(a) L-TBA (0.01–1 nmol) dose-dependently attenuates glutamate-induced pain in SNI (ANOVA P=0.0069), but not sham, rats (vehicle, veh). N=6 rats per group. (b) WAY+UCPH (1–100 nmol) dose-dependently potentiates glutamate-induced pain in SNI, but not sham, rats (ANOVA P=0.003). N=6 rats per group. (c) Paw-withdrawal thresholds (PWTs) of SNI rats are increased by L-TBA (1 nmol), but not WAY+UCPH (100 nmol) (ANOVA 30 min P<0.0001, 60 min P=0.0004). (***P<0.001 versus vehicle; legend as in d). N=8 rats/group. (d) PWTs of sham rats are reduced by WAY+UCPH (ANOVA 30–120 min P<0.001), but not L-TBA (***P<0.001). N=8 rats per group. (e) SNI, but not naive, rats show conditioned place preference (CPP) to L-TBA (1 nmol, CPP index=64.03%, ANOVA P=0.0099). Naive rats exhibit conditioned place aversion to WAY+UCPH (ANOVA 100 nmol, CPP index=37.16%, P=0.0118 (*P<0.05). N=8 rats per group. (f) Representative glutamate-induced Fos in ipsilateral SCDH (outlined with dashed lines) of sham and SNI animals following spinal pretreatment with L-TBA (1 nmol) or WAY+UCPH (100 nmol). Scale bar 100 μm. (g) For both SNI and sham rats, Fos in the ipsilateral SCDH is reduced by L-TBA (ANOVA P=0.0313), but conversely ipsilateral Fos is increased by WAY+UCPH in sham, but not SNI rats (ANOVA P=0.0313). (*P<0.05 with respect to vehicle). In both shams and SNI rats, L-TBA attenuates Fos more effectively than WAY+UCPH. (†††P<0.001 L-TBA versus LY393053). Six to 12 sections were averaged for each animal, with N=6 animals per group. (h) Representative glutamate-induced Jun in ipsilateral SCDH (outlined with dashed lines) of sham and SNI animals following spinal pretreatment with L-TBA (1 nmol) or WAY+UCPH (100 nmol). Scale bar, 100 μm. (i) Neither L-TBA nor WAY+UCPH significantly affected Jun in sham or SNI rats (ANOVA). Six to 12 sections were averaged per animal, with N=6 animals per group. All values in figure are expressed as mean±s.e.m.