INHIBITION OF POSTSYNAPTIC PKC OR CAMKII BLOCKS INDUCTION BUT NOT EXPRESSION OF LTP
INHIBITION OF POSTSYNAPTIC PKC OR CAMKII BLOCKS INDUCTION BUT NOT EXPRESSION OF LTP
复制标题
DOI：
10.1126/science.2549638
复制
发表时间：
1989-08-25
期刊：
影响因子：
56.9
通讯作者：
TSIEN, RW
中科院分区：
文献类型：
--
作者：
MALINOW, R;SCHULMAN, H;TSIEN, RW
突触传递的长时程增强（LTP）是突触可塑性的一个广泛研究的细胞例子。然而，身份，定位和生化信号之间的相互作用，潜在的LTP仍然不清楚。细胞内微电极已被用于记录突触电位和传递蛋白激酶抑制剂到突触后CA 1锥体细胞。LTP的诱导被细胞内递送H-7（一种通用蛋白激酶抑制剂）或PKC（19-31）（一种选择性蛋白激酶C（PKC）抑制剂）或CaMKII（273-302）（一种多功能Ca 2 +-钙调蛋白依赖性蛋白激酶（CaMKII）的选择性抑制剂）阻断。建立后，LTP出现突触后H-7反应迟钝，虽然它仍然对外部应用H-7敏感。因此，突触后PKC和CaMKII都是诱导LTP所必需的，而突触前蛋白激酶似乎是LTP表达所必需的。
Long-term potentiation (LTP) of synaptic transmission is a widely studied cellular example of synaptic plasticity. However, the identity, localization, and interplay among the biochemical signals underlying LTP remain unclear. Intracellular microelectrodes have been used to record synaptic potentials and deliver protein kinase inhibitors to postsynaptic CA1 pyramidal cells. Induction of LTP is blocked by intracellular delivery of H-7, a general protein kinase inhibitor, or PKC(19-31), a selective protein kinase C (PKC) inhibitor, or CaMKII(273-302), a selective inhibitor of the multifunctional Ca2+-calmodulin-dependent protein kinase (CaMKII). After its establishment, LTP appears unresponsive to postsynaptic H-7, although it remains sensitive to externally applied H-7. Thus both postsynaptic PKC and CaMKII are required for the induction of LTP and presynaptic protein kinase appears to be necessary for the expression of LTP.