Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
enabled [disable] Abstract
Number of results

Results found: 8

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  NIFEDIPINE
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
EN
Chronic, but not acute, electroconvulsive treatment reduced the immobility time of rats in the forced swimming test; nifedipine facilitated that effect.
EN
Chronic electroconvulsive treatment applied immediately after a training session or with a 15 min delay impairs spatial learning and memory in the Morris water maze paradigm, and this impairment is not counteracted, but rather aggravated by co-administration of a calcium channel blocker, nifedipine.
EN
Chronic administration of nifedipine (5 mg/kg/day for 10 days) induced some biochemical effects consistent with those of antidepressants: a significant depression in cortical alfa2-adrenoceptor density and reduction of beta-adrenoceptor affinity; nifedipine co-administration with electroconvulsive treatment potentiated the beta-downregulatory effect of the latter.
EN
The effect of long-term administration of imipramine (10 mg/kg po, twice daily, 30 days) with or without nifedipine (5 mg/kg ip, twice daily, 28 days) on the G protein alfa subunit, Gs-alfa, Go-alfa and Gi-alfa mRNA levels was investigated in the rat hippocampus. An in situ hybridization histochemistry showed that imipramine decreased the Go-alfa mRNA level in CA1 (by ca. 40%) and CA3 (by ca. 37%) hippocampal fields and, to a lesser extent, in the dentate gyrus (by ca. 25%), but had no effect on the Gs-alfa and Gi-alfa mRNA levels in those structures. Nifedipine decreased (by ca. 30%) the Gs-alfa level in the studied fields of hippocampal formation, having no imfluence on the level of mRNA which codes other subunits of G protein, Coadministration of nifedipine and imipramine reversed the imipramine effect on Go-alfa, but had no effect on the nifedipine induced decrease at the Gs-alfa mRNA level. These results suggest that inhibition of L calcium channels modifies the effect of imipramine at the level of intracellular signal transduction.
EN
Nifedipine administered for either 10 or 28 dayz did not affect the cAMP response to noradrenalina or isoproterenol; however it decreased the inhibitory effect of ECS on the noradrenaline-stimulated cAMP generation.
EN
A 7-day incubation of neuronal and glial cells with (2 myM) did not reduce cAMP response to or , however such an effect was observed when the cells were incubated with imipramine in the calcium channel antagonist nifedipine (1myM).
EN
Chronic co-administration of nifedipine and ECT or imipramine results in an increase in responsiveness of cerebral cortical alfa1-adrenoceptor as measured by accumulation of inositol phosphate in cortical slices after noradrenaline stimulation; the responsiveness of beta-adrenoceptor, measured by accumulation of cyclic AMP, was depressed similarly by antidepressant treatment with and without nifedipine.
EN
This is an overview of the symposium concerned with the action of electroconvulsive treatment and some antidepressant drugs (mainly imipramine) applied during blockade of voltage-dependent calcium channels with nifedipine. The results in general suggest that a combination of calcium channel blockers with antidepressant drugs of ECT may be of clinical value in treatment of depression.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.