Research Papers:
Association of myelinated primary afferents impairment with mechanical allodynia in diabetic peripheral neuropathy: an experimental study in rats
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Abstract
Chenlong Liao1, Min Yang1, Wenxiang Zhong1, Pengfei Liu1 and Wenchuan Zhang1
1Department of Neurosurgery, Xinhua Hospital Affiliated to Shanghai JiaoTong University School of Medicine, Shanghai, P. R. China
Correspondence to:
Wenchuan Zhang, email: [email protected]
Keywords: diabetic peripheral neuropathy, nerve decompression, mechanical allodynia, neuropathic pain
Abbreviations: DPN: diabetic peripheral neuropathy; MA: mechanical allodynia; PWL: paw withdrawal latency; PWT: paw withdrawal threshold; STZ: streptozotocin
Received: April 05, 2017 Accepted: June 16, 2017 Published: July 18, 2017
ABSTRACT
To investigate the mechanisms underlying the efficacy of surgical treatment for painful diabetic peripheral neuropathy. Rats were initially divided into 3 groups (I, control rats, II, streptozotocin-induced diabetic rats, III, streptozotocin-induced diabetic rats with latex tube encircling the sciatic nerve without compression). When mechanical allodynia (MA) became stable in the third week, one third of group III rats were sacrificed and the remainder were further divided into subgroups depending on whether the latex tube was removed. Except for some rats in group III, all rats were sacrificed in the fifth week. Morphometric analysis of nerve fibers was performed. Expression level of GABAB receptor protein in spinal dorsal horn was determined. Changes of GABAB receptor within areas of primary afferents central terminal were identified. Chronic nerve compression caused by the interaction of diabetic nerves swelling and the encircling latex tube increased the incidence of MA in diabetic rats, and nerve decompression could ameliorate MA. In diabetic rats with MA, demyelination of myelinated fibers was noted and reduction of GABAB receptor was mainly detected in the area of myelinated afferent central terminals. MA in DPN should be partially attributed to compression impairment of myelinated afferents, supporting the rationale for surgical decompression.
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