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Rhythmic feeding behavior is critical for regulating phase and amplitude in the ≈24-h variation of heart rate (RR intervals), ventricular repolarization (QT intervals), and core body temperature in mice. We hypothesized changes in cardiac electrophysiology associated with feeding behavior were secondary to changes in core body temperature. Telemetry was used to record electrocardiograms and core body temperature in mice during ad libitum-fed conditions and after inverting normal feeding behavior by restricting food access to the light cycle. Light cycle-restricted feeding modified the phase and amplitude of 24-h rhythms in RR and QT intervals, and core body temperature to realign with the new feeding time. Changes in core body temperature alone could not account for changes in phase and amplitude in the ≈24-h variation of the RR intervals. Heart rate variability analysis and inhibiting β-adrenergic and muscarinic receptors suggested that changes in the phase and amplitude of 24-h rhythms in RR intervals were secondary to changes in autonomic signaling. In contrast, changes in QT intervals closely mirrored changes in core body temperature. Studies at thermoneutrality confirmed that the daily variation in QT interval, but not RR interval, primarily reflected daily changes in core body temperature (even in ad libitum-fed conditions). Correcting the QT interval for differences in core body temperature helped unmask QT interval prolongation after starting light cycle-restricted feeding and in a mouse model of long QT syndrome. We conclude feeding behavior alters autonomic signaling and core body temperature to regulate phase and amplitude in RR and QT intervals, respectively. NEW & NOTEWORTHY: We used time-restricted feeding and thermoneutrality to demonstrate that different mechanisms regulate the 24-h rhythms in heart rate and ventricular repolarization. The daily rhythm in heart rate reflects changes in autonomic input, whereas daily rhythms in ventricular repolarization reflect changes in core body temperature. This novel finding has major implications for understanding 24-h rhythms in mouse cardiac electrophysiology, arrhythmia susceptibility in transgenic mouse models, and interpretability of cardiac electrophysiological data acquired in thermoneutrality. [ABSTRACT FROM AUTHOR]

Our previous studies have shown that light at night (LAN) impaired cognitive performance and affected neurogenesis and neurochemistry in the cognition‐associated brain regions, particularly the hippocampus (HP) and lateral caudal nidopallium (NCL) of Indian house crows (Corvus splendens). Here, we examined the cytoarchitecture and mapped out the morphology of neurons and glia–neuron density in HP and NCL regions of crows that were first entrained to 12‐hr light (LL): 12‐hr darkness (LD) and then exposed to the light regime in which 12‐hr darkness was either replaced by daytime light (i.e., constant light, LL) or by dim light (i.e., dim light at night, dLAN), with controls continued on LD 12:12. Compared with LD, there was a significant decrease in the soma size, suggesting reduced neuronal plasticity without affecting the neuronal density of both HP and NCL of crows under LL and dLAN conditions. In parallel, we found a reduced number of glia cells and, hence, decreased glia–neuron ratio positively correlated with soma size in both, HP and NCL regions. These results for the first time demonstrate LAN‐induced negative effects on the brain cytoarchitecture of a diurnal species and give insight for possible influence on the brain health and functions in animals including humans that might be inadvertently exposed to LAN in an emerging night‐illuminated urban environment. Highlights: We report light at night effects on brain cytoarchitecture in diurnal crows.LAN‐induced decrease in soma size of neurons in the hippocampus and nidopallium.We suggest functional association of soma size with the glia–neuron ratio. Artificial light at night affects neuronal soma size, and reduces glia number and glia‐neuron ratio. [ABSTRACT FROM AUTHOR]