Emergency Med Medical News about leptin, adipocyte, neuropathic pain

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Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation
Proceedings of the National Academy of Sciences of the United States of America, 08/06/09

Maeda T et al. – Findings suggest that leptin induces recruited macrophages to produce pronociceptive mediators for development of tactile allodynia. Adipocytes associated with primary afferent neurons may be involved in development of neuropathic pain through adipokine secretion.

Methods

Murine model to show leptin as critical for development of tactile allodynia via macrophage activation in mice with partial sciatic nerve ligation (PSL)

Results

PSL increased leptin expression in adipocytes at epineurium of injured sciatic nerve (SCN)
Absent PSL-induced tactile allodynia in leptin-deficient animals, ob/ob mice, reversed by leptin administration to injured SCN
Perineural injection of neutralizing antibody against leptin reproduced this attenuation
Macrophages recruited to SCN perineurium expressed the leptin receptor and phosphorylated signal transducer and activator of transcription 3 (pSTAT3), a transcription factor downstream of leptin
PSL upregulated accepted mediators of neuropathic pain in injured SCN, with transcriptional activation of their gene promoters by pSTAT3
Mediators: cyclooxygenase-2, inducible nitric oxide synthase, matrix metalloprotease-9
Upregulation partly reproduced in macrophage cell line treated with leptin
Administration of leptin-treated peritoneal macrophages to injured SCN reversed failure of ob/ob mice to develop PSL-induced tactile allodynia

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