Laser irradiation of the rabbit iris produces an injury response consisting of prolonged miosis, uveal vasodilation and a transient rise of intraocular pressure (IOP) accompanied by a breakdown of the blood-aqueous barrier. This response has hitherto been attributed partly to prostaglandin (PG) mediation and partly to mediation by a non-cholinergic nervous pathway thought to be sensory in fuction. Responses of the rabbit eye to laser irritation were examined at specified intervals after diathermic coagulation of the epigasserian nerve tract. Both the intensity of the pupillary constriction and the increase in IOP were almost unaltered at 90 minutes but progressively decreased until at 4 days there was essentially no response to high energy laser irradiation in the denervated eye. It was evident that manifestation of the response is largely dependent upon the presence of intact and functional sensory nerves, and it is proposed that endogenous PGs exert some, if not all of their effects via sensory nerve endings. It is suggested that those terminals which are directly stimulated, whether by laser irradiation or by PGs formed during the injury, release some mediator to cause pupillary constriction. From thes terminals impulses pass orthodromically and antidromically by axon reflex to release further mediator from terminals in the region of the ciliary vessels or the major arterial circle. In this way the response is propagated and augmented.