Moult Peter R, Schnabel Rebecca, Kilpatrick Ian C, Bashir Zafar I, Collingridge Graham L
MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, University Walk, Bristol BS8 1TD, UK.
Neuropharmacology. 2002 Aug;43(2):175-80. doi: 10.1016/s0028-3908(02)00110-7.
A form of long-term depression (LTD) of synaptic transmission can be induced by bath application of the group I metabotropic glutamate (mGlu) receptor agonist (RS)-3,5-dihydroxyphenylglycine (DHPG). The mechanisms responsible for the induction and expression of DHPG-induced LTD in the CA1 region of the hippocampus are currently the subject of intense investigation. Here we show that two protein tyrosine kinase (PTK) inhibitors (10 microM lavendustin A or 30 microM genistein) have little effect on DHPG-induced LTD. In contrast two protein tyrosine phosphatase (PTP) inhibitors (1 mM orthovanadate or 15 microM phenyl-arsine oxide) significantly inhibited DHPG-induced LTD. These data suggest that DHPG-induced LTD involves activation of a protein tyrosine phosphatase.
通过在浴槽中应用I型代谢型谷氨酸（mGlu）受体激动剂（RS）-3,5-二羟基苯甘氨酸（DHPG），可以诱导出一种突触传递的长期抑制（LTD）形式。目前，海马体CA1区中DHPG诱导的LTD的诱导和表达机制是深入研究的主题。在这里，我们表明两种蛋白酪氨酸激酶（PTK）抑制剂（10微摩尔拉芬斯汀A或30微摩尔染料木黄酮）对DHPG诱导的LTD影响很小。相比之下，两种蛋白酪氨酸磷酸酶（PTP）抑制剂（1毫摩尔原钒酸盐或15微摩尔苯胂氧化物）显著抑制了DHPG诱导的LTD。这些数据表明，DHPG诱导的LTD涉及蛋白酪氨酸磷酸酶的激活。
