Skip to main content
Fig. 5 | Molecular Pain

Fig. 5

From: Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available riluzole in a rat model of arthritis pain

Fig. 5

Involvement of SK, but not BK, channels in the CeA, but not BLA, in the inhibitory effects of riluzole in arthritis. a, b Systemic riluzole (8 mg/kg, i.p.) had no effect on audible (a) and ultrasonic (b) vocalizations compared to predrug values, when an SK channel blocker (apamin, 1 μM, concentration in the microdialysis probe, 15 min) was administered stereotaxically into the CeA of arthritic rats (n = 9 rats; 5 h postinduction). When ACSF was administered into the CeA, systemic riluzole inhibited vocalizations of arthritic rats significantly compared to predrug values (n = 9 rats). n.s. non-significant; **P < 0.01; paired t test. c, d Stereotaxic application of a BK channel blocker (charybdotoxin, ChTx, 1 μM, concentration in the microdialysis probe, 15 min) into the CeA (n = 5 rats) or stereotaxic application of apamin (1 μM, concentration in the microdialysis probe, 15 min) into the BLA (n = 6 rats) did not block the significant inhibitory effects of systemic riluzole on audible (c) and ultrasonic (d) vocalizations of arthritic rats compared to predrug values. n.s. non-significant; *,**P < 0.05; paired t test. Bar histograms show mean ± SEM

Back to article page