Department of Physiology and Biophysics, School of Medicine, Eulji University, Daejeon 301-746, Republic of Korea.
Neuroscience. 2012 Dec 13;226:348-55. doi: 10.1016/j.neuroscience.2012.08.055. Epub 2012 Sep 15.
Activation of protein kinase C (PKC) by bryostatin-1 affects various functions of the central nervous system. We explored whether bryostatin-1 influenced synaptic plasticity via a process involving PKC. Our purpose was to examine whether bryostatin-1 affected the induction of hippocampal long-term potentiation (LTP) in Schaffer-collateral fibers (CA1 fibers) of the hippocampus, and/or influenced the intracellular Ca(2+) level of hippocampal neurons. We also determined the PKC isoforms involved in these processes. We found that bryostatin-1 strongly facilitated LTP induction, in a dose-dependent manner, upon single-theta burst stimulation (TBS). Further, intracellular Ca(2+) levels also increased with increasing concentration of bryostatin-1. The facilitative effects of bryostatin-1 in terms of LTP induction and enhancement of intracellular Ca(2+) levels were blocked by specific inhibitors of PKCα and PKCε, but not of PKCδ. Our results suggest that bryostatin-1 is involved in neuronal functioning and facilitates induction of LTP via activation of PKCα and/or PKCε.
岩沙海葵毒素-1 通过激活蛋白激酶 C（PKC）影响中枢神经系统的各种功能。我们探索了岩沙海葵毒素-1 是否通过涉及 PKC 的过程影响突触可塑性。我们的目的是检查岩沙海葵毒素-1 是否影响海马 CA1 纤维中突触长时程增强（LTP）的诱导，和/或影响海马神经元的细胞内 Ca(2+)水平。我们还确定了参与这些过程的 PKC 同工型。我们发现岩沙海葵毒素-1 在单次 theta 爆发刺激（TBS）下以剂量依赖性方式强烈促进 LTP 诱导。此外，细胞内 Ca(2+)水平也随岩沙海葵毒素-1 浓度的增加而增加。PKCα 和 PKCε 的特异性抑制剂而非 PKCδ 可阻断岩沙海葵毒素-1 在 LTP 诱导和增强细胞内 Ca(2+)水平方面的促进作用。我们的结果表明，岩沙海葵毒素-1 参与神经元功能，并通过激活 PKCα 和/或 PKCε 促进 LTP 的诱导。
