Cholinergic activation of a population of corneal afferent nerves

It is concluded that a specific population of C-fiber afferents exist in the rabbit cornea which are stimulated by acetylcholine possibly acting via a neuronal nicotinic receptor and may be involved in the production of pain following tissue injury or ischemia.

Abstract

The in vivo rabbit cornea was used to investigate the effect of acetylcholine on "free" nerve endings from A-delta and C-fibers in the long-ciliary (corneal) nerve. Extracellular electrophysiologic recordings were obtained from 67 corneal nerve fibers. Acetylcholine in concentrations of 10(-5) to 10(-3) M stimulated a specific population of these corneal afferents that were not activated by mechanical or thermal stimuli. Their conduction velocity was determined to be 1.14 +/- 0.34 m/s (mean +/- SD). The other three previously characterized corneal nerve populations (mechanical, mechano-heat, and cold) were not stimulated by the cholinergic agonists or antagonists. Acetylcholine sensitive afferents were also stimulated by carbachol (10(-5) to 10(-3) M) and nicotine (10(-6) to 10(-4) M) but not by bethanecol (10(-5) to 10(-3) M). Acetylcholine-induced activity was abolished by d-tubocurare (10(-4) M) and kappa-bungarotoxin (10(-6) M). The cAMP analog 8-bromoadenosine 3'5'-cyclic monophosphate activated the same population of chemosensitive C-fibers as acetylcholine. It is concluded that a specific population of C-fiber afferents exist in the rabbit cornea which are stimulated by acetylcholine possibly acting via a neuronal nicotinic receptor. Physiologically, these nerves may be involved in the production of pain following tissue injury or ischemia.