Characterization of cyclic AMP-mediated wound closure of the rabbit corneal epithelium

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Abstract
Cholera toxin (CTX)-stimulated synthesis of AMP enhances the rate of wound closure of a 7 mm diameter corneal epithelial defect following heptanol debridement, but not after mechanical scraping. Pretreatment with topical epinephrine or topical timolol does not alter the rate of wound closure following either trauma. Corneal glycogen levels decrease after heptanol debridement but glycogenolysis is not influenced by compounds which increase intracellular cAMP levels. Apparently, cAMP increases the rate of wound closure towards a maximum; the 1st messenger for activating the pathway is not a catecholamine, and the mechanism for enhancing closure is not via mobilization of glycogen stores.

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