期刊
JOURNAL OF NEUROSCIENCE
卷 26, 期 2, 页码 479-489出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3915-05.2006
关键词
arrhythmia; behavior; circadian rhythms; desynchronization; Drosophila; sodium channel
资金
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [0757242] Funding Source: National Science Foundation
- Intramural NIH HHS Funding Source: Medline
- NIDA NIH HHS [R21 DA016352, R21 DA016352-02] Funding Source: Medline
- NINDS NIH HHS [R01 NS046750, R01 NS046750-04, R01-NS046750] Funding Source: Medline
Coupling of autonomous cellular oscillators is an essential aspect of circadian clock function but little is known about its circuit requirements. Functional ablation of the pigment-dispersing factor-expressing lateral ventral subset (LNV) of Drosophila clock neurons abolishes circadian rhythms of locomotor activity. The hypothesis that LN(V)s synchronize oscillations in downstream clock neurons was tested by rendering the LNVs hyperexcitable via transgenic expression of a low activation threshold voltage-gated sodium channel. When the LNVs are made hyperexcitable, free-running behavioral rhythms decompose into multiple independent superimposed oscillations and the clock protein oscillations in the dorsal neuron 1 and 2 subgroups of clock neurons are phase-shifted. Thus, regulated electrical activity of the LNVs synchronize multiple oscillators in the fly circadian pacemaker circuit.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据