Axon Reflex in Ocular Injury: Sensory Mediation of the Response of the Rabbit Eye to Laser Irradiation of the Iris

Abstract

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 function. 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 these 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.The response of the rabbit eye to injury consists of a miosis, anterior uveal vasodilation, a rise in the intraocular pressure (IOP) and a breakdown of the blood-aqueous barrier, leading to a rapid infiltration of plasma protein into the aqueous humour. To some extent, the mechanism would seem to depend upon the nature of the stimulus. The response to mechanical trauma, e.g. scratching the iris, appears to be mediated mainly by prostaglandins (PG) whereas that to chemical irritation involves a non-cholinergic nervous component believed to be identical to that with sensory function [

Experimental Trigeminal Nerve Injury

“…The trunk of the ophthalmic nerve is rarely damaged clinically, and experimental data on it are absent. Interest in the ophthalmic nerve is focused on its role in the inflammatory response to injuries of the cornea (e.g., Butler et al, 1980;Unger et al, 1985). In this respect, the observations made on it closely parallel those made on dental pulp and periapical tissues to elucidate the role of sensory afferents in response to pulpal injury (e.g., Byers, 1994).…”

Review: Mediation of the Ocular Response to Injury

“…The response of IOP and pupil to intracameral bradykinin, capsaicin, neutral formaldehyde and PGE-, and PGE2 are abolished in rabbit eyes deprived of functional somatic sensory innervation (1,26,87). Moreover, sensitivity of the eye to iris laserirradiation is progressively lost following destruction of the Gasserian ganglion (27). It was essentially intact 90 minutes and 24h after damage to the ganglion and then decreased gradually to become completely averted by 4-7 days, indicating that mediation of the irritative response does not follow an orthodromic central nervous pathway but occurs within sensory afférents by antidromic stimulation, propagated through branched axons and possibly colateral fibres.…”

“…It is seen in small cell bodies of the Gasserian ganglion (95)(96)(97). Since sensory fibres are known to be bipolar (98) neuropeptide transcribed in the cell body will be translocated along both central and somatic projections and appear in the anterior uvea (27,(99)(100)(101). Substance P immunoreactivity has been localised within the iris-ciliary bodies to fibres derived from the trigeminal nerve of the rabbit, rat, guinea pig, cat, monkey, man (102)(103)(104)(105)(106)(107)(108)(109).…”

“…In the past two decades, research into mediation of the ocular response to trauma has concentrated on the involvement of prostaglandin and role of sensory neuropeptides in mediating these ocular changes. The current view, as discussed below, is that the response is mediated primarily by antidromic activation of sensory elements in the anterior uvea, facilitated in many situations by the release and action of prostaglandins (PCs) (26)(27)(28).…”