Demonstration of presynaptic protein kinase C activation following long-term potentiation in rat hippocampal slices.
Demonstration of presynaptic protein kinase C activation following long-term potentiation in rat hippocampal slices.
复制标题
大鼠海马切片长期增强后突触前蛋白激酶 C 激活的演示。
DOI：
10.1016/0306-4522(93)90406-6
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发表时间：
1993
期刊：
影响因子：
3.3
通讯作者：
Vallano,ML
中科院分区：
文献类型：
--
作者：
Leahy,JC;Luo,Y;Kent,CS;Meiri,KF;Vallano,ML
Pharmacological and biochemical evidence implicate the Ca2+and phospholipid-dependent protein kinase C in long-term potentiation. Thein vitrohippocampal slice preparation was used to demonstrate redistribution of protein kinase C from cytosol to membrane and protein kinase C-dependent phosphorylation of the presynaptic growth-associated protein-43 substrate following long-term potentiation induction in area CA1. Protein kinase C translocation was assessed using both quantitative immunoblotting with a monoclonal antibody recognizing a common epitope in the α and β isoforms of protein kinase C and Ca2+and phospholipid-dependent phosphorylation of exogenous histone substrate. Slices examined 5 min after tetanus-induced spike potentiation showed no change in protein kinase C redistribution, whereas slices examined at 15-, 30- and 60-min intervals all showed a similar degree of protein kinase C translocation to membrane, although only at 15 min was the effect statistically significant. Additionally, an increase in protein kinase C-dependent growth-associated protein 43 phosphorylation was observed 10 min after high-frequency stimulation. The translocation of protein kinase C and phosphorylation of growth-associated protein 43 were dependent upon high-frequency (repetitive 400 Hz) afferent stimulation, as no effects were observed in slices receiving low-frequency (1 Hz) or no stimulation. TheN-methyl-d-aspartate receptor antagonist,dl-2-amino-5-phosphonovaleric acid (50 μM), inhibited induction of long-term potentiation, redistribution of protein kinase C and phosphorylation of growth-associated protein 43. A significant redistribution of the predominantly presynaptic protein kinase C isoform, protein kinase C-α, was also detected 15 min after induction of long-term potentiation using an α-isoform-specific monoclonal antibody. These observations support a presynaptic role for protein kinase C and growth-associated protein 43 in the early maintenance phase of LTP, and further suggest that a retrograde messenger produced postsynaptically followingN-methyl-d-aspartate receptor activation mediates these effects.
