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. Author manuscript; available in PMC: 2017 Oct 19.
Published in final edited form as: Neuron. 2016 Oct 6;92(2):493–504. doi: 10.1016/j.neuron.2016.09.029

Figure 2. Stress Attenuates Ethanol-induced DA Signaling In Vivo.

Figure 2

A) Animals were exposed to a 1-hr restraint stress and microdialysis experiments were conducted 15 hrs later.

B) Time course of DA release in the NAc following in vivo ethanol administration in control rats (black), in stressed rats (red), and in rats injected with RU486 (i.p.) prior to stress exposure (grey). Ethanol (1.5 g/kg) was injected i.v. during the 5-min period (shaded vertical grey bar). *Significantly different from the control group and from the RU486+Stress group by ANOVA with repeated measures, p < 0.05, n = 7–9 rats/group.

C) The spontaneous firing rate of VTA DA neurons was measured in vivo using single-unit recordings in anesthetized animals.

D) Putative DA neuron recording sites in the VTA for control (black) and stressed animals (red).

E) Representative recordings from putative DA neurons before and after ethanol administration (0.6–1.5 g/kg) in the control (black) and stressed (red) groups. No significant differences in the mean basal firing rate were detected between control and stressed groups: 6.3 ± 0.7 Hz in control vs. 8.0 ± 1.0 Hz after stress, n = 8–13, p > 0.05.

F) In the control group (black), ethanol increased the firing rate of putative DA neurons. In the stressed group (red), ethanol failed to increase the firing rate of putative DA neurons. **Significantly different from the control group by t-test, p < 0.01, n = 8–13 rats/group.