In general, ethanol consumption and/or exposure to low or moderate doses of ethanol elevate glutamatergic transmission and/or extracellular levels of glutamate in the nucleus accumbens (Acb)108; Acb shell (AcbSh)88,89,109–111; basolateral amygdala (BLA)112; cortex113; Hippocampus114,115; ventral teg-mental area (VTA)116; and posterior VTA (pVTA).110,117 It has also been shown that genetics influence ethanol-induced increases in extracellular glutamate within the Acb and/or PFC, such that rats with a predisposition for higher ethanol intake (P and Lewis rats) display greater elevations in glutamate relative to rats with a predisposition for lower ethanol intake (NP and F344 rats).118,119 Interestingly, similar relations have been observed between alcohol-preferring versus nonpreferring inbred strains of mice.86,120 In addition, these elevations in glutamatergic activity can be conditioned to the environment in which the animal had access to ethanol, with glutamatergic increases seen in the Acb core (AcbCo) or basolateral Amyg (BLA).103,121,122
