Figure 4.

Blockade of glutamate reuptake reveals increased tonic NMDAR-mediated currents following cocaine self-administration and D1DR stimulation. A, NMDAR-mediated tonic currents were measured as a shift of baseline holding current following application of dl-AP5 (solid black lines) in the absence (top row) and presence (bottom row) of SKF38393 pretreatment. Dotted lines are centered at the mean holding current before application of dl-AP5. To the left of the traces are Gaussian-fitted distributions of the amplitude of baseline noise before (black) and after (gray) dl-AP5 application. The displayed fits are to the portions of the distributions not skewed by synaptic events. Notice the differences in the onset of dl-AP5 block likely due to variation in cell accessibility between slices. B, Bar histograms summarizing tonic NMDAR-mediated current amplitudes across the experimental groups (t₍₁₆₎ = 2.35 for saline SKF; t₍₁₇₎ = 2.15 for cocaine no SKF; t₍₁₅₎ = 2.21 for cocaine SKF; *p < 0.05 vs saline no SKF; n = 8–11 cells).