Clock mutation lengthens the circadian period without damping rhythms in individual SCN neurons.
Spontaneous discharges of individual neurons in the suprachiasmatic nucleus (SCN) of Clock mutant mice were recorded for over 5 days in organotypic slice cultures and dispersed cell cultures using a multi-electrode dish. Circadian rhythms with periods of about 27 hours were detected in 77% of slice cultures and 15% of dispersed cell cultures derived from Clock/Clock homozygotes. These findings indicate that the Clock mutation lengthens the circadian period but does not abolish the circadian oscillation, and suggest an important role of intercellular communication in the expression of circadian rhythm in the SCN.
Nakamura
Wataru
W
Department of Physiology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.
Honma
Sato
S
Shirakawa
Tetsuo
T
Honma
Ken-ichi
K
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001683:Biological Clocks / Q000502:physiology; D056926:CLOCK Proteins; D002940:Circadian Rhythm / Q000502:physiology; D066298:In Vitro Techniques; D051379:Mice; D008817:Mice, Mutant Strains; D009154:Mutation; D009474:Neurons / Q000378:metabolism*; D010507:Periodicity; D013493:Suprachiasmatic Nucleus / Q000166:cytology / Q000378:metabolism*; D013997:Time Factors; D015534:Trans-Activators / Q000235:genetics* / Q000378:metabolism
D015534:Trans-Activators; D056926:CLOCK Proteins; C538944:Clock protein, mouse