Huntington mice with 84 CAG trinucleotide repeats produces less pain behavior in inflammatory pain model

摘要

Huntington's disease (HD) a genetically neurodegenerative disease was well-known for affecting nervous system and lead to mental and motor dysfunctions Previous studies had shown that Huntington's disease was caused by the exon 1 region of Huntington (HTT) gene with expanded CAG trinucleotide repeats and results in an abnormally long polyglutamine tract at N-terminus However little research focuses on the relationship of HD and pain We used a previous published transgenic HD mice (7-9 weeks) carrying with mutant HTT exon 1 containing 84 CAG trinucleotide repeats to evaluate the relationship of HD and pain Inflammatory pain models were induced by either formalin or Complete Freund’s adjuvant injection over left hind paw Spinal cord dorsal root ganglion (DRG) and local hind-paw skin tissues were harvested at the end of the inflammatory pain for evaluation Immunofluorescence assay Western blotting and ELISA were used to identify the change of cells and cytokines within tissues Our data demonstrated that the pre-onset Huntington mice produced less pain behavior (both mechanical allodynia and heat sensitivity) in both young and aged mice Western blotting and immunohistological examination of lumbar spinal cord tissue and DRG were also demonstrated less activation of glial cells and astrocyte in young HD mice The expression of c-Fos was less in lumbar spinal cord The production of inflammatory cytokine TNF-? and IL-1β were also less in young HD mice compared with wild type animals The pain-related neuropeptide substance P was less in young HD mice However we also found that the expression of MPO and CD68 were also less in local hind-paw skin tissues of young HD mice Huntington protein may be involved in the mechanism of inflammatory pain and morphine analgesia Further studies were needed to investigate the possible role of HD in various pain models

獎項日期	2014 7月 14
原文	English
監督員	Sheng-Nan Wu (Supervisor)