Abstract
The aim of the present study was to investigate whether the MAPK pathways were involved in the mechanism of neuropathic pain in rats with chronic compression of the dorsal root ganglion. We determined the paw withdrawal mechanical threshold (PWMT) of rats before and after CCD surgery and then after p38, JNK, or ERK inhibitors administration. Western blotting, RT-PCR, and immunofluorescence of dorsal root ganglia were performed to investigate the protein and mRNA level of MAPKs and also the alternation in distributions of positive neurons in dorsal root ganglia. Intrathecal administration of MAPKs inhibitors, SB203580 (p38 inhibitor), SP600125 (JNK inhibitor), and U0126 (ERK inhibitor), resulted in a partial reduction in CCD-induced mechanical allodynia. The reduction of allodynia was associated with significant depression in the level of both MAPKs mRNA and protein expression in CCD rats and also associated with the decreased ratios of large size MAPKs positive neurons in dorsal root ganglia. In conclusion, the specific inhibitors of MAPKs contributed to the attenuation of mechanical allodynia in CCD rats and the large size MAPKs positive neurons in dorsal root ganglia were crucial.
Highlights
Neuropathic pain caused by lesion or inflammation results from the dysfunction and derangement in transmission and signal processing within the nervous system
To detect whether the inhibitors of Mitogen-activated protein kinases (MAPKs) attenuated CCD-induced neuropathic pain, paw withdrawal mechanical threshold (PWMT) were examined before surgery, 4 days after surgery, and 2 h after inhibitors administration
CCD-induced allodynia was attenuated by SB203580, SP00125, and U0126 (n = 8 in each group; #P < 0.05), while there was no significant difference between sham group and control group (n = 8 in each group)
Summary
Neuropathic pain caused by lesion or inflammation results from the dysfunction and derangement in transmission and signal processing within the nervous system. It is characterized by the symptoms of allodynia, hyperalgesia, and spontaneous pain [1, 2] and it does not depend on the continued presence of tissue-damaging stimuli and is recognized as a disease in itself [3]. Pain and hyperalgesia that are produced by tissue damage or infection are common features of the inflammatory process [4]. Evidence demonstrates that a substantial proportion of mediators are involved in the symptoms of neuropathic pain, including cytokines, bradykinin, ATP and adenosine, serotonin, eicosanoids, and neurotrophins [1]. Kinds of drugs are used to alleviate neuropathic pain, but they exhibit limited efficacy and undesirable side effects, and neuropathic pain responds poorly to such drug treatments [5]
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