| In clinic, a few patients suffer serious neurophathic pain caused by brachial plexus injury, on which there is still no effective treatment to relieve the pain yet. Although the injury causes sensation and movement disability, the neuropathic pain is the most conspicuous symptom the patient can not tolerate. Although researchers had put a lot of effort on study of the mechanism of neuropathic pain, most of the animal models are focused on the nerve of hind limb to attempt to mimic the observed clinical consequences of nerve injury. Although most of these models have been useful in the experimental analysis of the pathological processes in the nerve itself, few of them reproduce changes in pain sensation like those that accompany peripheral neuropathies in humans. Therefore, new and reliable models of neuropathic persistent pain are still needed. Brachial plexus injury, caused by spinal cord root avulsion and particularity, produces a characteristic constant crushing and intermittent shooting pain that is often intractable. This lesion may lead to important pathological changes responsible for increased pain sensations. The main characteristics of brachial plexus injury are the rapid onset of pain, which occurs immediately after the trauma, and the development of a trigger point, which may be distant to the site of the lesion, either on the ipsilateral or contralateral side.The brachial plexus avulsion (BPA) has been recently described for rats as a new model of long-lasting neuropathic pain. This lesion may lead to pathological plasticity of the central nervous system that is associated with altered pain sensations (Carvalho et al., 1997). The main characteristics of BPA are the rapid onset of pain (an effect which occurs immediately after the trauma) and the long-lasting development of neuropathy, which may be evidenced distant from the site of the lesion, either on the ipsilateral or contralateralside.It has been proved immune and inflammatory mechanisms play important role in the development of neuropathic pain, during the development MAPK signal pathway and C-Fos is often take part in.In the present study, we aimed at reproducing a rat model previously described by Rodrigues-Filho et al. (2003), giving special attention to the definition of the activity of neutrophages infiltration, the activity of ERK and the C-Fos expression in the development of neuropathic pain.Main result:1. Rat model of brachial plexus injury was successfully reproduced. Von Frey fligament were used to identity the development of mechanical allodynia. The result proved that the significant mechanical hyperalgesia was formed in the experimental animals.2. ERK-LI that constantly expressed in Schwann cells was down-regulated transiently 5h after the low branch of brachial plexus were cut. Twenty-four hors after cutting, the ERK-LI is slowly up-regulated, and 3d latter it has recovered to the level as control.3. Lower branch of the brachial plexus avulsion caused more serious neutrophages infiltration, ERK1/2 signal pathway was strongly activated along the lower trunk, c-Fos was strongly up-regulated in the same trunk.4. Lower branch of the brachial plexus avulsion activated ERK pathways in the dorsal horn of gray matter. In addition, ERK pathways of the glia cell in fasciculus cuneatus was also strongly activated and lasted at least thirty days after avulsion.Conclusion:In this study, we proved that brachial plexus avulsion causes serious neutrophages infiltration in the lower trunk, ERK pathway was strongly activated and C-Fos expression was strongly upregulated in the lower trunk. In the spinal cord, ERK 1/2 in the gray matter and in the glia cell of fasciculus cuneatus is strongly activated. These changes might be related to the production and maintenance of neuropathic pain following bronchial plexus avulsion. |
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