Open AccessPromotion of thermal analgesia and neuropeptidergic skin reinnervation by 4‐methylcatechol in resiniferatoxin‐induced neuropathy
Author(s) -
Hsiao TinHsin,
Fu YawSyan,
Ho WanYi,
Chen TziHsuan,
Hsieh YuLin
Publication year - 2013
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2012.12.001
Subject(s) - calcitonin gene related peptide , resiniferatoxin , medicine , reinnervation , anesthesia , substance p , pharmacology , endocrinology , denervation , neuropeptide , trpv1 , anatomy , receptor , transient receptor potential channel
To investigate whether 4‐methylcatechol (4MC) could decrease the duration of the thermosensation disorder and promote the innervation of peptidergic intraepidermal nerve fibers (IENFs), we developed a resiniferatoxin (RTX)‐induced neuropathic mouse model with thermal analgesia and skin denervation that was followed by daily 4MC treatment. On day 7 after RTX administration (RTXd7), the substance P (SP)(+) IENFs were completely depleted compared with the vehicle group ( p < 0.0001), whereas the calcitonin gene‐related peptide (CGRP)(+) IENFs were dramatically, but not completely, depleted ( p < 0.0001). While SP(+) IENFs remained depleted ( p = 0.0043), CGRP(+) IENFs were recovered by RTXd84 ( p = 0.78). 4MC had no effect on the reinnervation of SP(+) IENFs, but markedly promoted the reinnervation of CGRP(+) IENFs on RTXd35 ( p = 0.035). On RTXd56, CGRP(+) IENFs were comparable with the vehicle group ( p = 0.39). In addition, 4MC normalized thermal analgesia on RTXd35 compared with RTX group ( p = 0.007). In the current study, the significant promotion of reinnervation of CGRP(+) IENFs and thermal latencies on RTXd35 by 4MC indicated that CGRP(+) IENFs were responsible for the thermal transmission in chronic phase of RTX‐induced neuropathy.