Drugs online research references
J Neurochem. 1998 Apr;70(4):1547-55.
Down-regulation of the human norepinephrine transporter in intact 293-hNET cells exposed to desipramine.
Zhu MY, Blakely RD, Apparsundaram S, Ordway GA.
Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson 39216, USA.
The effects of continuous exposure of cultured cells expressing the human norepinephrine transporter (hNET) to the hNET inhibitor desipramine on hNET expression and function were studied. Exposure of HEK-293 cells transfected stably with the hNET cDNA (293-hNET cells) to desipramine for 3 days reduced the specific binding of [3H]nisoxetine in membrane homogenates in a concentration-dependent manner. The magnitude of the reductions in [3H]nisoxetine binding to hNET was dependent on the length of time of the exposure to desipramine, reaching 77% after a 21-day exposure. The reduction of [3H]nisoxetine binding returned to control levels within 72 h after a 3-day exposure to desipramine. Reductions in [3H]nisoxetine binding to hNET were accompanied by time-dependent and exposure concentration-dependent reductions in hNET protein levels as determined by western blotting. Similar to binding, hNET protein levels returned to control levels 72 h after cessation of desipramine exposure. Northern blotting indicated that exposure of 293-hNET cells to desipramine did not significantly alter hNET mRNA levels. Uptake of [3H]norepinephrine by 293-hNET cells was markedly reduced after a 3-day exposure to desipramine. However, desipramine exposure had no effect on uptake of [3H]glutamate or [3H]alanine. The present findings imply that down-regulation of the hNET in 293-hNET cells induced by desipramine results from a selective reduction in hNET protein levels, presumably a consequence of either a reduction in the translation of hNET mRNA or from an enhanced degradation of hNET protein.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9523572&dopt=Abstract
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Brain Res Mol Brain Res. 1998 Feb;54(1):64-73.
Serotonergic regulation of neuropeptide and glutamic acid decarboxylase mRNA levels in the rat striatum and globus pallidus: studies with fluoxetine and DOI.
Mijnster MJ, Galis-de Graaf Y, Voorn P.
Graduate School Neurosciences Amsterdam, Vrije Universiteit, Department of Anatomy and Embryology, The Netherlands.
The serotonergic regulation of neuropeptide and glutamic acid decarboxylase (GAD) mRNA level in the rat basal ganglia was investigated by determining the effects of chronic treatment with the serotonin uptake blocker fluoxetine and the serotonin 5-HT2 agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrobromide (DOI). Fluoxetine (10 mg/kg) induced a reduction of preproenkephalin and GAD65 mRNA levels in the caudate-putamen and nucleus accumbens core and shell after 5 days of treatment. In addition, GAD65 mRNA levels were reduced in the globus pallidus. These changes appeared to be transient as they were not found after 15 days of fluoxetine treatment. DOI (7 mg/kg), administered for 9 days, induced a decrease of preprodynorphin mRNA levels in the caudate-putamen and the nucleus accumbens core and shell. No regional differentiation in the effects of fluoxetine and DOI was observed. Based on the present results, we propose that an increased 5-HT tone may reduce enkephalin and GABA mRNA levels in striatal regions and in the globus pallidus. Our results further show that preproenkephalin mRNA is not affected by chronic 5-HT2 receptor stimulation, indicating that the fluoxetine-induced decrease in preproenkephalin mRNA levels involves other 5-HT receptors than the 5-HT2 receptor. Preprodynorphin mRNA levels, on the other hand, were found to be reduced after chronic 5-HT2 receptors than stimulation. This observation, together with our previous finding that the 5-HT2 antagonist ritanserin tends to increase preprodynorphin mRNA levels, suggests a 5-HT2-mediated tonic inhibition of preprodynorphin mRNA levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526047&dopt=Abstract
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Prog Neuropsychopharmacol Biol Psychiatry. 1998 Jan;22(1):147-58.
Pinch-induced catalepsy in mice: a useful model to investigate antidepressant or anxiolytic drugs.
Fundaro A.
Department of Anatomy, Pharmacology and Forensis Medicine, University of Turin, Italy.
1. Repeated pinching at the scruff produces, in experimental test/retest sessions, prolonged cataleptic-like immobility in mice that may mimic immobilities seen in some natural situations. 2. In the first experiment, on male mice, imipramine and amitriptiline (20 and 30 mg/kg i.p.) augmented the number of pinches necessary to reach the criterion of induced catalepsy and reduced the total time of catalepsy. 3. In the second experiment, on female mice, compounds that modulate the central 5-HT transmission, like fluvoxamine, fluoxetine (20 mg/kg i.p.) and ondansetron (0.1 and 1 mg/kg i.p.), retarded the occurrence and shortened the duration of pinch induced catalepsy at doses that did not modify the open field performances. Maprotiline (a selective inhibitor of the NA reuptake) did not modify the mice's performances in respect to controls. 4. Female mice presented a more rapid occurrence and a prolonged duration of pinch-induced catalepsy in respect to male controls. The present behavioral test may become a simple experimental model to detect new antidepressant or anxiolytic compounds and the significant sex difference could make the test a more useful tool in investigating anxiety behaviour in rodents.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9533172&dopt=Abstract
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