蛋白激酶C的激活抑制了表达谷氨酸受体亚基的卵母细胞中由红藻氨酸诱导的电流。

Activation of protein kinase C inhibits kainate-induced currents in oocytes expressing glutamate receptor subunits.

作者信息

Dildy-Mayfield J E, Harris R A

机构信息

Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.

出版信息

J Neurochem. 1994 Apr;62(4):1639-42. doi: 10.1046/j.1471-4159.1994.62041639.x.

DOI:10.1046/j.1471-4159.1994.62041639.x

PMID:8133291

Abstract

The effect of protein kinase C (PKC) activation on maximal kainate (KA)-induced currents was studied in Xenopus oocytes expressing the glutamate receptor (GluR) subunits GluR3, GluR1 + 3, GluR2 + 3, and GluR6. The PKC activator phorbol 12-myristate 13-acetate (PMA) inhibited peak KA responses in a time-dependent manner. The magnitude of inhibition was greatest in GluR6-expressing oocytes. Desensitizing KA currents characterized by a peak, transient current followed by a slower, desensitizing current were observed in oocytes expressing GluR3 and GluR1 + 3 receptors. PMA inhibited the desensitization, and this effect could be observed before PMA's inhibition of peak current amplitude. PMA-mediated inhibition of both desensitization and peak current amplitude was prevented by intracellular injection of the protein kinase C (PKC) inhibitor peptide. These results suggest that the function of GluRs is regulated by PKC-dependent phosphorylation.

摘要

在表达谷氨酸受体（GluR）亚基GluR3、GluR1 + 3、GluR2 + 3和GluR6的非洲爪蟾卵母细胞中，研究了蛋白激酶C（PKC）激活对最大红藻氨酸（KA）诱导电流的影响。PKC激活剂佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯（PMA）以时间依赖性方式抑制KA反应峰值。在表达GluR6的卵母细胞中，抑制幅度最大。在表达GluR3和GluR1 + 3受体的卵母细胞中观察到了脱敏KA电流，其特征为峰值瞬态电流后跟随较慢的脱敏电流。PMA抑制脱敏作用，且这种效应可在PMA抑制峰值电流幅度之前观察到。通过细胞内注射蛋白激酶C（PKC）抑制肽可阻止PMA介导的对脱敏和峰值电流幅度的抑制。这些结果表明，GluRs的功能受PKC依赖性磷酸化调节。