Intra-articular injection of LPA caused knee joint neuropathy, joint damage and pain. Pharmacological blockade of LPA receptors inhibited joint nerve damage and hindlimb incapacitance. Thus, LPA is a candidate molecule for the development of OA nerve damage and the origin of joint neuropathic pain.
nociceptors. MSCs were recorded in the cell-attached configuration and were stimulated with a high-speed pressure clamp (HSPC) device. Results: Our behavioral observations indicate that MIA-injected mice become hypersensitive to knee flexion and extension. Electrophysiology recordings from acutely dissociated knee nociceptors indicate that there are no changes in the resting membrane potential. However, our data indicates that the activation threshold of MSCs in the nociceptors of OA mice is significantly lower than that of nociceptors from naïve mice. Moreover, there is a greater elicited mechanosensitive current in OA nociceptors. Conclusions: Our data suggest that the lowered threshold of MSCs may contribute to the mechanical hypersensitivity observed in behavioral tests. MSCs in nociceptors may be a novel therapeutic target in the treatment of OA pain.
LYSOPHOSPHATIDIC ACID CONTRIBUTES TO THE DEVELOPMENT OF NEUROPATHIC PAIN IN RODENT KNEE JOINTS
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