Evidence from the effect of aspiration lesions of the entorhinal cortex (EC) has shown that this region is involved in conditioned odor-aversion (COA) learning--that is, the avoidance of an odorized tasteless solution the ingestion of which precedes toxicosis--by rendering COA tolerant to long odor-toxicosis delay. The present study examined whether neurotoxic lesions restricted to the lateral or medial parts of the EC, in comparison with large aspiration lesions, were sufficient to produce this effect. Male Long-Evans rats received odor-intoxication pairing with either a short (5-min) or long (120-min) delay between the presentation of the odor and toxicosis. All groups, including sham-lesioned controls, showed COA at the 5-min odor-toxicosis delay interval, but only rats with lateral EC damage displayed COA at the longer delay. These data show that the lateral EC is part of the substrate involved in the control of the olfactory memory trace during COA.