When ingestion of a taste stimulus is paired with internal malaise the animal remembers the taste and rejects its ingestion thereafter. A model of neural substrate for this conditioned taste aversion (CTA) is presented on the basis of our recent experiments. To establish the CTA in rats, 0.01 M saccharin was paired with i.p. injection of 0.15 M LiCl. Behavioral lesion experiments by means of ibotenic acid showed that the parabrachial nucleus (PBN), medial thalamus (MT), and lateral part of the amygdala (LPA) were crucial to establish the CTA. c-fos immunoreactivity studies showed that ingestion of saccharin induced a remarkable activation of the central lateral (cl) subnucleus of the PBN in normal rats, however, rats with the CTA to saccharin showed c-fos neurons in the ventral lateral (vl) subnucleus of the PBN. These findings suggest that the recipient zone for saccharin taste switches from the cl to vl subnuclei after acquisition of a CTA. The taste pathway from the vl subnucleus to the LPA through the MT may be a neural substrate for taste aversion learning. The switching may result from a plastic change involving long-term potentiation and depression due to a convergence of the taste input of saccharin and general visceral information of LiCl injection.
