Several studies have shown that taste-aversion conditioning can modify the neural coding of taste in rodents. Chang and Scott (1984) reported that after aversive conditioning to saccharin, rats declined to drink saccharin solution, and, simultaneously, the neural code in the first relay, the nucleus of the solitary tract (NST), showed drastic changes compared with the neural code analyzed in unconditioned rats. Similarly, after aversive conditioning, c-fos staining showed changes in the locations of saccharin-responding neurons in the parabrachial nuclei (PBN) (Yamamoto, 1993) and in the NST (Houpt et al., 1994, 1996). Preference conditioning has been shown to produce changes in neural activation patterns in the NST (Giza et al., 1997).
In rodents, taste afferent pathways lead, on the one hand, to cortical taste areas through the NST, the PBN (the pontine taste relay), and thalamus and, on the other hand, to the amygdala, the lateral hypothalamus, and the bed nucleus of the stria terminalis (BST). In primates, the pontine taste relay is bypassed, and the NST projects directly to the parvicellular region of the thalamic ventroposteromedial nucleus (VPMpc). Efferent pathways from the amydgala, lateral hypothalamus, and BST have been traced down to the pons and the NST (Norgren, 1985). We know from a study by Mora, Rolls, and Burton (1976) that in primates, the lateral hypothalamus contains neurons responding to highly integrative information, such as the sight of a taste stimulus that a monkey likes.