Chronic irregular photoperiod disrupts locomotor rhythms and hypothalamic clock gene expression without metabolic imbalance in the male volcano mouse Neotomodon alstoni.

Circadian rhythms in physiology are coordinated daily variations driven by endogenous oscillators and synchronized by environmental light-dark cycles. Chronic disruption of the natural photoperiod has been associated with circadian desynchronization and physiological impairment. To examine these effects, we exposed adult lean male Neotomodon alstoni to an irregular photoperiod composed of alternating short and long cycles over a week, with abrupt phase shifts and maintained for three consecutive months. Behavioral, physiological, and molecular parameters were assessed, focusing on hypothalamic expression of circadian clock genes (Per1, Bmal1), metabolic regulators (Mchr1, Crh, Prepro-orexin, Sirt1), and feeding-related genes (Npy, Lepr). The irregular photoperiod differentially altered locomotor rhythms depending on phase delays or advances and increased food consumption during the photophase. Nocturnal expression of clock and metabolism-related genes was also modified in the hypothalamus. However, body weight, total food intake, and glucose handling remained unchanged. These findings indicate that in N. alstoni, chronic exposure to an irregular photoperiod disrupts circadian organization of activity and hypothalamic gene expression suggesting that a compensatory mechanisms may preserve overall metabolic homeostasis.