Drugs online research references
Br J Pharmacol. 1998 Jul;124(6):1141-8.
Evidence from microdialysis and synaptosomal studies of rat cortex for noradrenaline uptake sites with different sensitivities to SSRIs.
Hughes ZA, Stanford SC.
Department of Pharmacology, University College London.
1. Microdialysis of the frontal cortex of freely-moving rats and uptake of [3H]noradrenaline into cortical synaptosomes were used to evaluate changes in efflux of noradrenaline in vivo and uptake of [3H]noradrenaline in vitro, respectively, induced by the selective serotonin reuptake inhibitors (SSRIs), fluoxetine and citalopram, and the tricyclic antidepressant, desipramine. 2. Noradrenaline efflux was increased during local infusion into the cortex of each of these drugs. All three agents also inhibited synaptosomal uptake of [3H]noradrenaline; this inhibition was unaffected by a substantial (50%) lesion of central 5-hydroxytrytaminergic neurones induced by intracerebroventricular infusion of 5,7-DHT (150 microg). 3. A noradrenergic lesion (70%), induced by pretreatment with the selective neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4, 40 mg kg(-1) i.p.), 5 days earlier, abolished the increase in noradrenaline efflux caused by local infusion of fluoxetine. In contrast, the desipramine-induced increase in efflux was greater than in non-lesioned rats whereas the effect of citalopram on noradrenaline efflux was unaffected by DSP-4 pretreatment. 4. The combined results of all these experiments suggest that there could be more than one, functionally distinct, noradrenaline uptake site in rat frontal cortex which can be distinguished by their different sensitivities to desipramine and the SSRIs, fluoxetine and citalopram.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9720784&dopt=Abstract
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Br J Urol. 1998 Aug;82(2):237-40.
In vivo evaluation of serotonergic agents and alpha-adrenergic blockers on premature ejaculation by inhibiting the seminal vesicle pressure response to electrical nerve stimulation.
Hsieh JT, Chang HC, Law HS, Hsieh CH, Cheng JT.
Department of Urology, College of Medicine, National Taiwan University, Taipei, Taiwan.
OBJECTIVE: To evaluate the effect of drugs on premature ejaculation using a rat animal model in which the seminal vesicle was electrically stimulated via its lesser splanchnic nerve and changes in the pressure response monitored. MATERIALS AND METHODS: Male Wistar rats (aged 12-14 weeks) were injected intravenously with prazosin and serotonergic agents (serotonin, clomipramine, fluoxetine, imipramine and indatraline) at various concentrations 10 min before electrical nerve stimulation (ENS) of the lesser splanchnic nerve; the initial increase in seminal vesicle pressure in response to ENS was then compared. RESULTS: The pressure response to ENS was reduced in the presence of prazosin or serotonergic agents. The mean (SEM) maximum inhibition values were 84.1 (8.9%) by fluoxetine at 0.1 mg/kg, 67.9 (8.7)% by prazosin at 0.1 mg/kg, 60.9 (11.0)% by serotonin at 3 mg/kg, 54.9 (4.6)% by clomipramine at 3 mg/kg, 30.0 (11.0)% by imipramine at 0.1 mg/kg, and 20.9 (4.3)% by indatraline at 0.1 mg/kg. From the concentration-response curve, the potency of prazosin was lower than that of fluoxetine, but was higher than that of serotonin or clomipramine. CONCLUSIONS: Like serotonin, fluoxetine and clomipramine can reduce the pressure response of the seminal vesicle to ENS. Among these inhibitory agents, including prazosin, fluoxetine was the most effective and may be valuable for the clinical treatment of ejaculatory dysfunction in man.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9722759&dopt=Abstract
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Prog Neuropsychopharmacol Biol Psychiatry. 1998 Jul;22(5):787-802.
Effect of chronic antidepressant treatment on transcription factor binding activity in rat hippocampus and frontal cortex.
Frechilla D, Otano A, Del Rio J.
Department of Pharmacology, University of Navarra Medical School, Pamplona, Spain.
1. The effect of chronic antidepressant administration on CRE-, SP1- and GRE-binding activity was studied in rat hippocampus and frontal cortex. 2. Fluoxetine and desipramine (3 and 10 mg/kg/day respectively) were given to rats for 21 consecutive days. The animals were killed 3 hr after the last injection and nuclear extracts were prepared to perform the DNA-protein reaction with consensus CRE, SP1 and GRE oligonucleotides. 3. Gel-shift assays showed that CRE-binding activity was increased in both frontal cortex and hippocampus by chronic fluoxetine treatment. Desipramine, however, only enhanced this activity in the frontal cortex. 4. Chronic fluoxetine decreased SP1-binding activity in the two selected brain regions. Again, desipramine only produced a significant reduction in the frontal cortex. 5. GRE-binding in the hippocampus was only enhanced by desipramine. Since chronic desipramine, and not fluoxetine, is able to increase hippocampal glucocorticoid receptor (GR) expression, interactions of GR with CREB and SP1 may determine the lack of effect of desipramine on binding activity of the two latter transcription factors in this brain region. 6. Overall, the results show a differential and region-specific effect of chronic, and not acute, antidepressant treatment on the DNA-binding activities studied and are consonant with the possible role of changes in gene expression in the mechanism of antidepressant action.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9723120&dopt=Abstract
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