Objective To establish a neuropathic pain model of mice through the chronic constrictive injury (CCI) method, and to discuss the effects of transient receptor potential ankyrin 1 (TRPA1) in the nucleus accumbens (Nac) on neuropathic pain. Methods According to the random number table method, 10 male Kunming mice were divided into two groups (n=5): a sham operation (SHAM) group and a CCI group. On day 7 after modeling, Western blot was used to detect the expression of TRPA1 protein in the NAc of both groups. Furthermore, according to the random number table method, 24 mice were divided into four groups (n=6): a CCI+A96 group (where the mice were injected with A967079 (A96) , a CCI+PBS group (where the mice were injected with PBS), a SHAM+A96 group (where the mice were injected with A967079) and a SHAM+PBS group (where the mice were injected with PBS). On day 7 after modeling, the TRPA1 antagonist A967079 or PBS was injected into the contralateral NAc and thermal withdrawal latency (TWL) was measured before and 2, 4 h, and 6 h after treatment. Results On day 7 after modeling, mice in the CCI group presented remarkable increases in the expression of TRPA1 in the contralateral NAc region than the SHAM group (P<0.05). Compared with the CCI+PBS group, the CCI+A96 group presented significant increases in TWL 2 h and 4 h after treatment (P<0.05), but after microinjection for 6 h basically returned to the level before treatment (P>0.05). Moreover, there was no significant difference in TWL between the SHAM+A96 group and SHAM+PBS group (P>0.05). Conclusions TRPA1 in the NAc region may take part in the regulation of neuropathic pain induced by CCI in the sciatic nerve.