In experimental studies with rats, systemic administration of Riluzole at a dose of 8 mg/kg (intraperitoneally) has been shown to decrease the duration of ultrasonic vocalizations, but not audible vocalizations, evoked by noxious stimulation of the knee joint compared to vehicle control, indicating its potential analgesic effects in conditions of pain (P<0.05). Additionally, in arthritic rats, the same dose of Riluzole significantly reduces vocalizations compared to pre-drug and vehicle treatments, suggesting its effectiveness in managing arthritic pain (P<0.05 to P<0.001)^[2].

Riluzole, classified as an anticonvulsant, functions as a use-dependent sodium channel blocker and also exhibits the ability to inhibit GABA uptake, with an IC50 of 43 μM. It shows slight inhibition of peak autaptic IPSCs at a concentration of 20 μM, but it reliably prolongs IPSCs at this level. More notably, Riluzole significantly enhances responses to 2 μM GABA in a concentration-dependent and readily reversible manner. At a higher concentration of 300 μM, it leads to apparent desensitization of GABA currents during prolonged exposure to 2 μM GABA. The effective concentration (EC50) for Riluzole's potentiation of GABA responses is approximately 60 μM^[1].