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. 2019 Sep 6;13:202. doi: 10.3389/fnbeh.2019.00202

Figure 2.

Figure 2

Effects of nicotine and cocaine on firing rate of VTA dopamine neurons in prenatal Poly I:C and adolescent THC treated offspring and their controls. (A) Representative firing rate histograms of VTA dopamine neurons recorded from vehicle-vehicle, Poly I:C-vehicle, vehicle-THC and Poly I:C-THC rats showing the effects of a bolus dose of nicotine (0.2 mg/kg, i.v.). Arrows indicate the times of nicotine injection. The graph shows that the combination of prenatal Poly I:C and adolescent THC prevented nicotine-induced increase of firing rate (vehicle-vehicle, n = 8; Poly I:C-vehicle, n = 6; vehicle-THC, n = 6 and Poly I:C-THC, n = 6; two-way ANOVA and Sidak’s test, *P < 0.05). (B) Representative firing rate histograms of VTA dopamine neurons recorded from vehicle-vehicle, Poly I:C-vehicle, vehicle-THC and Poly I:C-THC rats showing the effects of cumulative doses of cocaine (0.25–2.0 mg/kg, i.v.). Arrows indicate the times of cocaine injections (0.25, 0.25, 0.5, 1.0 mg/kg). The bottom graph displays the dose–response curves of the effect of cumulative doses of cocaine on the firing rate of VTA DA neurons recorded from vehicle-vehicle (n = 5), Poly I:C-vehicle (n = 6), vehicle THC (n = 4) and Poly I:C-THC (n = 4). Results are presented as mean ± SEM of firing rate expressed as a percentage of baseline levels.