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Published on: May 27, 2010
Interval timing is intact in arrhythmic Cry1/Cry2-deficient mice.
Efstathios B Papachristos1, Edwin H Jacobs, Ype Elgersma
1Department of Neuroscience, Erasmus University Medical Center, Rotterdam, the Netherlands. stathis.papachristos@gmail.com
Journal of Biological Rhythms
|July 22, 2011
Summary
Mice lacking the Cry1 and Cry2 genes showed normal interval timing, suggesting these genes are not essential for this process. This indicates separate biological mechanisms for circadian and interval timing in the brain.
Area of Science:
- Neuroscience
- Chronobiology
- Molecular Biology
Background:
- The brain's ability to track time is crucial for daily functioning, yet impaired in disorders like schizophrenia.
- The molecular basis of circadian (24-hour) timing is understood, but interval timing (seconds to hours) remains unclear.
- It is unknown if circadian and interval timing share common biological mechanisms.
Purpose of the Study:
- To investigate the role of the circadian clock genes Cry1 and Cry2 in interval timing.
- To determine if the circadian clock is necessary for accurate interval timing.
Main Methods:
- Cry1/Cry2 double knockout mice were trained on an interval timing task.
- Mice were maintained under constant light conditions to eliminate external time cues.
- Temporal memory accuracy and precision were assessed in knockout and control mice.
Main Results:
- Cry1/Cry2 knockout mice exhibited interval timing performance comparable to control mice.
- The absence of Cry1 and Cry2 did not impair temporal memory accuracy or precision.
- Proper interval timing calibration was observed independently of a functional circadian clock.
Conclusions:
- The Cry1 and Cry2 genes are not critical components of the interval timing system.
- Circadian clock genes and mechanisms are not required for interval timing.
- Circadian and interval timing likely operate via distinct and independent biological pathways.

