Modulation of Protein Kinase C and cAMP-Dependent Protein Kinase by δ-Opioid

doi:10.1006/bbrc.1997.7027

Biochemical and Biophysical Research Communications

Volume 236, Issue 3, 30 July 1997, Pages 626-629

https://doi.org/10.1006/bbrc.1997.7027 Get rights and content

Abstract

Modulation of protein kinase C (PKC) and cAMP-dependent protein kinase (PKA) activities by δ-opioid receptor specific agonist [d-Pen²,d-Pen⁵]-enkephalin (DPDPE) was investigated in neuroblastoma × glioma hybrid NG 108-15 cells. DPDPE activated PKC in a dose-dependent manner, with the maximal response at 5 min. The DPDPE-stimulated PKC activation could be blocked by naltrindole. The activation of PKC by DPDPE was dependent on Ca²⁺and was inhibited by chelerythrine chloride (10 μM), but not by H89 (1 μM). Pretreatment of NG 108-15 cells with pertussis toxin (100 ng/ml for 24 h) completely abolished DPDPE-stimulated PKC activation. In contrast to the result from the acute treatment with DPDPE, which had no significant effect on PKA activity, chronic treatment of DPDPE (1 μM for 24 h) increased PKA activity, but reduced the basal activity of PKC. These results demonstrated that DPDPE differentially modulated PKC and PKA activities via a receptor-mediated, PTX sensitive pathway.

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Neurosteroid dehydroepiandrosterone sulfate enhances spontaneous glutamate release in rat prelimbic cortex through activation of dopamine D1 and sigma-1 receptor
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Citation Excerpt :
The assay was based on the change in the net charge of the fluorescent PKA substrate before and after phosphorylation. The change in the net charge of the substrate allowed the phosphorylated and nonphosphorylated version of the substrate to be rapidly separated on an agarose gel at neutral pH. The intensity of the fluorescence of phosphorylated peptides was measured (Lou and Pei, 1997) and the number of units of kinase activity in each slice of agarose was calculated as per the manufacturer's instructions (Promega). Off-line data analysis was performed using Mini Analysis Program (Synaptosoft), SigmaPlot (Jandel Scientific) and Origin (Microcal Software Inc.).
This paper studied the effect of neurosteroid dehydroepiandrosterone sulfate on spontaneous glutamate release in the prelimbic cortex by using electrophysiological and biochemical methods combined with a pharmacological approach and made some comparisons with those in the hippocampus. The results showed that dehydroepiandrosterone sulfate increased the frequency of miniature excitatory postsynaptic currents in the prelimbic cortex and hippocampus; sigma-1 receptor antagonist partially blocked the effect of dehydroepiandrosterone sulfate in the prelimbic cortex, but completely blocked it in the hippocampus; D1 receptor antagonist, adenylyl cyclase inhibitor and protein kinase A inhibitor completely blocked the effect of dehydroepiandrosterone sulfate in the prelimbic cortex; dehydroepiandrosterone sulfate increased the activity of protein kinase A in the prelimbic cortex and hippocampus; the effect of dehydroepiandrosterone sulfate on protein kinase A was completely blocked by sigma-1 receptor antagonist in the hippocampus, but was partially blocked in the prelimbic cortex; interestingly, here again, the effect of dehydroepiandrosterone sulfate on protein kinase A was completely blocked by D1 receptor antagonist in the prelimbic cortex. These results suggest that dehydroepiandrosterone sulfate promotes presynaptic glutamate release in the prelimbic cortex via activation of D1 and sigma-1 receptors.
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Citation Excerpt :
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Regular ArticleModulation of Protein Kinase C and cAMP-Dependent Protein Kinase by δ-Opioid

Abstract

Neuron

J. Biol. Chem.

Mol. Cell Endocr.

Brain Res.

Brain Res.

Pain

Biochem. Biophys. Res. Commun.

Eur. J. Pharmacol.

FEBS Lett.

J. Biol. Chem.

Brain Res.

Neuroscience

Clin. Neuropharmacol.

Regular Article
Modulation of Protein Kinase C and cAMP-Dependent Protein Kinase by δ-Opioid