Gating of CaMKII by cAMP-regulated protein phosphatase activity during LTP

被引:338
作者
Blitzer, RD [1 ]
Conner, JH
Brown, GP
Wong, T
Shenolikar, S
Iyengar, R
Landau, EM
机构
[1] Bronx VA Med Ctr, New York, NY 10029 USA
[2] CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA
[3] Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC 27712 USA
[4] CUNY Mt Sinai Sch Med, Dept Pharmacol, New York, NY 10029 USA
关键词
D O I
10.1126/science.280.5371.1940
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Long-term potentiation (LTP) at the Schaffer collateral-CA1 synapse involves interacting signaling components, including calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) pathways. Postsynaptic injection of thiophosphorylated inhibitor-1 protein, a specific inhibitor of protein phosphatase-1 (PP1), substituted for cAMP pathway activation in LTP. Stimulation that induced LTP triggered cAMP-dependent phosphorylation of endogenous inhibitor-1 and a decrease in PP1 activity. This stimulation also increased phosphorylation of CaMKII at Thr(286) and Ca2+-independent CaMKII activity in a cAMP-dependent man ner. The blockade of LTP by a CaMKII inhibitor was not overcome by thiophosphorylated inhibitor-1. Thus, the cAMP pathway uses PP1 to gate CaMKII signaling in LTP.
引用
收藏
页码:1940 / 1943
页数:4
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