Fig. 4
From: The sigma-1 receptor modulates methamphetamine dysregulation of dopamine neurotransmission

In vivo σ1R activation in the dorsal striatum inhibits METH-induced dopamine efflux. METH was locally applied into the dorsal striatum of anesthetized mice. Representative oxidation currents (converted to a micromolar concentration using a calibration factor determined in vitro) are shown in (a) and (b). METH signals produced after pretreatment are overlaid with signals obtained after the secondary treatment for ease of comparison. a Representative oxidation traces produced by METH-induced dopamine efflux after pretreatment aCSF treatment (black lines) or subsequent aCSF (red line) or PRE-084 (blue line) treatment. b Representative oxidation currents produced by METH-induced dopamine efflux after BD1063 pretreatment (black lines) or subsequent aCSF (gray line) or PRE-084 (purple line) treatment. c Comparison of the signal amplitude percent change over baseline (pre-aCSF or pre-PRE-084) reveals that intrastriatal application of PRE-084 (n = 9) but not aCSF (n = 6) significantly decreased the amplitude of dopamine release. Application of BD1063 prior to PRE-084 prevented this effect (n = 4 BD1063 + aCSF, n = 6 for BD1063 + PRE-084, F (1,21) = 6.06, P = 0.0226, Sidak’s test for multiple comparisons, *P = 0.0222). Data is represented as mean ± SEM