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首页> 外文期刊>The European Journal of Neuroscience >Involvement of T-type Ca2+ channels in the potentiation of synaptic and visual responses during the critical period in rat visual cortex.
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Involvement of T-type Ca2+ channels in the potentiation of synaptic and visual responses during the critical period in rat visual cortex.

机译：在大鼠视觉皮层的关键时期，T型Ca2 +通道参与了突触和视觉反应的增强。

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Neocortical neuronal circuits are refined by experience during the critical period of early postnatal life. The shift of ocular dominance in the visual cortex following monocular deprivation has been intensively studied to unravel the mechanisms underlying the experience-dependent modification. Synaptic plasticity is considered to be involved in this process. We previously showed in layer 2/3 pyramidal neurons of rat visual cortex that low-frequency stimulation-induced long-term potentiation (LTP) at excitatory synapses, which requires the activation of Ni(2+)-sensitive (R-type or T-type) voltage-gated Ca(2+) channels (VGCCs) for induction, shared a similar age and experience dependence with ocular dominance plasticity. In this study, we examined whether this LTP is involved in ocular dominance plasticity. In visual cortical slices, LTP was blocked by mibefradil, kurtoxin and R-(-)-efonidipine, T-type VGCC blockers, but not by SNX-482, an R-type VGCC blocker, indicating that LTP induction requires T-type VGCC activation. Mibefradil did not affect synaptic transmission even at a dose about 30 times higher than that required for LTP blockade. Therefore, this drug was used to test the effect of T-type VGCC blockade on ocular dominance shift produced by 6 days of monocular deprivation during the critical period using visual evoked potentials (VEPs). Although this monocular deprivation commonly produced both depression of deprived eye responses and potentiation of nondeprived eye responses, only the former change occurred when mibefradil was infused into the visual cortex during monocular deprivation. Mibefradil infusion produced no acute effects on VEPs. These results suggest that T-type VGCC-dependent LTP contributes to the experience-dependent enhancement of visual responses.
机译：在出生后早期的关键时期，经验会完善新皮质神经元回路。深入研究了单眼剥夺后视觉皮质中眼优势的转移，以揭示依赖于经验的修饰的机制。突触可塑性被认为与该过程有关。我们先前在大鼠视觉皮层的2/3层锥体神经元中表明，低频刺激在兴奋性突触中诱导长期增强（LTP），这需要激活Ni（2+）敏感的（R型或T型型）电压门控Ca（2+）通道（VGCC）的感应，共享相似的年龄，并经历与眼优势可塑性的依赖。在这项研究中，我们检查了这种LTP是否与眼部优势可塑性有关。在视觉皮层切片中，LTP被米贝拉地尔，kurtoxin和R-（-）-efonidipine T型VGCC阻断剂阻断，但未被SNX-482（R型VGCC阻断剂）阻断，这表明LTP诱导需要T型VGCC激活。咪贝地尔不影响突触传递，即使其剂量比LTP阻断所需的剂量高约30倍。因此，该药物用于使用视觉诱发电位（VEP）来测试T型VGCC阻滞对关键时期单眼剥夺6天所产生的眼优势转移的影响。尽管这种单眼剥夺通常会同时导致被剥夺的眼睛反应的压抑和未剥夺的眼睛反应的增强，但是当单眼剥夺期间将咪贝夫地尔注入到视皮层时，只有前一种变化发生。咪贝地尔输注对VEP没有产生急性影响。这些结果表明，T型VGCC依赖性LTP有助于视觉响应的经验依赖性增强。

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