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The effect of chronic treatment with imipramine on the G-proteins mRNA level in the rat hippocampus - an interaction with a calcium channel antagonist

100%
Lason W., Przewlocki R.
Polish Journal of Pharmacology
|
1993
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vol. 45
|
issue 2
219-226
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.
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Sphingolipid derivatives modulate intracellular Ca2+ in rat synaptosomes

88%
Miguel B. G., Calcerrada M. C., Catalan R. E., Martinez A. M.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 2
113-117
EN
Sphingosylphosphorylcholine (SPC) induces a rapid increase of intracellular Ca2+ concentration in isolated synaptosomes. This effect is dose-dependent and is also dependent on extracellular Ca2+. Sphingosine (SPH) has a smaller effect and treatment with psychosine (PSY) is ineffective, which suggests that phosphorylation of the 1-carbon of SPH is required for the SPC to act as a Ca2+ release agonist in synaptosomes. Experiments performed in the presence of heparin or ryanodine indicate that SPC-elicited Ca2+ release is not mediated by IP3 or ryanodine receptors. Finally, our results show that the effect of SPC on Ca2+ concentration is nimodipine-sensitive, suggesting that SPC possibly activates a specific sphingolipid-gated Ca2+ channel in synaptosomes.
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