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C. Belmonte, S. Quirce-Vazquez, A. Parra-Martin, T. Donovan-Rodriguez; Surgical Lesion Alters Electrical Activity and Pharmacological Responses of Cold Sensory Receptors in the Cornea. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3470.
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To characterize cold sensory receptor activity in the guinea-pig cornea in two different models of surgical lesion.
We recorded activity of corneal cold receptors after performing two types of surgical lesion to the mid-stromal level in guinea-pigs: trephine (circular cut) and microkeratome (incomplete circular flap). Nerve terminal impulses (NTIs) were recorded 3-10 days post-lesion in the excised cornea in vitro. Corneas were pinned in a recording chamber superfused with physiological saline at 35 °C. Extracellular recordings of NTIs were made with glass electrodes and thermal stimuli (cooling to 22 °C and heating to 52 °C) were delivered using a Peltier device. Cold receptors were identified by their spontaneous activity (SA), which increases on cooling and silences on warming. Drugs were tested via application to the bathing solution.
NTIs recorded in the vicinity of both lesion types showed significantly increased SA, lower cooling thresholds and increased cold-evoked peak frequencies compared to intact corneas. In trephine lesions no activity was recorded within the lesion area suggesting total denervation. In microkeratome lesions NTIs were recorded within the hinge and flap area. Here some receptors displayed normal activity and others showed sensitization, suggesting the presence of intact, injured, and regenerating fibers. Lidocaine (0.01%) ablated electrical activity in intact corneas, and normalized SA and cold-evoked activity in lesioned corneas. Phenytoin and carbamazepine dose-dependently reduced SA in intact and lesioned corneas.
Photorefractive surgery (PRS), which damages sensory nerves in the cornea, is used widely to correct refractive defects. Common sequelae include disesthesias such as sensations of ocular dryness. Abnormal electrical activity in severed nerve fibers due to altered expression of sodium channels is well documented. Our results indicate that injured/regenerating corneal cold nerve endings maintain their characteristic activity, albeit at higher frequencies. This may be the consequence of an increased expression of sodium channels. Sodium channel blocking drugs may therefore represent a novel treatment for certain disesthesias caused by PRS.
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