Balduzzi Raffaella, Cupello Aroldo, Robello Mauro
Unità INFM, Dipartimento di Fisica, Università di Genova, Via Dodecaneso 33, 16146 Genoa, Italy.
Biochim Biophys Acta. 2002 Aug 19;1564(1):263-70. doi: 10.1016/s0005-2736(02)00460-1.
The expression of GABA(A) receptors in rat cerebellar granules in culture has been studied by beta(2/3) subunit immunocytochemistry and fluorescence confocal microscopy. These cells show labeling all over the cell bodies' plasma membrane and dendrites. Treatment with the protein tyrosine kinase (PTK) inhibitor genistein results in a decrease of the labeling associated with the beta(2/3) subunit in both cell bodies and dendrites. No effect was found with an inactive genistein analogue, daidzein. A similar effect was found with a protein kinase C (PKC) activator, phorbol myristate acetate (PMA). The effects of genistein and PMA are additive.The interpretation of the results is that PTK inhibition blocks exocytotic deposit of newly synthesized GABA(A) receptors onto the neuronal plasma membrane. On the other hand, PKC activation speeds up endocytotic removal of GABA(A) receptors.
通过β(2/3)亚基免疫细胞化学和荧光共聚焦显微镜研究了培养的大鼠小脑颗粒细胞中GABA(A)受体的表达。这些细胞在整个细胞体的质膜和树突上均显示出标记。用蛋白酪氨酸激酶（PTK）抑制剂染料木黄酮处理会导致细胞体和树突中与β(2/3)亚基相关的标记减少。而无活性的染料木黄酮类似物大豆苷元则没有效果。用蛋白激酶C（PKC）激活剂佛波酯肉豆蔻酸酯（PMA）处理也发现了类似的效果。染料木黄酮和PMA的作用是相加的。这些结果的解释是，PTK抑制作用会阻断新合成的GABA(A)受体向神经元质膜的胞吐沉积。另一方面，PKC激活会加速GABA(A)受体的内吞清除。
