Enhancement of the anticonvulsant effect of fluoxetine following blockade of 5-HT1A receptors. Sensitive measurement of agonist-stimulated [3H]inositol monophosphate accumulation in rat cortical miniprisms. Concomitant use of selective serotonin reuptake inhibitors with other cytochrome P450 2D6 or 3A4 metabolized medications: how often does it really happen? Rx drugs

Drugs online research references

Eur J Pharmacol. 1997 Oct 1;336(1):1-6.
Enhancement of the anticonvulsant effect of fluoxetine following blockade of 5-HT1A receptors.

Browning RA, Wood AV, Merrill MA, Dailey JW, Jobe PC.

Department of Physiology, Southern Illinois University School of Medicine, Carbondale, USA.

Serotonin reuptake inhibitors, such as fluoxetine, have been shown to exert anticonvulsant effects in several animal models of epilepsy. In view of recent studies showing that 5-HT1A receptor antagonists (somatodendritic autoreceptor antagonists) enhance the increase in extracellular 5-hydroxytryptamine (5-HT, serotonin) produced by serotonin reuptake inhibitors, it was of interest to determine if these antagonists also enhance the anticonvulsant effect of fluoxetine in Genetically Epilepsy-Prone Rats (GEPRs). The 5-HT1A receptor antagonists (-)-pindolol and LY 206130 (1-[1-H-indol-4-yloxy]-3-[cyclohexylamino]-2-propanol maleate) were examined in the present study and both enhanced the anticonvulsant action of fluoxetine in severe seizure GEPRs (GEPR-9s). The latter effect of LY 206130 was found to be dose- and 5-HT-dependent. These findings provide further evidence that the increase in extracellular serotonin observed after administering fluoxetine in combination with a 5-HT1A receptor antagonist is physiologically important and that the anticonvulsant effect of fluoxetine in the GEPR is mediated through an increase in extracellular 5-HT.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9384247&dopt=Abstract

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Brain Res Brain Res Protoc. 1997 May;1(2):139-44.
Sensitive measurement of agonist-stimulated [3H]inositol monophosphate accumulation in rat cortical miniprisms.

Erfurth A, Wurtman RJ.

Department of Brain and Cognitive Sciences, E25-604 Massachusetts Institute of Technology, Cambridge 02142-1323, USA.

Phosphoinositide (PI) breakdown is an important transmembrane signaling mechanism in rat brain and numerous transmitter receptors are linked to this mechanism. Since agonist-stimulated PI breakdown is often changed after drug pretreatment, assessment of changes in PI breakdown represents an important tool in drug development. PI breakdown is commonly monitored by assaying [3H]inositol monophosphate ([3H]IP1) accumulation in the presence of lithium as an inhibitor of inositol monophosphatase. The present protocol presents a lithium-inhibited [3H]IP1 accumulation assay that enhances relatively weak agonist-stimulated [3H]IP1 accumulation signals by thorough oxygenation during agonist stimulation. The protocol is particularly useful in the measurement of [3H]IP1 accumulation after in vitro exposure to relatively weak stimulants, such as serotonin (5-HT), and/or after animal pretreatments that decrease the response to the agonist. In the case of 5-HT stimulation the monoamine oxidase (MAO) inhibitor, tranylcypromine, was added to the incubation medium to inhibit breakdown of exogenous serotonin. We used this protocol to measure 5-HT- and carbachol-stimulated [3H]IP1 accumulation in cortical miniprisms obtained from rats pretreated with D-fenfluramine. D-Fenfluramine is a drug that acutely releases 5-HT into the synaptic cleft and blocks its reuptake.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9385077&dopt=Abstract

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J Affect Disord. 1997 Oct;46(1):59-67.
Concomitant use of selective serotonin reuptake inhibitors with other cytochrome P450 2D6 or 3A4 metabolized medications: how often does it really happen?

Gregor KJ, Way K, Young CH, James SP.

Outcomes Research, PCS Health Systems, Inc., Scottsdale, Arizona 85260, USA.

This study retrospectively examines the one-month concomitant use of cytochrome P450 2D6 or 3A4 metabolized medications in 544,309 patients who were also receiving selective serotonin reuptake inhibitors (SSRIs). Overall, 25.53% of SSRI patients experienced concomitant use with at least one of the 33 studied CYP 2D6 or 3A4 metabolized medications. Certain drugs and drug classes were more likely to be used concurrently among SSRI patients (e.g., benzodiazepines, tricyclic antidepressants, calcium channel blockers). Similarly, of the SSRI patients experiencing concomitant use, this concurrent use was twice as likely with cytochrome P450 medications metabolized by the 3A4 isoenzyme as with those metabolized by the 2D6 isoenzyme. Finally, the vast majority (80.9%) of SSRI patients experiencing concomitant use did so with one CYP 2D6 or 3A4 metabolized medication. In sum, concomitant use generally was not extensive and did not appear to be differential among the fluoxetine, paroxetine, or sertraline patient comparison groups.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9387087&dopt=Abstract

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