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Published on: September 12, 2017
Serotonergic stimulation and nonphotic phase-shifting in hamsters
K J Bobrzynska1, M H Godfrey, N Mrosovsky
1Department of Zoology, University of Toronto, Ontario, Canada. kasia@zoo.utoronto.ca
Physiology & Behavior
|February 1, 1996
Summary
Serotonin (5-HT) agonists can shift hamster circadian rhythms. This study shows that these shifts are not solely due to increased activity, suggesting a direct role for serotonin in clock resetting.
Area of Science:
- Chronobiology
- Neuroscience
- Circadian Rhythms
Background:
- Nonphotic stimuli, like activity, alter circadian clocks.
- Serotonergic (5-HT) pathways projecting to the suprachiasmatic nucleus (SCN) are implicated in nonphotic clock resetting.
- The precise role of 5-HT in mediating activity-induced phase shifts remains unclear.
Purpose of the Study:
- To investigate the contribution of locomotor activity to phase shifts induced by the 5-HT1A and 5-HT7 receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT).
- To determine if 5-HT receptor agonists directly affect circadian clock resetting independent of their motor effects.
Main Methods:
- Hamsters received 8-OH-DPAT at circadian time 8 to assess phase advances.
- Locomotion was prevented in a subset of animals after 8-OH-DPAT administration.
- The effects of varying 8-OH-DPAT doses on activity levels and phase shifts were examined.
- Quipazine, a non-specific 5-HT agonist, was administered during the subjective day.
Main Results:
- Preventing locomotion did not abolish the phase shifts induced by 8-OH-DPAT.
- Higher doses of 8-OH-DPAT reduced activity but did not alter the amplitude of phase shifts.
- Quipazine did not induce phase shifts in hamsters, contrasting with findings in rats.
Conclusions:
- The phase-shifting effects of 8-OH-DPAT in hamsters are not solely mediated by increased locomotor activity.
- Serotonin likely plays a direct role in the nonphotic resetting of the circadian clock in hamsters.
- Species-specific differences exist in the response of circadian rhythms to non-specific 5-HT agonists like quipazine.

