Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 2, Pages 479-489Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3915-05.2006
Keywords
arrhythmia; behavior; circadian rhythms; desynchronization; Drosophila; sodium channel
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Funding
- 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
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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.
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