Fig. 4: Expression of constitutively active CRTC1 in the NAcsh increases cocaine reinforcement and motivation and rescues the actions of AMPK activation.
From: Novel role of AMPK in cocaine reinforcement via regulating CRTC1
A Timeline of the experiment. Four weeks after the injection of AAV-GFP or AAV-CA-CRTC1 in the NAcsh, the rats were trained to self-administer intravenous injections of cocaine under an FR1 schedule in daily 3 h sessions. The response requirement was gradually increased to FR5, and training continued until cocaine intake stabilized. Following acquisition and stabilization, the rats received intra-NAcsh infusions of saline or the AMPK activator AICAR. The rats then underwent a between-session dose-response test and progressive-ratio test. B Photomicrographs of AAV-CA-CRTC1 injection sites in the NAcsh (scale bar = 200 μm [left], 50 μm [right]). Infusions (C), active nosepokes (D), and inactive nosepokes (E) during daily 3 h self-administration sessions. F The expression of CA-CRTC1 shifted dose-response curves upward, which was prevented by AICAR treatment (n = 8–10/group). G The expression of CA-CRTC1 increased breakpoints during the progressive-ratio test, which was prevented by AICAR treatment (n = 8–10/group). The data are expressed as mean ± SEM. Post hoc analyses were performed using the Tukey test. *p < 0.05, **p < 0.01, compared with GFP + saline group; #p < 0.05, ##p < 0.01, ####p < 0.0001, compared with CA-CRTC1 + AICAR group.
