Fig. 2

Effect of the injection of dopamine receptor agonists/antagonists into the NAc on neuropathic pain. a Schematic diagram showing the injection site of the NAcMed (a-i) or NAcLat (a-ii). b Latency in the response to thermal stimulation under a neuropathic pain-like state by administration of the selective dopamine D1 receptor agonist Chloro-APB into the NAcMed (b-i) and NAcLat (b-ii). Data are presented as the mean ± SEM of 5-6 animals. ^***p < 0.001 vs. saline ligation contralateral paw; ^#p < 0.05, ^###p < 0.001 vs. Chloro-APB ligation contralateral paw; ^$$$p < 0.001 vs. saline ligation ipsilateral paw. c Latency in the response to thermal stimulation under a neuropathic pain-like state by the administration of the selective dopamine D2 receptor agonist quinpirole into the NAcMed (c-i) and NAcLat (c-ii). Data are presented as the mean ± SEM of 5-6 animals. ^**p < 0.01, ^***p < 0.001 vs. saline ligation contralateral paw; ^##p < 0.01, ^###p < 0.001 vs. quinpirole ligation contralateral paw; ^$$p < 0.01, ^$$$< 0.001 vs. saline ligation ipsilateral paw. d Effects of the selective dopamine D1 receptor antagonist SCH23390 in the NAcMed and NAcLat in mice. Latency in the response to thermal stimulation under a neuropathic pain-like state by SCH23390 of the NAcMed (d-i) and NAcLat (d-ii). Data are presented as the mean ± SEM of 5-6 animals. ^***p < 0.001 vs. saline ligation contralateral paw; ^###p < 0.001 vs. SCH23390 ligation contralateral paw. e Latency in the response to thermal stimulation under a neuropathic pain-like state by the administration of dopamine D2 receptor antagonist sulpiride of the NAcMed (e-i) and NAcLat (e-ii). Data are presented as the mean ± SEM of 5-6 animals. ^***p < 0.001 vs. vehicle ligation contralateral paw; ^###p < 0.001 vs. sulpiride ligation contralateral paw