Drugs online research references
intra.nida.nih.gov
Repeated administration of D,L-fenfluramine (FEN) is known to cause prolonged depletion of forebrain serotonin (5-HT) in animals. Ironically, few studies have evaluated functional consequences of such FEN-induced 5-HT loss. In the present work, we examined neuroendocrine and behavioral responses evoked by acute FEN injection in rats that had previously received a 4 d FEN-dosing regimen known to deplete forebrain 5-HT (D,L-FEN, 20 mg/kg, s.c., b. i.d.). Rats were fitted with indwelling jugular catheters before the study to allow for repeated intravenous challenge injections and stress-free blood sampling. At 1 and 2 weeks after the 4 d dosing regimen, acute FEN (1.5 or 3.0 mg/kg, i.v.) produced dose-related elevations in plasma corticosterone and prolactin; these hormonal responses were markedly attenuated in FEN-pretreated rats. Behavioral effects of acute FEN, namely flat body posture and forepaw treading, were also blunted in FEN-pretreated rats. Interestingly, rats exposed to repeated FEN did not display overt abnormalities in hormonal or behavioral parameters under basal (i.e., unprovoked) conditions, despite dramatic decreases in postmortem tissue levels of 5-HT in numerous brain areas. Our results suggest that FEN-induced 5-HT depletion is accompanied by multiple impairments in 5-HT function. Although the clinical relevance of our data are debatable, the findings clearly show the utility of the FEN challenge test for uncovering in vivo functional deficits that might otherwise go undetected. FEN should remain an important pharmacological tool for determining the role of 5-HT neurons in mediating diverse physiological and behavioral processes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9787010&dopt=Abstract
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Biol Psychiatry. 1998 Oct 1;44(7):617-21.
Effect of antidepressants on intracellular Ca++ mobilization in human frontal cortex.
Jagadeesh SR, Subhash MN.
Neurochemistry Department, National Institute of Mental Health and Neurosciences, Bangalore, India.
BACKGROUND: It is well documented that central serotonin (5-HT)2 receptor dysfunction is involved in the biochemistry and pathophysiology of depression and might be corrected by antidepressant drug treatment. METHODS: The effect of imipramine (IMI) and fluoxetine (FLX) on 5-HT2A receptor-mediated intracellular calcium ([Ca++]i) mobilization in synaptosomes of human frontal cortex was studied. [Ca++]i was measured using Fura-2AM. RESULTS: It was observed that in response to 5-HT (10 mumol/L) there was a significant increase (254%; p < .001) in [Ca++]i compared to basal level (140.00 +/- 31.77 nmol/L/mg protein). Both IMI and FLX (10-1000 nmol/L) induce mobilization of basal [Ca++]i in a dose-dependent manner. IMI and FLX antagonize the 5-HT-stimulated [Ca++]i mobilization in a dose-dependent manner. IMI showed higher antagonizing effect at lower concentration (10 nmol/L); however, FLX showed maximum antagonizing effect at higher concentration (1000 nmol/L). CONCLUSIONS: It is observed that imipramine and fluoxetine have different effects on antagonizing the 5-HT response in frontal cortex. One mode of action of these antidepressants might be by decreasing the intracellular calcium.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9787886&dopt=Abstract
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cep.u-psud.fr
We studied the ability of WAY 100635 [N-[4-(2-methoxyphenyl)-1-piperazinyl]-N-(2-pyridinyl) cyclo-hexanecarboxamide], 0.5 mg/kg, i.v. and (-)-5-Me-8-OH-DPAT [(-)-5-methyl-8-hydroxy-2-(di-n-propylamino)tetralin], 3 mg/kg, i.v. two selective 5-HT1A receptor antagonists, to potentiate: (1) the enhancement of extracellular 5-HT levels ([5-HT(ext)]) induced by a single administration of 5 mg/kg i.p. fluoxetine using in vivo microdialysis in the ventral hippocampus of conscious rats, (2) the decrease in food intake induced by this antidepressant drug in food-deprived rats. The effects of fluoxetine were significantly potentiated, by 30-40%, by WAY 100635 as well as by (-)-5-Me-8-OH-DPAT in the two sets of experiments. Thus, fluoxetine increased [5-HT(ext)] in serotonergic nerve terminal areas and consequently, induced hypophagia, both effects being limited by indirect activation of somatodendritic 5-HT1A autoreceptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9797034&dopt=Abstract
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