Central and peripheral release of oxytocin following chronic homotypic stress in rats

Accumulation of continuous life stress (chronic stress) often causes gastric symptoms. Centrally released oxytocin has anxiolytic and anti-stress effects. We have recently shown that impaired gastric and colonic motility observed in acute restraint stress was restored following repeated restraint stress for 5 consecutive days (chronic homotypic stress) in mice and rats. Chronic homotypic stress upregulates oxytocin mRNA expression and downregulates corticotrophin-releasing factor (CRF) mRNA expression at the hypothalamus. However, it still remains unclear whether stress responses induced by chronic homotypic stress are accompanied by the central or peripheral release of oxytocin. Adult male SD rats were chronically implanted with microdialysis probes at the hypothalamic paraventricular nucleus (PVN) and jugular vein catheters. Microdialysis and blood sampling were performed following 1st, 3rd and 5th of chronic homotypic stress. Oxytocin levels in the dialysates and plasma were measured by radioimmunoassay (RIA). On day 1 of chronic homotypic stress, oxytocin release was slightly, but not significantly, increased in the PVN and plasma. Oxytocin release was significantly increased in the PVN on day 3 (12.7 ± 1.3 pg/sample, n = 5, P < 0.05) and day 5 (28.2 ± 2.4 pg/sample, n = 5, P < 0.05) from basal (6.9 ± 1.8 pg/sample, n = 5). In contrast, there were no significant changes observed in the plasma on day 3 and day 5. This suggests that central, but not peripheral, release of oxytocin plays an important role in response to chronic homotypic stress in rats.