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M Carmen Acosta, Carolina Luna, Susana Quirce, Carlos Belmonte, Juana Gallar; Changes In Corneal Cold Thermoreceptor Activity Induced By Repetitive Allergen Challenges, In A Guinea-Pig Model Of Allergic Conjunctivitis. Invest. Ophthalmol. Vis. Sci. 2013;54(15):903.
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© ARVO (1962-2015); The Authors (2016-present)
To test in a guinea-pig model of allergic conjunctivitis whether exposure to the allergen evokes changes in blinking, tearing and corneal cold sensory nerve activity and the contribution of TRPA1 and TRPV1 channels of sensory nerves to the allergic response.
Sensitization to ovalbumin (OVA) was evoked by i.p. injection of 100µg OVA+20mg Al(OH)3 in 1ml PBS. On days 14th to 18th, 10% OVA (10µl drop) was applied to both eyes and tearing and blinking rates were measured immediately afterwards during 5 min. Nerve activity from cold-sensitive corneal nerve terminals (CNTs) was recorded in the superfused cornea in vitro, in response to thermal changes (exposure to bath temperature variations from the basal temperature of 34°C, down to 20°C or up to 50°C) at different days after the allergic challenge. In some experiments a 10µl drop of the TRPA1 channel blocker HC-030031, 10µM or of the TRPV1 channel blocker Capsazepine, 5mM was applied topically, 20 to 60 min before ocular instillation of the OVA.
Tearing and blinking rates were significantly increased and the response to cooling of CNTs was decreased after a single exposure to the allergen (Table 1). These effects were more pronounced after repeated exposures to OVA (RE) (see table) Blockade of TRPA1 and TRPV1 channels attenuated the tearing and blinking response to repeated exposure to the allergen. Only capsazepine reversed in part the depression of cold receptors by the allergic inflammation, possibly through its anti-inflammatory effect.
Inflammatory mediators released during allergic conjunctivitis, inhibit TRPM8 decreasing cold receptor activity, and activate TRPV1 and TRPA1 channels enhancing blinking through polymodal nociceptor excitation.
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