Different Roles for VIP Neurons in the Neonatal and Adult Suprachiasmatic Nucleus.
Different Roles for VIP Neurons in the Neonatal and Adult Suprachiasmatic Nucleus.
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DOI：
10.1177/0748730420932073
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发表时间：
2020-10
影响因子：
3.5
通讯作者：
Herzog ED
中科院分区：
文献类型：
--
作者：
Mazuski C;Chen SP;Herzog ED
视交叉上核（SCN）通过耦合的单细胞振荡驱动运动中的昼夜节律。神经肽Vip或其受体Vipr2的整体遗传缺失导致SCN细胞之间的日常同步性以及运动行为和糖皮质激素分泌的日常节律严重不足。为了测试这种表型是否依赖于SCN中的VIP神经元，我们通过caspase3介导的表达cree的VIP神经元的凋亡通路，在成年雄性小鼠体内切除VIP SCN神经元。我们发现成年小鼠VIP SCN神经元的消融导致了与VIP和Vipr2缺失小鼠不同的表型。缺乏VIP神经元的小鼠保持有节奏的运动活动，昼夜节律周期缩短，起病变化更大，每日活动持续时间缩短。昼夜激素的输出，特别是皮质酮的节律受到严重抑制。相比之下，新生儿SCN VIP神经元的缺失显著降低了培养的SCN中昼夜节律基因的表达，模仿了VIP或Vipr2的整体缺失的效果。这些结果表明，SCN VIP神经元在延长成人昼夜节律周期和刺激糖皮质激素的日常激增以及在发育中的SCN中同步和维持细胞之间的日常节律中发挥作用。
The suprachiasmatic nucleus (SCN) drives circadian rhythms in locomotion through coupled, single-cell oscillations. Global genetic deletion of the neuropeptide, Vip or its receptor Vipr2, results in profound deficits in daily synchrony among SCN cells and daily rhythms in locomotor behavior and glucocorticoid secretion. To test whether this phenotype depends on VIP neurons in the SCN, we ablated VIP SCN neurons in vivo in adult, male mice through Caspase3-mediated induction of the apoptotic pathway in cre-expressing VIP neurons. We found that ablation of VIP SCN neurons in adult mice caused a phenotype distinct from Vip- and Vipr2- null mice. Mice lacking VIP neurons retained rhythmic locomotor activity with a shortened circadian period, more variable onsets and decreased duration of daily activity. Circadian hormonal outputs, specifically corticosterone rhythms were severely dampened. In contrast, deletion of neonatal SCN VIP neurons dramatically reduced circadian gene expression in the cultured SCN, mimicking the effects of global deletion of Vip or Vipr2. These results suggest that SCN VIP neurons play a role in lengthening circadian period and stimulating the daily surge in glucocorticoids in adults and in synchronizing and sustaining daily rhythms among cells in the developing SCN.
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影响因子：
16.2
作者：
Mazuski C;Abel JH;Chen SP;Hermanstyne TO;Jones JR;Simon T;Doyle FJ 3rd;Herzog ED
通讯作者：
Herzog ED
影响因子：
7.2
作者：
Herzog, Erik D.;Hermanstyne, Tracey;Hastings, Michael H.
通讯作者：
Hastings, Michael H.
影响因子：
64.8
作者：
Gueler, Ali D.;Ecker, Jennifer L.;Hattar, Samer
通讯作者：
Hattar, Samer
影响因子：
4.1
作者：
Loh, Dawn H.;Abad, Catalina;Waschek, James A.
通讯作者：
Waschek, James A.
影响因子：
3.4
作者：
Reed, HE;Meyer-Spasche, A;Piggins, HD
通讯作者：
Piggins, HD