Figure 1.

μ- and δ-opioid receptor agonists inhibit single-spike-evoked DA overflow. a, Single-spike-evoked DA responses constructed using fast-scan cyclic voltammetry before and after successive 10 min bath applications of the μ-opioid EM-1 (1 μm) and the μ-opioid receptor antagonist naloxonazine (1 μm). The insets are subtracted voltammograms obtained at the peak of evoked DA responses in each condition. b, Summary of the effect of 1 μm EM-1 on evoked DA responses in the dorsal medial NAc shell (n = 24). Each data point reflects a single stimulus pulse, unless noted by 2P, 4P, or 6P, indicating two, four, or six stimulus pulses, respectively, delivered at 25 Hz (in this and subsequent figures). Average DA concentration elicited by single spikes during control conditions was normalized to 1 for each recording. EM-1 significantly inhibited single-spike-evoked DA overflow (t = 17.6, p < 0.001, n = 24) and naloxonazine induced significant recovery (t = −12.1, p < 0.001, n = 24). Baseline single-spike dopamine levels during control averaged 0.59 ± 0.10 μm. c, The difference between DA release from burst and single stimuli were determined by subtracting the peak DA overflow responses to single spikes from that measured after two, four, or six stimuli at 25 Hz. Statistical comparison by repeated-measures ANOVA revealed significant effects of pulse number (F_(2,69) = 25.6, p < 0.0001), EM-1 (F_(1,69) = 31.1, p < 0.0001), and an interaction (F_(2,69) = 4.4, p = 0.0157). d, Summary of the effect of 1 μm deltorphin II, a δ-opioid receptor agonist, followed by 1 μm BNTX, an δ₁-opioid receptor antagonist, on evoked DA responses in the NAc shell (n = 6). The 25 Hz burst stimuli of two, four, or six stimulus pulses are indicated. Deltorphin II induced significant inhibition of single-spike-evoked DA overflow (t = 8.9, p < 0.001, n = 6) and BNTX induced significant recovery (t = −2.5, p < 0.05, n = 6).