Blockade of Kinin B1receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice

Menopause is related to a decline in ovarian estrogen production, affecting the perception of the somatosensory stimulus, changing the immune-inflammatory systems, and triggering depressive symptoms. Inhibition of kinin B 1 and B 2 receptors (B 1 R and B 2 R) inhibits the depressive-like behavior and mechanical allodynia induced by immune-inflammatory mediators in mice. However, there is no evidence on the role of kinin receptors in depressive-like and nociceptive behavior in female mice submitted to bilateral ovariectomy. This study shows that ovariectomized mice (OVX) developed time-related mechanical allodynia and increased immobility time in the tail suspension test (TST). The genetic deletion of B 1 R, or the pharmacological blockade by selective kinin B1R antagonist R-715 (acute, i.p), reduced the increase of immobility time and mechanical allodynia induced by ovariectomy. Neither genetic deletion nor pharmacological inhibition of B 2 R (HOE 140, i.p) prevented the behavioral changes elicited by OVX. Our data suggested a particular modulation of kinin B 1 R in the nociceptive and depressive-like behavior in ovariectomized mice. Selective inhibition of the B 1 R receptor may be a new pharmacological target for treating pain and depression symptoms in women on the perimenopause/menopause period.