Physiological deficits in the visual system of mice infected with Semliki Forest virus and their correlation with those seen in patients with demyelinating disease.
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.
D000818:Animals; D005074:Evoked Potentials, Visual; D006801:Humans; D051379:Mice; D008815:Mice, Inbred Strains; D009103:Multiple Sclerosis / Q000503:physiopathology*; D009186:Myelin Sheath / Q000503:physiopathology*; D009900:Optic Nerve / Q000503:physiopathology; D010775:Photic Stimulation; D012672:Semliki forest virus; D013477:Superior Colliculi / Q000503:physiopathology; D014036:Togaviridae Infections / Q000503:physiopathology*; D014796:Visual Perception / Q000502:physiology