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Journal of Virology, October 2006, p. 10270-10273, Vol. 80, No. 20
0022-538X/06/$08.00+0     doi:10.1128/JVI.01272-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Rabies Virus Infection of Primary Neuronal Cultures and Adult Mice: Failure To Demonstrate Evidence of Excitotoxicity{dagger}

Simon C. Weli,1,2 Courtney A. Scott,2,4 Christopher A. Ward,3 and Alan C. Jackson1,2,4*

Departments of Medicine (Neurology),1 Microbiology and Immunology,2 Physiology,3 Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada4

Received 16 June 2006/ Accepted 31 July 2006

Cultures derived from the cerebral cortices and hippocampi of 17-day-old mouse fetuses infected with the CVS strain of rabies virus showed loss of trypan blue exclusion, morphological apoptotic features, and activated caspase 3 expression, indicating apoptosis. The NMDA (N-methyl-D-aspartate acid) antagonists ketamine (125 µM) and MK-801 (60 µM) were found to have no significant neuroprotective effect on CVS-infected neurons, while the caspase inhibitor Ac-Asp-Glu-Val aspartic acid aldehyde (25 µM) exerted a marked neuroprotective effect. Glutamate-stimulated increases in levels of intracellular calcium were reduced in CVS-infected hippocampal neurons. Ketamine (120 mg/kg of body weight/day intraperitoneally) given to CVS-infected adult mice produced no beneficial effects. We have found no supportive evidence that excitotoxicity plays an important role in rabies virus infection.

* Corresponding author. Mailing address: Kingston General Hospital, 76 Stuart Street, Connell 725, Kingston, ON, Canada K7L 2V7. Phone: (613) 548-1316. Fax: (613) 548-1317. E-mail: jacksona{at}post.queensu.ca.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, October 2006, p. 10270-10273, Vol. 80, No. 20
0022-538X/06/$08.00+0     doi:10.1128/JVI.01272-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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