Syrian hamsters in a lighting schedule of 14 h of light per day (LD 14:10) and housed in cages equipped with running wheels exhibited a clear onset of locomotor activity during the 1st h after lights off. Implantation of osmotic minipumps containing clorgyline (2 mg . kg-1 . day-1), an irreversible inhibitor of monoamine oxidase type A, caused a 1.5-h delay in the onset of wheel running by the 7th day of treatment. Increasing dosages of clorgyline (0.5, 1, 2, or 4 mg . kg-1 . day-1) caused increasing delays. Hamsters shifted from LD 14:10 to LD 10:14 underwent a 3-h advance in the onset of wheel running. Animals treated with clorgyline (2 mg . kg-1 . day-1) exhibited a markedly slowed rate of advance in activity onset, which did not prevent the short photoperiod from inhibiting reproductive function. Additionally, removal of the pineal gland did not affect wheel-running onset and did not prevent the delay in activity onset during clorgyline treatment. Hamsters in LD 14:10 were "released" into constant darkness (DD) for 3 days to prevent masking of activity onsets and offsets by light. Delays in activity onset in LD 14:10 caused by clorgyline (2 mg . kg-1 . day-1) persisted when these animals were released into DD. Activity offset in LD 14:10 occurred at lights on before and during clorgyline treatment but was delayed when the treated animals were maintained in DD. Drug-induced delays in both activity onset and offset suggest that clorgyline is not simply shortening the duration of activity or changing the expression of activity relative to the light-dark cycle, but is delaying the phase position of the circadian rhythm in locomotor activity. Clorgyline may act directly on the central oscillatory mechanism that drives the rhythm.
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http://dx.doi.org/10.1152/ajpregu.1983.245.2.R215 | DOI Listing |
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