Cerebral Cortex Advance Access originally published online on August 5, 2004
Cerebral Cortex 2005 15(4):378-384; doi:10.1093/cercor/bhh140
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Cerebral Cortex V 15 N 4 © Oxford University Press 2004; all rights reserved
Use of a Recombinant Pseudorabies Virus to Analyze Motor Cortical Reorganization after Unilateral Facial Denervation
1 Department of Comparative Physiology, Faculty of Science, University of Szeged, H-6726 Szeged, Hungary, 2 Department of Psychiatry, Faculty of Medicine, University of Szeged, Szeged, Hungary, 3 Laboratory of Neuromorphology, Department of Anatomy, Faculty of Medicine, University of Budapest, Budapest, Hungary, 5 Department of Medical Informatics, Faculty of Medicine, University of Szeged, Szeged, Hungary, 4 Present address: Department of Medical Biology, Faculty of Medicine, University of Szeged, Szeged, Hungary
Address correspondence to J. Toldi, Department of Comparative Physiology, University of Szeged, POB 533, H-6726 Szeged, Hungary. Email: toldi{at}bio.u-szeged.hu.
A unilateral facial nerve injury (n7x) was found to influence the transcallosal spread of the attenuated strain of pseudorabies virus (PRV Bartha) from the affected (left) primary motor cortex (MI) to the contralateral MI of rats. We used Ba-DupLac, a recombinant PRV strain, for the tracing experiments since this virus was demonstrated to exhibit much more restricted transportation kinetics than that of PRV Bartha, and is therefore more suitable for studies of neuronal plasticity. Ba-Duplac injection primarily infected several neurons around the penetration channel, but hardly any transcallosally infected neurons were observed in the contraleral MI. In contrast, after right facial nerve injury, Ba-DupLac was transported from the primarily infected neurons in the left MI to the contralateral side, and resulted in the labeling of several neurons due to a transneuronal infection. These results reveal that a peripheral nerve injury induces changes in the Ba-DupLac infection pattern in the related cortical areas. These findings and the literature data suggest that this phenomenon may be related to the changes in the expression or to the redistribution of cell-adhesion molecules, which are known to facilitate the entrance and/or transmission of PRV into neurons.
Key Words: herpes • neuronal plasticity • peripheral nerve injury • primary motor cortex • pseudorabies virus
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