Fig. 1: GluA1 deletion does not alter intrinsic VTA-NAcc DA pathway release properties.
a Electrical stimulation of the VTA and FSCV measurement of NAcc DA release in anaesthetized WT and Gria1−/− mice. Outline of stimulation protocol involving a baseline session before and after the stimulus response curve protocol. Baseline stimulation parameters were 30 Hz, 40 pulses, 2 ms pulse width, 300 µA. b Average traces showing the time course of electrically evoked DA release during baseline stimulations before and after the stimulation response curves (shown in f and g). Peak DA (c), latency to peak (d), and rate of decay (e) of these baseline stimulations did not differ between genotypes. Rate of decay was quantified using the t50 from model fit of negative exponential decay for traces during the baseline period with model fit R2 > 90%. Box and whisker plots show range (error bars), 25th–75th percentile (box limits), and median values (line), and individual animal data points. f Effects of varying number of stimulation pulses on the peak DA release expressed as a percentage of release to the maximum (40) pulses. g Effects of varying stimulation amplitude on the peak DA release expressed as a percentage of release to the maximum (300 µA) amplitude. Varying the number of pulses and stimulation amplitude significantly changed DA release but this did not depend on genotype. Significant main effect of stimulation amplitude (F5,45 = 59.87, p < 0.001), and number of pulses (F4,45 = 83.91, p < 0.001), but no significant main effects of genotype or genotype × stimulation interactions (all Fs < 0.59, ps > 0.61, and Fs < 1.57, ps > 0.22 respectively). See Supplementary Fig. 1 for histology and additional analyses. All error bars represent ± standard error of the mean.
