Pretreatment with ethanol was shown to further enhance the dopamine levels in the NAc shell in response to a challenge dose of ethanol in the posterior VTA, indicating that VTA neurons sensitize to this acute effect of ethanol causing larger ethanol-induced dopamine release in the shell (Ding, Rodd et al. 2009). At the same time, a recent report shows blunted dopamine levels after chronic ethanol exposure, an effect mediated by kappa opioid receptors (Karkhanis, Huggins et al. 2016). Stress also can change the acute ethanol response in the VTA from inhibition in naïve animals to excitation of GABA neurons in the VTA of animals pre-expose to stress. As consequences of this switch, dopamine neuron firing is decreased and the ethanol-induced dopamine signals in the NAc is blunted by stress pre-exposure (Ostroumov, Thomas et al. 2016). It is possible that this effects of stress can explain, at least partially, the discrepancy on the sensitized or blunted dopamine levels in response to acute ethanol after chronic exposure. (Valenta, Job et al. 2013)
