Although permanent lesion studies have demonstrated that the area postrema (AP), a chemoreceptor trigger zone, is part of the neural mechanism for conditioned taste aversions (CTAs), its exact role remains questionable. It has been suggested that the attenuated acquisition of a CTA after permanent lesions of the AP is the result of an inability to recognize the conditioned taste as novel. The present series of experiments was designed to test the hypothesis that lesions of the AP interfered with LiCl processing and not recognition of taste novelty. This was accomplished by using the reversible lesioning procedure, cooling, only during administration of the illness-inducing agent. In Expt. 1, measurement of thermal lines around the tip of the cold probe in the AP indicated that our cooling procedures allowed the majority of the AP to be cooled to temperatures that suppress neuronal activity and transsynaptic transmission, but not axonal transmission. In Expts. 2 and 3, rats were injected with either LiCl or apomorphine after consumption of a 10% sucrose solution. Cooling of the AP was initiated 5 min before administration of one of the illness-inducing agents and was continued for 55 min after injection. The rats were tested later for acquisition while the neural function of the AP was preserved. Our experimental results demonstrated that cooling the AP could attenuate the CTA induced by LiCl, but had no effect on the CTA induced by apomorphine. Since the AP was functional when the rats encountered the novel sucrose solution both before and after conditioning, but not functional when LiCl was given, these results do not support the recognition of taste novelty hypothesis.