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BioMed Research International
Volume 2016 (2016), Article ID 3819052, 9 pages
Research Article

Transneuronal Degeneration of Thalamic Nuclei following Middle Cerebral Artery Occlusion in Rats

1School of Dentistry, National Yang-Ming University, No. 155, Section 2, Li-Non Street, Taipei 112, Taiwan
2Department and Graduate Institute of Biology and Anatomy, National Defense Medical Center, No. 161, Section 6, Minquan E. Road, Taipei 114, Taiwan

Received 18 February 2016; Revised 22 June 2016; Accepted 8 July 2016

Academic Editor: Andrea Vecchione

Copyright © 2016 Shu-Jen Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. Postinfarction transneuronal degeneration refers to secondary neuronal death that occurs within a few days to weeks following the disruption of input or output to synapsed neurons sustaining ischemic insults. The thalamus receives its blood supply from the posterior circulation; however, infarctions of the middle cerebral arterial may cause secondary transneuronal degeneration in the thalamus. In this study, we presented the areas of ischemia and associated transneuronal degeneration following MCAo in a rat model. Materials and Methods. Eighteen 12-week-old male Sprague-Dawley rats were randomly assigned to receive middle cerebral artery occlusion surgery for 1, 7, and 14 days. Cerebral atrophy was assessed by 2,3,5-triphenyltetrazolium hydrochloride staining. Postural reflex and open field tests were performed prior to animal sacrifice to assess the effects of occlusion on behavior. Results. Myelin loss was observed at the lesion site following ischemia. Gliosis was also observed in thalamic regions 14 days following occlusion. Differential degrees of increased vascular endothelial growth factor expression were observed at each stage of infarction. Increases in myelin basic protein levels were also observed in the 14-day group. Conclusion. The present rat model of ischemia provides evidence of transneuronal degeneration within the first 14 days of occlusion. The observed changes in protein expression may be associated with self-repair mechanisms in the damaged brain.