Fig. 2

Intra-DMS injection of HU210 and AM281 impaired NPL and alleviated the impairment of NRL, respectively. A, F A simplified scheme illustrating the injection sites and the experimental paradigms (A: intracranial injection of HU210; F: combined administration of AM281 and HU210). B–D Compared with the vehicle group, the HU210 group exhibited significantly increased tELS (B), failures (C), and TMCS (D) during NRL. E Escape latency curves of two groups in the intracranial injection of HU210 experiment (vehicle vs. HU210). G–I Compared with the “Vehicle + HU210” group, the “AM281 + HU210” group exhibited significantly decreased tELS (G), failures (H), and TMCS (I) during NRL. J Escape latency curves of two groups (vehicle + HU210 vs. AM281 + HU210). Vehicle, mice were administrated with vehicle (i.c.); HU210, mice were administrated with HU210 (i.c.); Vehicle + HU210, mice were administrated with vehicle (i.c.) and HU210 (i.p.); AM281 + HU210, mice were administrated with AM281 (i.c.) and HU210 (i.p.). HU210, mice were administrated with HU210 (i.c.). Vehicle: n = 8; HU210: n = 7; Vehicle + HU210: n = 9; AM281 + HU210: n = 9. Data shown as mean ± SEM. ANOVA (E, J), unpaired t-test (B, G), and Mann-Whitney test (C, D, H, I): **p < 0.01, ***p < 0.001