medication, but were not relieved by benzodiazepines or by moclobemide. A role has been suggested for serotonin in coordinating sensory and autonomic function with motor activity. We suggest that this may lead to useful hypotheses about the pathophysiology of withdrawal symptoms from serotonin reuptake inhibitors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8889907&dopt=Abstract

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