Diclofenac inhibition of sodium currents in rat dorsal root ganglion neurons.

Abstract:

:The effects of diclofenac, a nonsteroidal anti-inflammatory drug (NSAID), on the fast tetrodotoxin-sensitive (TTX-S) and the slow tetrodotoxin-resistant (TTX-R) sodium currents in rat dorsal root ganglion neurons were investigated using the whole-cell patch-clamp method. Diclofenac suppressed both sodium currents in a dose-dependent manner. The apparent dissociation constants for the diclofenac suppression of TTX-S and TTX-R sodium currents were estimated to be 14 and 97 microM, respectively, at a holding potential of -80 mV. Diclofenac had no effect on the kinetic parameters of the activation process in either type of sodium current. However, diclofenac produced shifts of the steady-state inactivation curves in the hyperpolarizing direction in both types of sodium currents in a dose-dependent manner. At sufficiently negative holding potentials, the inhibitory effects of diclofenac on both types of sodium currents were minimal. The results suggested that diclofenac might bind to sodium channels with a greater affinity when they are in the inactivated state than when they are in the resting state. Effects of other NSAIDs (acetylsalicylic acid, antipyrin, indomethacin and flufenamic acid) on sodium currents were tested. Among these, only flufenamic acid suppressed the sodium currents to a considerable extent. Thus, the chemical structure of each NSAID, not the inhibition of cyclooxygenase, seems to be an important determinant in the sodium current inhibition. The suppression of sodium currents in sensory neurons by diclofenac and flufenamic acid would contribute to their analgesic activity in addition to their inhibition of cyclooxygenase.

journal_name

Brain Res

journal_title

Brain research

authors

Lee HM,Kim HI,Shin YK,Lee CS,Park M,Song JH

doi

10.1016/j.brainres.2003.08.048

subject

Has Abstract

pub_date

2003-11-28 00:00:00

pages

120-7

issue

1

eissn

0006-8993

issn

1872-6240

pii

S0006899303036424

journal_volume

992

pub_type

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