Long-term changes in excitability induced by protein kinase C activation in Aplysia sensory neurons.
Long-term changes in excitability induced by protein kinase C activation in Aplysia sensory neurons.
复制标题
海兔感觉神经元中蛋白激酶 C 激活引起的兴奋性的长期变化。
DOI：
10.1152/jn.1998.79.3.1210
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Castellucci,VF
中科院分区：
文献类型：
--
作者：
Manseau,F;Sossin,WS;Castellucci,VF
Manseau, fracei, Wayne S. Sossin和Vincent F. Castellucci。蛋白激酶C活化对大鼠神经兴奋性的影响。中国生物医学工程学报，2009,31(2):387 - 398。蛋白激酶A （PKA）和C （PKC）在学习障碍的简单形式中起着细胞内转导的核心作用。这两种蛋白质似乎以一种状态和时间依赖的方式协同调节防御反射行为改变的不同形式的可塑性。虽然机械感觉神经元和反射运动神经元之间连接的突触效能的短期和长期变化已经被很好地表征，但也有一个明显的可塑性中间阶段尚未被很好地理解。生化和生理实验表明PKC在诱导和表达这种形式的促进中起作用。在本报告中，我们证明PKC激活可以诱导感觉神经元（SNs）兴奋性的中期和长期变化。短时间应用4β-苯酚酯12,13-二丁酸酯（PDBU），一种有效的PKC激活剂，在去极化电流脉冲下，SNs激发的尖峰数量持续增加。这种效应在分离细胞培养和完整神经节中观察到；它被一种选择性PKC抑制剂（chelerythrine）阻断。有趣的是，在治疗后的中期时间点（3小时）测量的兴奋性增加与蛋白质合成无关，而在长期时间点（24小时）被一般蛋白质合成抑制剂大霉素破坏。除了表明PKC和PKA参与了持久的兴奋性变化之外，这些发现还支持了记忆形成涉及多个阶段的观点，这些阶段在生化水平上是机械不同的。
Manseau, Frédéric, Wayne S. Sossin, and Vincent F. Castellucci.Long-term changes in excitability induced by protein kinase C activation inAplysiasensory neurons.J. Neurophysiol.79: 1210–1218, 1998. Protein kinases A (PKA) and C (PKC) play a central role as intracellular transducers during simple forms of learning inAplysia. These two proteins seem to cooperate in mediating the different forms of plasticity underlying behavioral modifications of defensive reflexes in a state- and time-dependent manner. Although short- and long-term changes in the synaptic efficacy of the connections between mechanosensory neurons and motoneurons of the reflex have been well characterized, there is also a distinct intermediate phase of plasticity that is not as well understood. Biochemical and physiological experiments have suggested a role for PKC in the induction and expression of this form of facilitation. In this report, we demonstrate that PKC activation can induce both intermediate- and long-term changes in the excitability of sensory neurons (SNs). Short application of 4β-phorbol ester 12,13-dibutyrate (PDBU), a potent activator of PKC, produced a long-lasting increase in the number of spikes fired by SNs in response to depolarizing current pulses. This effect was observed in isolated cell culture and in the intact ganglion; it was blocked by a selective PKC inhibitor (chelerythrine). Interestingly, the increase in excitability measured at an intermediate-term time point (3 h) after treatment was independent of protein synthesis, while it was disrupted at the long-term (24 h) time point by the general protein synthesis inhibitor, anisomycin. In addition to suggesting that PKC as well as PKA are involved in long-lasting excitability changes, these findings support the idea that memory formation involves multiple stages that are mechanistically distinct at the biochemical level.
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DOI：
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