Elsevier

Brain Research

Volume 160, Issue 2, 12 January 1979, Pages 307-326
Brain Research

A fine-grained anatomical analysis of the role of the rat suprachiasmatic nucleus in circadian rhythms of feeding and drinking

https://doi.org/10.1016/0006-8993(79)90427-XGet rights and content

Abstract

Recent experiments have suggested that the suprachiasmatic nuclei (SCN) represent a neural timekeeper responsible for the maintenance of circadian rhythms of sleeping, drinking, general activity, plasma corticosterone, and pinealN-acetyltransferase. A rigorous evaluation of this proposal has been hampered, however, by the fact that past experiments have employed lesions many times larger than the volume of the SCN. To test the hypothesis that the SCN, as such, are necessary for certain circadian rhythms, the present study examined periodic variations in feeding and drinking before and after small (i.e. median size: 75% of total SCN volume) radiofrequency lesions and discrete knife cuts in the area of the SCN. The two behaviors were monitored in 120 male rats over a 7-week period. The animal room, kept at a constant temperature, was on a 12:12 light-dark cycle. Eating and drinking data were grouped in 6 four-hour time bins per day and analyzed using both autocorrelation coefficients and light-dark ratios. Brain-damaged animals were compared with sham-operated controls and blinded rats.

Total damage to the suprachiasmatic nuclei, with little insult to adjacent areas (e.g. tractus infundibularis, supraoptic commissures. optic chiasm, area anterior to the SCN), was sufficient to eliminate circadian rhythms of both feeding and drinking. Conversely, lesions or knife cuts anterior, ventral or lateral to the SCN had little effect on the circadian rhythms. Damage directly posterior to the SCN abolished the circadian rhythms, probably by destroying efferents of the SCN. Loss of rhythms was sometimes seen with less than total destruction of the SCN. Rats with partial damage of the SCN showed a decrease in the autocorrelation coefficient describing their circadian rhythm. A computer-assisted procedure compared the three-dimensional reconstruction of each lesion with the circadian rhythm indicators, autocorrelation coefficients, and confirmed that the SCN and their immediate surround were necessary for the manifestation of circadian rhythms.

Destruction of at least 50% of the SCN was sometimes associated with the appearance of a significant 8-h ultradian rhythm. This ultradian rhythm was not seen in any sham-operated control or blinded rat.

The findings of the present study lend strong support to earlier suggestions that the SCN per se represent a critical area necessary for manifestation of certain circadian rhythms.

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    Present address and reprint requests to: Section of Neurosurgery, Yale University School of Medicine, New Haven, Ct. 06510, U.S.A.

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