Journal article
A neuronal ryanodine receptor mediates light-induced phase delays of the circadian clock
Nature (London), Vol.394(6691), pp.381-384
07/23/1998
DOI: 10.1038/28639
PMID: 9690474
Abstract
Circadian clocks are complex biochemical systems that cycle with a period of approximately 24 hours. They integrate temporal information regarding phasing of the solar cycle, and adjust their phase so as to synchronize an organism's internal state to the local environmental day and night,. Nocturnal light is the dominant regulator of this entrainment. In mammals, information about nocturnal light is transmitted by glutamate released from retinal projections to the circadian clock in the suprachiasmatic nucleus of the hypothalamus. Clock resetting requires the activation of ionotropic glutamate receptors, which mediate Ca2+ influx. The response induced by such activation depends on the clock's temporal state: during early night it delays the clock phase, whereas in late night the clock phase is advanced. To investigate this differential response, we sought signalling elements that contribute solely to phase delay. We analysed intracellular calcium-channel ryanodine receptors, which mediate coupled Ca2+ signalling. Depletion of intracellular Ca2+ stores during early night blocked the effects of glutamate. Activators of ryanodine receptors induced phase resetting only in early night; inhibitors selectively blocked delays induced by light and glutamate. These findings implicate the release of intracellular Ca2+ through ryanodine receptors in the light-induced phase delay of the circadian clock restricted to the early night.
Details
- Title: Subtitle
- A neuronal ryanodine receptor mediates light-induced phase delays of the circadian clock
- Creators
- Dong Chen - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramShelley A Tischkau - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramKevin P Campbell - Howard Hughes Medical Institute and Department of Physiology, College of Medicine, University of IowaLia E Faiman - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramLiana Kuriashkina - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramJoan M Alster - Computing and Communications Services Office, University of IllinoisMartha U Gillette - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramJian M Ding - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience ProgramPeter S McPherson - Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill UniversityGordon F Buchanan - Departments of Cell and Structural Biology, Molecular and Integrative Physiology, the Neuroscience Program
- Resource Type
- Journal article
- Publication Details
- Nature (London), Vol.394(6691), pp.381-384
- DOI
- 10.1038/28639
- PMID
- 9690474
- ISSN
- 0028-0836
- eISSN
- 1476-4687
- Language
- English
- Date published
- 07/23/1998
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute
- Record Identifier
- 9984020650802771
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