Fig. 2: Esketamine administration causes mixed effects on spontaneous dopaminergic transmission.

A Schematic representation of dopamine sensor expression in the NAc. B Representative immunohistochemical image of dLight1.3b expression in the NAc. Scale bar: 1 mm. C Average trace detected from the fluorescent signal of dLight1.3b in the NAc after saline or esketamine (10 mg/kg and 30 mg/kg) administration. D Representative traces of the corrected dLight1.3b in the NAc after saline or esketamine (10 mg/kg and 30 mg/kg) administration. E–J Peaks per minute, dopamine transient amplitude and dopamine transient duration on day 1 and day 5 of esketamine administration with and without pretreatment with naloxone (3 mg/kg) (each dot represents one animal). K Schematic representation of the viral strategy for expression dopamine and calcium biosensors in the NAc and VTA-originated terminals, respectively, and representative traces of Dlight1.3b, RCaMP1.07 and isosbestic control signals. L–N Peaks per minute, transient amplitude, and transient duration of calcium in the NAc (each dot represents one animal). In all panels, statistical significance, evaluated by Tukey’s post-hoc multiple comparisons test, * p < 0.05 and ** p < 0.01). O, P Correlation between extracellular dopamine and intracellular calcium from terminals from VTA neurons in the NAc. All correlations were statistically significant with p < 0.001 and esketamine treatment did not alter Pearson’s r coefficients on amplitude (p = 0.52) nor duration (p = 0.58).