Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system.
Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later. While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up).
Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling.
