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Pineal N-Acetyltransferase Activity in 10-Day-Old Rats: A Paradigm for Studying the Developing Circadian System^*

Laboratory of Developmental Chronobiology, Children’s Service, Massachusetts General Hospital, and Harvard Medical School Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Dr. Steven M. Reppert, Children’s Service, Massachusetts General Hospital, Boston, Massachusetts 02114.

Abstract

Pineal N-acetyltransferase (NAT) activity in 10-day-old rat pups was used to examine several aspects of the developing circadian timing system. When born and reared under constant darkness, 10-day-old animals manifested a clear daily rhythm of NAT activity whose phase was in time with the estimated circadian time of the mother (set by the lighting cycle during pregnancy). When pups were reared in constant darkness from birth by a foster mother whose circadian time was 180° (12 h) out of phase with that of the natural mother, the resulting population profiles of NAT activity were arrhythmic. Analysis of the individual litter profiles from this experiment showed a variable postnatal influence of the maternal circadian system on the timing of the developing circadian system. Neither cross-fostering per se nor social interactions among litter mates contributed significantly to the apparent maternal influence. The magnitude of the postnatal maternal influence was not the same throughout development, but was most apparent during the first 5 days of life. Neonatal blinding (within 24 h of birth) did not appreciably alter the maternal influence. Extraretinal photore-ception does not contribute to entrainment of the circadian clock during postnatal development, and retina-mediated photic entrainmerit is present by 10 days of age. The results indicate that pineal NAT activity monitored in 10-day-old rats provides a useful paradigm for studying the developing circadian system. (Endocrinology 115: 918–925, 1984)

Footnotes

^* This work was supported by USPHS Grant HD-14427 and Basil O’Connor Starter Research Grant 5-335 from the March of Dimes-Birth Defects Foundation.

Received November 23, 1983.

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