Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (21)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by TREMAIN, K. E.
Right arrow Articles by IKEDA, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by TREMAIN, K. E.
Right arrow Articles by IKEDA, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Brain, Vol. 106, No. 4, 879-895, 1983
© 1983 Guarantors of Brain

research-article

PHYSIOLOGICAL DEFICITS IN THE VISUAL SYSTEM OF MICE INFECTED WITH SEMLIKI FOREST VIRUS AND THEIR CORRELATION WITH THOSE SEEN IN PATIENTS WITH DEMYELINATING DISEASE

K. E. TREMAIN and HISAKO IKEDA

Vision Research Unit of Sherrington School, The Rayne Institute, St Thomas' Hospital London SE1 7EH

Electrophysiological recordings were made from the superior colliculus of mice infected with Semliki Forest virus (SFV) which produced patchy demyelination in many different locations within the central nervous system including the optic nerve. Over a wide range of light intensities, the visual latencies of both single cell and field potential responses from the superior colliculi of infected mice were longer than those of the corresponding control mice, and there was a greater interocular difference in visual latency in the infected mice than in control mice. In addition, the collicular neurons of infected mice revealed a loss of sensitivity to light of approximately 0.5 log units and a significant reduction in flicker fusion frequency. Using the same flash stimuli as in the mouse experiments, visual evoked potentials (VEPs) were recorded from patients with demyelinating disease. Patients diagnosed as suffering from multiple sclerosis showed a clear increase in peak latency of the VEP and a significantly reduced VEP flicker fusion frequency, as found in the SFV infected mice. These results suggest that mice infected with SFV may provide a suitable animal model of demyelinating disease.

Received January 25, 1983. Accepted March 29, 1983.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
S. F. Stasheff
Emergence of Sustained Spontaneous Hyperactivity and Temporary Preservation of OFF Responses in Ganglion Cells of the Retinal Degeneration (rd1) Mouse
J Neurophysiol, March 1, 2008; 99(3): 1408 - 1421.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.