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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Aberrant gating of photic input to the suprachiasmatic circadian pacemaker of mice lacking the VPAC2 receptor.
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Aberrant gating of photic input to the suprachiasmatic circadian pacemaker of mice lacking the VPAC2 receptor.

机译：缺乏VPAC2受体的小鼠视交叉上生物钟起搏器的光输入异常门控。

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摘要

VIP acting via the VPAC(2) receptor is implicated as a key signaling pathway in the maintenance and resetting of the hypothalamic suprachiasmatic nuclei (SCN) circadian pacemaker; circadian rhythms in SCN clock gene expression and wheel-running behavior are abolished in mice lacking the VPAC(2) receptor (Vipr2(-/-)). Here, using immunohistochemical detection of pERK (phosphorylated extracellular signal-regulated kinases 1/2) and c-FOS, we tested whether the gating of photic input to the SCN is maintained in these apparently arrhythmic Vipr2(-/-) mice. Under light/dark and constant darkness, spontaneous expression of pERK and c-FOS in the wild-type mouse SCN was significantly elevated during subjective day compared with subjective night; no diurnal or circadian variation in pERK or c-FOS was detected in the SCN of Vipr2(-/-) mice. In constant darkness, light pulses given during the subjective night but not the subjective day significantly increased expression of pERK and c-FOS in the wild-type SCN. In contrast, light pulses given during both subjective day and subjective night robustly increased expression of pERK and c-FOS in the Vipr2(-/-) mouse SCN. Although photic stimuli activate intracellular pathways within the SCN of Vipr2(-/-) mice, they do not engage the core clock mechanisms. The absence of photic gating, together with the general lack of overt rhythms in circadian output, strongly suggests that the SCN circadian pacemaker is completely dysfunctional in the Vipr2(-/-) mouse.
机译：通过VPAC（2）受体起作用的VIP参与维持和复位下丘脑超视交叉核（SCN）昼夜节律起搏器;在缺少VPAC（2）受体（Vipr2（-/-））的小鼠中，SCN时钟基因表达和昼夜运转行为的昼夜节律被消除。在这里，使用pERK（磷酸化的细胞外信号调节激酶1/2）和c-FOS的免疫组织化学检测，我们测试了在这些明显心律不齐的Vipr2（-/-）小鼠中是否维持了对SCN的光输入。在明亮/黑暗和恒定黑暗中，与主观夜晚相比，在主观白天，野生型小鼠SCN中pERK和c-FOS的自发表达明显升高;在Vipr2（-/-）小鼠的SCN中未检测到pERK或c-FOS的昼夜变化或昼夜节律变化。在持续的黑暗中，在主观夜晚而非主观白天给予的光脉冲显着增加了野生型SCN中pERK和c-FOS的表达。相反，在主观白天和主观夜晚都给予的光脉冲会在Vipr2（-/-）小鼠SCN中强烈增强pERK和c-FOS的表达。尽管光刺激激活Vipr2（-/-）小鼠的SCN内的细胞内通路，但它们不参与核心时钟机制。缺乏光控门控，以及昼夜节律输出中普遍缺乏明显的节律，强烈表明SCN昼夜节律起搏器在Vipr2（-/-）小鼠中完全功能失调。

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