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首页> 外文期刊>The European Journal of Neuroscience >Calcineurin regulates induction of late phase of cerebellar long-term depression in rat cultured Purkinje neurons.
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Calcineurin regulates induction of late phase of cerebellar long-term depression in rat cultured Purkinje neurons.

机译：钙调神经磷酸酶调节大鼠培养的浦肯野神经元的小脑长期抑郁晚期的诱导。

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摘要

Cerebellar long-term depression (LTD), a candidate cellular mechanism of motor learning, is induced by conjunctive activation of parallel fibres and a climbing fibre. Previous studies have shown that combinatorial application of high potassium and glutamate (K/glu) to cultured cerebellar neurons can mimic this conjunctive stimulation of presynaptic fibres and induces the LTD of miniature excitatory postsynaptic current (mEPSC) amplitudes lasting for more than 24 h. The late phase of this LTD (LLTD, > 3 h) depends on de novo transcription induced by prolonged conditioning. Here, the role of Calcineurin in the LLTD induction was examined. Application of a Calcineurin inhibitor FK506 mimicked the effect of K/glu-treatment by decreasing mEPSC amplitudes for more than 24 h. FK506-induced depression, as well as the K/glu-induced LLTD, was blocked by inhibitors of either mRNA synthesis or Ca/Calmodulin dependent kinase. In addition, the FK506-induced depression and K/glu-induced LLTD occluded each other, suggesting that they share the same mechanism. On the other hand, misexpression of the constitutively active form of Calcineurin in the Purkinje neuron nucleus blocked the LLTD induction by the K/glu-treatment. These results suggest that Calcineurin is involved in the induction of LLTD as a negative regulator. Furthermore, it was found that trapping superoxide, which is increased by neuronal activity and inactivates Calcineurin, suppressed the LLTD induction. Taken together, these results suggest that the LLTD might be induced by down-regulation of Calcineurin activity through superoxide in cultured Purkinje neurons.
机译：小脑长期抑郁症（LTD）是运动学习的一种候选细胞机制，是由平行纤维和攀爬纤维的联合激活引起的。以前的研究表明，将高钾和谷氨酸（K / glu）组合应用到培养的小脑神经元可以模拟突触前纤维的这种联合刺激，并诱导持续超过24小时的微型兴奋性突触后电流（mEPSC）振幅的LTD。该LTD的晚期（LLTD，> 3 h）取决于长时间调节所引起的从头转录。在这里，研究了钙调神经磷酸酶在LLTD诱导中的作用。钙调神经磷酸酶抑制剂FK506的应用通过降低mEPSC幅度超过24小时来模仿K / glu处理的效果。 FK506诱导的抑郁以及K / glu诱导的LLTD被mRNA合成或Ca /钙调蛋白依赖性激酶的抑制剂阻断。此外，FK506诱导的抑郁症和K / glu诱导的LLTD相互闭塞，表明它们具有相同的机制。另一方面，钙调神经磷酸酶的组成型活性形式在浦肯野神经元核中的错误表达通过K / glu处理阻止了LLTD的诱导。这些结果表明钙调神经磷酸酶作为负调节剂参与了LLTD的诱导。此外，发现通过神经元活性增加并使钙调神经磷酸酶失活的超氧化物捕集抑制了LLTD的诱导。两者合计，这些结果表明，LLTD可能是由培养的浦肯野神经元中的过氧化物通过下调钙调神经磷酸酶活性而诱导的。

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