Drugs online research references
Jpn J Pharmacol. 1997 Oct;75(2):123-8.
Inhibition by nitric oxide of the uptake of [3H]serotonin into rat brain synaptosomes.
Asano S, Matsuda T, Nakasu Y, Maeda S, Nogi H, Baba A.
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Osaka University, Japan.
[3H]Serotonin (5-HT) uptake by synaptosomes of rat brain was dose-dependently inhibited by nitric oxide (NO) donors such as sodium nitroprusside (SNP), 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamin e, 3-morpholinosydnonimine and S-nitroso-L-cysteine (NO-CYS). The inhibitory effect was blocked by reduced hemoglobin. The effect was not mimicked by ferrocyanide and ferricyanide. 8-Bromoguanosine 3',5'-cyclic monophosphate (8-bromo cGMP) did not affect [3H]5-HT uptake into rat cortical synaptosomes. The reduced activity of [3H]5-HT uptake into the cortical synaptosomes pretreated with NO-CYS was partially reversed by washing the preparation after the treatment. Kinetic analysis showed that NO-CYS (100 microM) decreased the Vmax value without any change in the Km value. NO-CYS did not affect the specific binding of [3H]paroxetine, a ligand that binds to the 5-HT transporter, in membranes. NO-CYS and SNP, like iodoacetic acid and sodium cyanide, decreased the ATP content in cortical synaptosomes, but the effect on ATP content was not related to that on [3H]5-HT uptake. These findings suggest that NO inhibits reversibly [3H]5-HT uptake into rat brain synaptosomes without affecting the recognition site of the 5-HT transporter in a cGMP-independent manner, and the observed effect is not due to its metabolic effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9414026&dopt=Abstract
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Br J Pharmacol. 1997 Dec;122(8):1725-31.
Influence of olfactory bulbectomy and subsequent imipramine treatment on 5-hydroxytryptaminergic presynapses in the rat frontal cortex: behavioural correlates.
Grecksch G, Zhou D, Franke C, Schroder U, Sabel B, Becker A, Huether G.
Psychiatric Clinic of the University of Gottingen, Germany.
1. Alterations of 5-hydroxytryptaminergic mechanisms are thought to play a special role in the pathogenesis of depression and antidepressant treatments are assumed to restore these changes. 2. We have used one of the most reliable models of depression, the olfactory bulbectomized rat to study the long term consequences of this manipulation and of subchronic imipramine treatment on two parameters of 5-hydroxytryptaminergic presynapses, 5-hydroxytryptamine (5-HT) transporter density and tryptophan hydroxylase apoenzyme concentration, in the frontal cortex as well as on active avoidance learning several weeks after bulbectomy. 3. The Bmax value of [3H]-paroxetine binding and the concentration of the 5-HT synthesizing enzyme were both significantly elevated in the frontal cortex of bulbectomized rats compared to sham-operated controls. 4. Imipramine treatment, either by daily injections or by subcutaneous implantation of slow release imipramine-containing polymers reduced the elevated tryptophan hydroxylase apoenzyme levels in the frontal cortex of bulbectomized, but not of sham-operated control rats and restored the deficient learning performance of bulbectomized rats. 5. Both effects were more pronounced after continuous drug administration by imipramine-releasing polymers compared to daily i.p. injections. 6. These findings indicate that bulbectomy leads to a compensatory 5-hydroxytryptaminergic hyperinnervation of the frontal cortex. Chronic antidepressant treatment seems to attenuate the increased output of the 5-hydroxytryptaminergic projections in the frontal cortex through the destabilization of the rate limiting enzyme of 5-HT synthesis of the 5-hydroxytryptaminergic nerve endings in this brain region.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9422820&dopt=Abstract
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J Pharm Sci. 1997 Dec;86(12):1497-500.
Evaluation of the neuropharmacodynamics of paroxetine in vivo utilizing microdialysis.
Ramaiya A, Johnson JH, Karnes HT.
Department of Pharmacy & Pharmaceutics, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298-980533, USA.
The effect of paroxetine, a selective serotonin reuptake inhibitor used in the treatment of depression, on extracellular serotonin levels was evaluated in freely moving conscious rats. Microdialysis, a powerful in vivo technique to monitor the extracellular levels of neurotransmitters, was used to monitor the baseline changes in the levels of serotonin in rat brain anterior lateral striatum post paroxetine administration, which is a measure of the neuropharmacodynamic effect of the drug. Microdialysis sampling was performed for 210 min prior to and for 240 min after intraperitoneal administration of paroxetine (10 mg/kg). Paroxetine caused a statistically significant increase in the extracellular levels of serotonin in the anterior lateral striatum sampled by microdialysis. The present study demonstrates the utility of microdialysis for studying the in vivo neuropharmacodynamics of paroxetine in conscious rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9423168&dopt=Abstract
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