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Recombinant Human Lymphokines Induce Changes in Visual Evoked Potentials in the Rabbit a

In response to antigenic stimulation, lymphocytes and macrophages secrete an array of inflammatory mediators that serve to activate and effect an immune response. The success achieved in cloning the genes for many of these mediators has led to the availability of relatively pure products and an increased understanding of the role that they play in the inflammatory process. Much of this information has been obtained from experimentation in vitro or from subcutaneous or systemic injection in vivo However, less is known about the effect of these cytokines on central nervous system (CNS) function. To establish a system that would permit longitudinal assessment of the role of cytokines in inducing electrophysiologic and structural changes associated with inflammation in the CNS, we explored the use of epidural visual evoked potentials (VEPs) in the rabbit. The rabbit visual system offers several advantages for these studies: the visual pathways are almost entirely crossed, which permits the response of one eye to be distinguished from the response in the other, allowing one eye to function as an internal control; the visual cortex is on the dorsolateral surface of the brain, which results in large amplitude cortical VEPs and a clearly defined topographic distribution of monocular and binocular responses; and factors to be tested can be injected into the vitreous, circumventing the blood-brain barrier with minimal trauma. In addition, axons of the retina are myelinated, which permits a study of the effect of inflammatory mediators on myelinated portions of the primary sensory axons. Injection of 1,000 U of recombinant human gamma-interferon increased the peak latency of the cortical response by 2 ms within 10 minutes of injection. No change in the morphology of the waveform was evident. Cortical responses were still delayed 3 hours postchallenge but had returned to baseline values by 24 hours postchallenge. The response could be reinduced by reinjection of rhIFN-y and again reversed within 24 hours. Injection of 1,000 U of tumor necrosis factor ( rhTNF)