Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive-compulsive disorder. Chronic fluoxetine administration increases the serotonin N-acetyltransferase messenger RNA content in rat hippocampus. Rx drugs

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Electrical or chemical stimulation of the superior colliculus (SC) in rats produces orienting and defensive responses. Defensive behaviors are modulated by serotonin (5-hydroxytryptamine, 5-HT), and serotonergic fibers provide a dense innervation of the SC. Here, we examined the role of 5-HT in modulating the behavioral responses of rats elicited by electrical SC stimulation. Low-intensity (107+/-12 microA) stimulation of the SC elicited orienting head movements, while higher intensities (204+/-20 microA) produced running and jumping responses. Treatment with the 5-HT depletor p-chlorophenylalanine (300 mg/kg/day x 3, i.p.) lowered current thresholds to elicit orienting and running by 40 and 21%, respectively. Conversely, concurrent administration of the 5-HT uptake inhibitor fluoxetine (10 mg/kg, i.p.) and the 5-HT(1A) receptor antagonist WAY 100635 (0.5 mg/kg, s.c.) increased threshold currents to produce head and running movements by 41 and 18%, respectively. We investigated the anatomical substrate of this inhibitory effect of 5-HT with intracerebral 5-HT application by means of reverse microdialysis. Application of 5-HT (1-50 mM) into the midbrain immediately adjacent to the SC stimulation electrode resulted in a pronounced (approximately four-fold for 50 mM 5-HT) dose- and time-dependent increase in stimulation thresholds to elicit head movements. Application of 5-HT into the frontal cortex (up to 100 mM) had no significant effect on SC-evoked behavioral responses. These results show that 5-HT exerts an inhibitory influence over orienting and defensive behaviors initiated in the mammalian SC. It appears that this inhibitory effect is mediated, to a large extent, by a direct action of 5-HT at the level of the midbrain.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12946599&dopt=Abstract

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Biol Psychiatry. 1999 Jan 15;45(2):164-74.
Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive-compulsive disorder.

Bergqvist PB, Bouchard C, Blier P.

Department of Psychiatry, McGill University, Montreal, Quebec, Canada.

BACKGROUND: Among all antidepressant treatments, including electroconvulsive shock (ECS) therapy and monoamine oxidase inhibitors (MAOIs), only the selective serotonin (5-HT) reuptake inhibitors (SSRIs) exert a clear therapeutic effect in obsessive-compulsive disorder (OCD). An 8-week, but not a 3-week treatment with the SSRI paroxetine results in an increased electrically evoked [3H]5-HT release and a desensitization of 5-HT autoreceptors in the guinea pig orbitofrontal cortex, a brain region implicated in OCD. METHODS: In the present study, the effect of long-term treatment with the SSRI fluoxetine, ECS, and the reversible type A MAOI moclobemide was investigated on evoked [3H]5-HT release from preloaded guinea pig brain slices prepared from the hypothalamus, cingulate cortex, and orbitofrontal cortex. RESULTS: Fluoxetine treatment yielded an enhanced [3H]5-HT release in the three brain areas, but a desensitization of the 5-HT autoreceptor only in the hypothalamus and orbitofrontal cortex. ECS treatment did not result in any alteration of the electrically evoked [3H]5-HT release or of 5-HT autoreceptor sensitivity in any of the brain regions. Moclobemide increased [3H]5-HT release only in the orbitofrontal cortex without any alteration in the 5-HT autoreceptor sensitivity. CONCLUSIONS: These findings indicate that only treatments effective in OCD have the capacity to desensitize the terminal 5-HT autoreceptor in the orbitofrontal cortex.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9951563&dopt=Abstract

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Biol Psychiatry. 1999 Jan 15;45(2):175-9.
Chronic fluoxetine administration increases the serotonin N-acetyltransferase messenger RNA content in rat hippocampus.

Uz T, Manev H.

Psychiatric Institute, University of Illinois at Chicago, USA.

BACKGROUND: It has been proposed that up-regulation of cyclic adenosine monophosphate response element binding protein is a common action of chronic antidepressant treatments that may regulate specific target genes in the hippocampus. We hypothesized that the serotonin N-acetyltransferase (AA-NAT; EC 2.3.1.87) gene is one such target. AA-NAT leads to formation of N-acetylserotonin from serotonin, and in the pineal gland, to melatonin synthesis. We investigated whether hippocampal AA-NAT expression can be modified by chronic administration of fluoxetine to rats. METHODS: Male Brown-Norway rats were administered 5 mg/kg fluoxetine or its vehicle either once (acute) or once daily for 21 days (chronic). They were sacrificed 18 hours after the last injection, and their hippocampi were processed for a quantitative reverse-transcription/polymerase-chain reaction assay of AA-NAT and cyclophilin (cyc) messenger (m)RNAs. The results are expressed as AA-NAT/cyc ratios. RESULTS: Chronic but not acute fluoxetine administration resulted in about a fivefold increase in hippocampal AA-NAT mRNA. CONCLUSIONS: Up-regulation of extrapineal, e.g., hippocampal, AA-NAT expression may play a role in mediating the therapeutic action of antidepressant drugs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9951564&dopt=Abstract

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