The nervous system has profound modulatory influences on many inflammatory processes, particularly within the eye. These properties are in part mediated via neuropeptides. The neurotoxin, capsaicin, has been utilized as a valuble experimental tool to study the role of neuropeptides in many organ systems. Retrobulbar injection of capsaicin into rats results in the loss of sensory nerve function with rapid onset of inflammation (6–12 hours) which is confined to the the anterior segment. The hallmark of the acute response at 24–48 hours is marked polymorphonuclear leukocyte (PMN)/mononuclear cell influx and opacification of the corneal stroma with degeneration and loss of the central epithelium. PMN/mononuclear cell infiltration was also evident within the angle, the anterior chamber, and the iris. The corresponding posterior segments were normal. There was extensive corneal neovascularization between 7 and 14 days. This keratouveitogenic response in rats was age-dependent and can be attenuated by prior systemic pretreatments with capsaicin. This model should prove to be useful useful in the study of mechanisms of intraocular neurogenic inflammation.