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. 2013 Jan 14;591(Pt 7):1951–1966. doi: 10.1113/jphysiol.2012.246983

Figure 1. Potentiation of glutamatergic synapses on hypocretin neurons following the establishment of cocaine-conditioned place preference (CPP).

Figure 1

A, sample traces of mEPSCs recorded from control and cocaine-treated mice are presented. B, mean frequency of mEPSCs detected in saline- and cocaine-treated mice showed no significant difference between these two groups. C, a significant increase in the mean amplitude of mEPSC events detected in cocaine-treated mice was indicated as compared to the control group (*P < 0.05, t test). D, a significant right-shift in the cumulative probability of mEPSC amplitude was detected in cocaine-treated mice as compared to control mice (P < 0.001, Kolmogorov–Smirnov test). E, sample traces of evoked EPSCs carried by AMPA receptors (AMPAR) and NMDA receptors (NMDAR) in control and cocaine-treated mice. F, the ratio of evoked EPSCs carried by AMPAR and NMDAR was enhanced in mice treated with cocaine as compared to controls (*P < 0.05, t test). Inset, bar graph indicates that mice spent more time in the cocaine-paired side of the testing apparatus after a 3-day training session. Blockade of the hypocretin-1 receptor pathway blocks cocaine CPP in mice.