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Heat hyperalgesia and mechanical hypersensitivity induced by calcitonin gene-related peptide in a mouse model of neurofibromatosis
Journal article   Open access   Peer reviewed

Heat hyperalgesia and mechanical hypersensitivity induced by calcitonin gene-related peptide in a mouse model of neurofibromatosis

Stephanie White, Blanca Marquez de Prado, Andrew F Russo and Donna L Hammond
PloS one, Vol.9(9), pp.e106767-e106767
2014
DOI: 10.1371/journal.pone.0106767
PMCID: PMC4153688
PMID: 25184332
url
https://doi.org/10.1371/journal.pone.0106767View
Published (Version of record) Open Access

Abstract

This study examined whether mice with a deficiency of neurofibromin, a Ras GTPase activating protein, exhibit a nociceptive phenotype and probed a possible contribution by calcitonin gene-related peptide. In the absence of inflammation, Nf1+/- mice (B6.129S6 Nf1/J) and wild type littermates responded comparably to heat or mechanical stimuli, except for a subtle enhanced mechanical sensitivity in female Nf1+/- mice. Nociceptive phenotype was also examined after inflammation induced by capsaicin and formalin, which release endogenous calcitonin gene-related peptide. Intraplantar injection of capsaicin evoked comparable heat hyperalgesia and mechanical hypersensitivity in Nf1+/- and wild type mice of both genders. Formalin injection caused a similar duration of licking in male Nf1+/- and wild type mice. Female Nf1+/- mice licked less than wild type mice, but displayed other nociceptive behaviors. In contrast, intraplantar injection of CGRP caused greater heat hyperalgesia in Nf1+/- mice of both genders compared to wild type mice. Male Nf1+/- mice also exhibited greater mechanical hypersensitivity; however, female Nf1+/- mice exhibited less mechanical hypersensitivity than their wild type littermates. Transcripts for calcitonin gene-related peptide were similar in the dorsal root ganglia of both genotypes and genders. Transcripts for receptor activity-modifying protein-1, which is rate-limiting for the calcitonin gene-related peptide receptor, in the spinal cord were comparable for both genotypes and genders. The increased responsiveness to intraplantar calcitonin gene-related peptide suggests that the peripheral actions of calcitonin gene-related peptide are enhanced as a result of the neurofibromin deficit. The analgesic efficacy of calcitonin gene-related peptide receptor antagonists may therefore merit investigation in neurofibromatosis patients.
Hyperalgesia - metabolism Neurofibromatoses - physiopathology Calcitonin Gene-Related Peptide - genetics Male Hot Temperature Neurofibromatoses - genetics Touch Hyperalgesia - physiopathology Animals Hyperalgesia - genetics Neurofibromatoses - metabolism Female Mice Calcitonin Gene-Related Peptide - metabolism Neurofibromin 1 - metabolism Neurofibromin 1 - genetics Disease Models, Animal

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