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Background. Models of cancer-induced neuropathy are designed by injectingcancer cells near the peripheral nerves. The interference of tissue-residentimmune cells does not allow a direct contact with nerve fibres which affectsthe tumor microenvironment and the invasion process. Methods. Anaplastictumor-1 (AT-1) cells were inoculated within the sciatic nerves (SNs) of maleCopenhagen rats. Lumbar dorsal root ganglia (DRGs) and the SNs were collectedon days 3, 7, 14, and 21. SN tissues were examined for morphological changesand DRG tissues for immunofluorescence, electrophoretic tendency, and mRNAquantification. Hypersensitivities to cold, mechanical, and thermal stimuliwere determined. HC-030031, a selective TRPA1 antagonist, was used to treatcold allodynia. Results. Nociception thresholds were identified on day 6.Immunofluorescent micrographs showed overexpression of TRPA1 on days 7 and 14and of CGRP on day 14 until day 21. Both TRPA1 and CGRP were coexpressed on thesame cells. Immunoblots exhibited an increase in TRPA1 expression on day 14.TRPA1 mRNA underwent an increase on day 7 (normalized to 18S). Injection ofHC-030031 transiently reversed the cold allodynia. Conclusion. A novel and apromising model of cancer-induced neuropathy was established, and the role ofTRPA1 and CGRP in pain transduction was examined.

A Novel Model of Cancer-Induced Peripheral Neuropathy and the Role of TRPA1 in Pain Transduction