RT Journal Article SR Electronic T1 Blockade of Kinin B1 receptor counteracts the depressive-like behavior and mechanical allodynia in ovariectomized mice JF bioRxiv FD Cold Spring Harbor Laboratory SP 2020.09.01.278416 DO 10.1101/2020.09.01.278416 A1 Izaque de Souza Maciel A1 Vanessa Machado Azevedo A1 Patricia Oliboni A1 Maria Martha Campos YR 2020 UL http://biorxiv.org/content/early/2020/09/02/2020.09.01.278416.abstract AB 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 B1 and B2 receptors (B1R and B2R) 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 B1R, 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 B2R (HOE 140, i.p) prevented the behavioral changes elicited by OVX. Our data suggested a particular modulation of kinin B1R in the nociceptive and depressive-like behavior in ovariectomized mice. Selective inhibition of the B1R receptor may be a new pharmacological target for treating pain and depression symptoms in women on the perimenopause/menopause period.Competing Interest StatementThe authors have declared no competing interest.OVXovariectomized mice;TSTtail suspension test;PWTpaw withdrawal threshold;FSHfollicle-stimulating hormone;HRThormone replacement therapy;ERestrogen receptors;MDmajor depression;BKbradykinin;CNScentral nervous system;LPSlipopolysaccharide;TNFÉ‘tumor necrosis factor-alpha;CSFcerebrospinal fluid;ACEangiotensin-converting enzyme;ROSreactive oxygen species.