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Takayoshi Masuoka, Carlos Belmonte, Juana Gallar; Effects of the sodium channel blocker amitriptyline on the spontaneous and stimulus-evoked activity of corneal cold-sensitive nerve terminals in intact and tear-deficient guinea-pig eyes.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):330.
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© ARVO (1962-2015); The Authors (2016-present)
To clarify the effect of amitriptyline, a tricyclic antidepressant commonly used for treatment of neuropathic pain, on the electrical activity of corneal cold nerve terminals recorded from corneas of control and lacrimodeficient guinea pigs.
Dry eye (DE) was induced in the guinea pig by removing the exorbital lacrimal gland. Four to 6 weeks after surgery, the isolated cornea was mounted in a recording chamber superfused at 340C. Corneal cold-sensitive nerve terminal impulse (NTI) activity was recorded from the corneal surface using a glass micropipette and conventional equipment for extracellular recording. Thermal stimuli were performed changing the temperature of the perfusion solution with a Peltier system, from the control temperature of 34°C down to 20°C (cooling ramp) or up to 50°C. The characteristics of the spontaneous and stimulus-evoked NTI activity recorded from DE and intact corneas before and during perfusion with 10-30 µM amitriptyline, were compared.
Amitriptyline (10 or 30 μM) reduced irreversibly the spontaneous NTI activity at 340C in a dose-dependent manner in both intact and dry eye corneas. The inhibition of spontaneous NTI by 10 μM amitriptyline was significantly less effective in DE corneas, where 42% of the recorded units were insensitive to 10 μM amitriptyline while all recorded unit were inhibited in intact corneas. Amitriptyline-insensitive units recorded from DE corneas were characterized by higher cooling thresholds and a higher temperature decrease needed to reach peak frequency during cooling ramps from 34°C to 20°C when compared with amitriptyline-sensitive units. Amitriptyline tends also to decrease the maximal response to cooling ramps in intact corneas but not in DE corneas.
Na+-channel blocker amitriptyline attenuates the spontaneous activity and cooling response of cold nerve terminals in intact corneas and less efficiently in DE corneas. This difference may be due to the changes induced by ocular dryness in the expression of the various voltage-sensitive Na+ channels responsible for impulse generation in corneal cold-sensitive terminals of DE corneas.
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