Purchase this article with an account.
C. Belmonte, V. Meseguer, G. Graff, F. Viana; Effects of the Nonsteroidal Anti–Inflammatory Drug Nepafenac on Sodium Channels in Cultured Mice Trigeminal Sensory Neurons . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2604.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate whether the ocular analgesic effects of nepafemac, a non–steroidal antiinflammatory drug, are mediated by a blockade of sodium currents in corneal peripheral endings of mouse trigeminal ganglion neurons.
Whole–cell patch–clamp recordings of sodium currents were made from adult mice trigeminal ganglion neurons. Neurons were isolated by a mechano–enzymatic dissociation procedure and kept in culture for 24–48 h. All recordings were performed at room temperature in small to medium size neurons. Drugs were applied by a gravity perfusion system. The effects of nepafenac and its active metabolite amfenac were compared with equivalent doses of diclofenac.
Nepafenac (1–50 µM) had no effect on sodium currents. The active metabolite, amfenac (50 µM), produced a transient enhancement followed by a slow, modest decline, that did not reverse upon wash of the drug. In contrast, diclofenac (50 µM) produced a robust, reversible inhibition of sodium currents.
The significant reduction in polymodal nociceptor activity observed after application of nepafenac to trigeminal afferents in vivo is unlikely to involve an anesthetic blockade of impulse activity through the reduction of sodium channel currents in corneal sensory fibers.
This PDF is available to Subscribers Only