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Riluzole hydrochloride is an anticonvulsant drug and belongs to the family of use-dependent Na+ channel blocker which can also inhibit GABA uptake with an IC50 of 43 μM.

Riluzole hydrochloride is an anticonvulsant drug and belongs to the family of use-dependent Na+ channel blocker which can also inhibit GABA uptake with an IC50 of 43 μM. At 20 μM, Riluzole hydrochloride inhibits peak autaptic IPSCs only slightly but prolongs IPSCs reliably. It is also found that Riluzole hydrochloride causes a strong, concentration-dependent, readily reversible enhancement of responses to 2 μM GABA. At higher concentrations of Riluzole hydrochloride, especially 300 μM, GABA currents exhibit apparent desensitization during prolonged co-exposure to 2 μM GABA and Riluzole hydrochloride. The EC50 of Riluzole hydrochloride potentiation of GABA responses is about 60 μM[1].

In normal nave rats, systemic injection of Riluzole hydrochloride (8 mg/kg, i.p.; n=6 rats) decreases the duration of ultrasonic but not audible vocalizations evoked by noxious stimulation of the knee joint compare to vehicle tested in the same rats (P<0.05). Systemic application of Riluzole hydrochloride (8 mg/kg, i.p.; n=19 rats) decreases the vocalizations of arthritic rats compare to predrug and vehicle significantly (P<0.05 to 0.001). Riluzole hydrochloride administered into the CeA significantly decreases the duration of audible and ultrasonic vocalizations evoked by noxious stimulation of the knee compare to predrug values (n=8 rats; P<0.05 to 0.01)[2].

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