Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation.

ABSTRACT: Nerve injury may result in neuropathic pain, characterized by allodynia and hyperalgesia. Accumulating evidence suggests the existence of a molecular substrate for neuropathic pain produced by neurons, glia, and immune cells. Here, we show that leptin, an adipokine exclusively produced by adipocytes, is critical for the development of tactile allodynia through macrophage activation in mice with partial sciatic nerve ligation (PSL). PSL increased leptin expression in adipocytes distributed at the epineurium of the injured sciatic nerve (SCN). Leptin-deficient animals, ob/ob mice, showed an absence of PSL-induced tactile allodynia, which was reversed by the administration of leptin to the injured SCN. Perineural injection of a neutralizing antibody against leptin reproduced this attenuation.

SUBMITTER: Maeda T 

PROVIDER: S-EPMC2722338 | biostudies-literature | 2009 Aug

REPOSITORIES: biostudies-literature