Role of linkage between cerebral activity and baroreflex control of heart rate via central vasopressin V1a receptors in food-deprived mice

We previously reported that cerebral activation at the onset of voluntary locomotion suppressed baroreflex control of heart rate (HR) and increased arterial pressure via vasopressin V1a receptors in the brain. Here, we examined whether these responses were associated with food seeking, a motivated behavior, using free-moving wild type (WT, = 10), V1a receptor knockout (KO, = 9), and wild-type mice locally infused with a V1a receptor antagonist into the nucleus tractus solitarii (BLK, = 10). For three consecutive days, mice were fed ad libitum (Fed), food deprived (FD), and refed (RF) under a dark/light cycle (1900/0700). Food was removed on and restored on at 1800. Throughout the protocol, cerebral activity was determined from the power density ratio of θ- to δ-wave band (θ/δ) by electroencephalogram every 4 s. Baroreflex was evaluated by the cross-correlation function [ ( )] between changes in HR and arterial pressure every 4 s. The cerebro-baroreflex linkage was then evaluated by the cross-correlation function between θ/δ and ( ). Behavior was recorded with CCD camera. We found that cerebro-baroreflex linkage, enhanced in WT at night after FD ( = 0.006), returned to Fed level after RF ( = 0.68). Similarly, food-seeking behavior increased after FD to a level twofold higher than during Fed ( < 0.001) and returned to Fed level after RF ( = 0.54). However, none of these changes occurred in KO or BLK ( > 0.11). Thus, the suppression of baroreflex control of HR linked with cerebral activation via central V1a receptors might play an important role at the onset of motivated behaviors, such as food seeking induced by FD. Motivated behaviors, characterized by goal-directed and persistent movements, are indispensable for living. However, how cerebro-cardiovascular adjustment occurs during such behaviors remains unknown. By focusing on food-seeking behavior in a food-deprived condition using free-moving mice, we found that this condition enhanced the linkage between cerebral activation and suppression of baroreflex control of heart rate through central vasopressin V1a receptors, making it easier to start motivated behaviors by enhancing pressor response.