Fig. 4. α-1A-selective antagonist enhances the therapeutic window between analgesia and sedation for intrathecal clonidine and tizanidine in wild-type mice. (  A–C ) Effect of intrathecal clonidine pretreatment, with (▴) or without (▪) 30 μg/kg intraperitoneal 5-methylurapidil (5-MU) on total pain scores in wild-type mice with (  A ) sulprostone-induced allodynia and (  B ) NMDA-induced allodynia, and on (  C ) activity counts in an exploratory chamber, expressed as percent sedation. (  D–F ) Effect of intrathecal tizanidine pretreatment, with (▴) or without (▪) 30 μg/kg intraperitoneal (5-MU) on total pain scores in wild-type mice with (  D ) sulprostone-induced allodynia and (  E ) NMDA-induced allodynia, and on (  F ) activity counts in an exploratory chamber, expressed as percent sedation. (  G ) Lack of effect of 30 μg/kg intraperitoneal 5-MU alone on total pain scores in wild-type mice with sulprostone- or NMDA-induced allodynia. 5-MU = 5-methylurapidil; NMDA =  N -methyl-  D -aspartate; Sulp = sulprostone. *  P < 0.05; **  P < 0.01, ***  P < 0.001  versus allodynic agent alone for pain score, +  P < 0.05, ++  P < 0.01, +++  P < 0.001  versus vehicle for sedation; N = 6 mice per group.