The circadian clock generates behavioural and physiological rhythms to maximize the efficacy of organismal functions. The circadian system with a major circadian pacemaker in the suprachiasmatic nucleus of the hypothalamus develops gradually and its proper function in adulthood depends on an appropriate neurochemical milieu during ontogeny [1]. Locomotor activity is under direct control by the circadian clock, and alterations in its rhythmicity indicate changes of circadian clock function. We evaluated circadian parameters of locomotor rhythms of adult male Wistar rats born to mothers that were exposed to a stable dose of 0.1 mg/ml of morphine in drinking water (36 ml water on average/day/each rat) from embryonic day 10 (E10) until weaning at postnatal day 28 (P28). Increasing the dose of morphine in drinking water was used to evaluate the changes in the rhythmic gene expression in the suprachiasmatic nucleus and in the livers of young rats at P20 [2]. At P90, we started measurement of endogenous rhythmicity for 12 days in constant darkness (DD), then we applied a 15 min light pulse at circadian time 15 (CT15) and followed the animals for the next 15 days in DD. We evaluated the magnitude of light-induced phase shift and compared the circadian parameters of free-running rhythmicity in the intervals before and after the light pulse. All data were also compared between morphine-exposed animals (M group) and controls (C group) that were not exposed to morphine. An unpaired t-test confirmed a significantly longer light-induced phase delay in M group compared with C group, a prolonged circadian period in M group in the interval after the light pulse, and greater amplitude for C group in the first interval, i.e. before the light pulse. No change in total activity counts between groups was confirmed.
Keywords: Circadian clock; Development; Locomotor activity; Morphine; Rat.
© 2022 The Author(s).