Animals, including rats, have a predisposition to process and use spatial information to organize and guide behavior. The hippocampus and related structures are critically involved in this function, and, consequently, it has been proposed that one function of the hippocampus is to construct "spatial cognitive maps" of environments. Lesions to the hippocampus or its connections produce a pattern of alterations in behavior which include shifts from the use of spatial information to guide behavior to the use of cue- or taxon-based information to guide behavior. Recently it was demonstrated that ethanol interacts with a specific group of neurotransmitter systems, i.e., N-methyl-D-aspartate receptors and GABA(A) receptors that exist in high proportions in the hippocampus and related structures. In this review, we seek to summarize the literature demonstrating that one effect of acute and chronic ethanol exposure is to produce behavioral alterations that are strikingly similar to those found following lesions to the hippocampal system. Furthermore, cellular and anatomical alterations resulting from similar ethanol exposure paradigms will be reviewed and offered as possible mechanisms for producing the alterations in behavior. Finally, several unanswered questions concerning the interaction between ethanol and spatial cognitive processing will be identified.