• Jie Zhang, Liang Chen, and Yu-Dong Gu.
• Department of Orthopedics, the Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, China.
• World Neurosurg. 2017 Oct 1; 106: 211-218.

ObjectiveMajor histocompatibility complex class I (MHCI), paired-immunoglobulin-like receptor B (PirB), and cluster of differentiation 3ζ (CD3ζ) negatively regulate neuronal plasticity in developing and adult brains. The aim of this study was to evaluate expressive changes of these factors in motor cortical representations of the brachial plexus (MCRBP) after total brachial plexus root avulsion (tBPRA).MethodsA total of 45 rats were randomly and equally divided into 3 groups for evaluating mRNA and protein expression levels of MHCI, PirB, and CD3ζ: 7 days, 3 months, and control. In the 7-day and 3-month groups, expressions were examined at 7 days and 3 months, respectively, after left tBPRA. In the control group, the brachial plexus was uninjured. Three rats from each group were used for examining expressions of MHCI, PirB, and CD3ζ proteins by immunofluorescence labeling, 6 rats for quantification of MHCI, PirB, and CD3ζ mRNAs by real-time quantitative polymerase chain reaction, and the remaining 6 animals for quantification of MHCI, PirB, and CD3ζ proteins by Western blotting.ResultsIn the original MCRBP, mRNA and protein expression levels of MHCI, PirB, and CD3ζ were down-regulated 7 days postinjury compared with control (P < 0.01). Interestingly, mRNA and protein expression levels of these factors were up-regulated at 3 months compared with 7 days (P < 0.01), excepting PirB protein, whose expression was not increasing (P > 0.05). Recovery of protein expressions were initiated from near the border region of the original MCRBP.ConclusionsMHCI, PirB, and CD3ζ may participate in motor cortical reorganization after tBPRA.Copyright © 2017 Elsevier Inc. All rights reserved.

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