Macrophage presence is essential for the regeneration of ascending afferent fibres following a conditioning sciatic nerve lesion in adult rats

BMC Neuroscience

Research Article

Malcolm Smith¹  Ernesto A Aguilar Salegio¹  Anthony N Pollard¹  Xin-Fu Zhou¹ 

[1] Department of Human Physiology and Centre for Neuroscience, Flinders University, GPO Box 2100, 5001, Adelaide, Australia;

关键词: Dorsal Root Ganglion;    Brain Derive Neurotrophic Factor;    Dorsal Root Ganglion Neuron;    Dorsal Column;    Sciatic Nerve Injury;   

DOI  :  10.1186/1471-2202-12-11

 received in 2010-03-21, accepted in 2011-01-20,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundInjury to the peripheral branch of dorsal root ganglia (DRG) neurons prior to injury to the central nervous system (CNS) DRG branch results in the regeneration of the central branch. The exact mechanism mediating this regenerative trigger is not fully understood. It has been proposed that following peripheral injury, the intraganglionic inflammatory response by macrophage cells plays an important role in the pre-conditioning of injured CNS neurons to regenerate. In this study, we investigated whether the presence of macrophage cells is crucial for this type of regeneration to occur. We used a clodronate liposome technique to selectively and temporarily deplete these cells during the conditioning phase of DRG neurons.ResultsRetrograde and anterograde tracing results indicated that in macrophage-depleted animals, the regenerative trigger characteristic of pre-conditioned DRG neurons was abolished as compared to injury matched-control animals. In addition, depletion of macrophage cells led to: (i) a reduction in macrophage infiltration into the CNS compartment even after cellular repopulation, (ii) astrocyte up-regulation at rostral regions and down-regulation in brain derived neurotrophic factor (BDNF) concentration in the serum.ConclusionActivation of macrophage cells in response to the peripheral nerve injury is essential for the enhanced regeneration of ascending sensory neurons.

【 授权许可】

Unknown   
© Salegio et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.