EFFECTS OF CAMP SIMULATE A LATE-STAGE OF LTP IN HIPPOCAMPAL CA1 NEURONS
EFFECTS OF CAMP SIMULATE A LATE-STAGE OF LTP IN HIPPOCAMPAL CA1 NEURONS
复制标题
DOI：
10.1126/science.8389057
复制
发表时间：
1993-06-11
期刊：
影响因子：
56.9
通讯作者：
KANDEL, ER
中科院分区：
文献类型：
--
作者：
FREY, U;HUANG, YY;KANDEL, ER
海马体长时程增强(LTP)被认为是在哺乳动物大脑中建立某些形式的外显记忆的基本机制。与行为记忆的情况一样，CA1区的LTP有几个阶段：一个持续1-3小时的短期早期增强，它独立于蛋白质合成，先于一个更晚、更长时间的阶段(L-LTP)，后者需要蛋白质合成。环磷酸腺苷(CAMP)依赖的蛋白激酶(PKA)抑制剂阻断L-LTP，cAMP类似物诱导的增强作用可阻断自然诱导的L-LTP。CAMP类似物的作用可被蛋白质合成的抑制剂阻断。因此，PKA的激活可能是L-LTP发生机制的一个组成部分。
Hippocampal long-term potentiation (LTP) is thought to serve as an elementary mechanism for the establishment of certain forms of explicit memory in the mammalian brain. As is the case with behavioral memory, LTP in the CA1 region has stages: a short-term early potentiation lasting 1 to 3 hours, which is independent of protein synthesis, precedes a later, longer lasting stage (L-LTP), which requires protein synthesis. Inhibitors of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) blocked L-LTP, and analogs of cAMP induced a potentiation that blocked naturally induced L-LTP. The action of the cAMP analog was blocked by inhibitors of protein synthesis. Thus, activation of PKA may be a component of the mechanism that generates L-LTP.