To evaluate the role of the STT pathway in the inhibition of cocaine-induced locomotor activity by ulnar MS, STT lesions were made by surgically cutting the ventrolateral columns at the C3 level 7–10 days before testing (Fig. 3A1 and A2). STT lesions did not alter the inhibitory effects of ulnar MS on cocaine locomotion (p > 0.05, STT X + MS vs. Sham + MS, Fig. 3A3), suggesting that the STT pathway does not play a role in these processes (Fig. 3A). In an experiment to evaluate the role of the VPL, the third-order neurons of the DC pathway, in the inhibition of cocaine-induced locomotor activation by ulnar MS, chemical lesion of the VPL by ibotenic acid (Fig. 3B1 and B2) effectively blocked the ulnar MS effects (VPL X + MS vs. Sham + MS; two-way ANOVA: group factor F = 7.010, p = 0.017; time factor F = 14.122, p < 0.001; interaction F = 2.584, p = 0.016; Fig. 3B3), confirming the VPL mediation of DC input.