Peripheral and central neuroplasticity in a mouse model of endometriosis

AbstractChronic pelvic pain (CPP) is the most debilitating symptom of gynaecological disorders such as endometriosis. However, it remains unclear how sensory neurons from pelvic organs affected by endometriosis, such as the female reproductive tract, detect and transmit nociceptive events and how these signals are processed within the central nervous system (CNS) Using a previously characterised mouse model of endometriosis we investigated whether the increased pain sensitivity occurring in endometriosis could be attributed to i) changes in mechanosensory properties of sensory afferents innervating the reproductive tract, ii) alterations in sensory input from reproductive organs to the spinal cord, or iii) neuroinflammation and sensitisation of spinal neural circuits. Mechanosensitivity of vagina-innervating primary afferents was examined using anex vivo single-unit extracellular recording preparation. Nociceptive signalling from the vagina to the spinal cord was quantified by phosphorylated MAP kinase ERK1/2 immunoreactivity. Immunohistochemistry was used to determine glial and neuronal circuit alterations within the spinal cord. We found that sensory afferents innervating the rostral, but not caudal portions of the mouse vagina, developed mechanical hypersensitivity in endometriosis. Nociceptive signalling from the vagina to the spinal cord was significantly enhanced in mice with endometriosis. Moreover, mice with endometriosis developed microgliosis, astrogliosis and enhan...
Source: Journal of Neurochemistry - Category: Neuroscience Authors: Tags: ORIGINAL ARTICLE Source Type: research