Rats with bilateral lesions of the lateral hypothalamus (LH) fail to exhibit sodium appetite. Lesions of the parabrachial nuclei (PBN) also block salt appetite. The PBN projection to the LH is largely ipsilateral. If these deficits are functionally dependent, damaging the PBN on one side and the LH on the other should also block Na appetite. First, bilateral ibotenic acid lesions of the LH were needed because the electrolytic damage used previously destroyed both cells and axons. The ibotenic LH lesions produced substantial weight loss and eliminated Na appetite. Controls with ipsilateral PBN and LH lesions gained weight and displayed robust sodium appetite. The rats with asymmetric PBN-LH lesions also gained weight, but after sodium depletion consistently failed to increase intake of 0.5 M NaCl. These results dissociate loss of sodium appetite from the classic weight loss after LH damage and prove that Na appetite requires communication between neurons in the LH and the PBN. ibotenic acid; lateral hypothalamus; asymmetric lesions; parabrachial nuclei SALT APPETITE ARISES DURING sodium need or its hormonal mimics. It is usually assessed by measuring NaCl intake at concentrations rejected by animals in hydromineral balance (5,38). Although the hormonal precursors of the Na (sodium) appetite and their neural targets are yielding to investigation, the neural mechanisms that change the hedonic value of the sapid stimulus remain elusive (6, 10). Bilateral lesions centered in the parabrachial nuclei (PBN), the second central gustatory relay in rodents, eliminate the expression of salt appetite (7,8,41,(43)(44)(45). Chronic decerebrate rats that have an intact PBN but no connections between the hind-and forebrain also fail to express Na appetite (12). Thus, the PBN is necessary for the expression of sodium appetite, but is not sufficient unless its axonal connections to the forebrain are intact. In the forebrain, however, neither the thalamic nor the cortical gustatory areas are required for the expression of this behavior (7,8,41,51,55). Based on these observations, it follows that the gustatory neural activity required for salt appetite reaches the forebrain via the PBN projections to the limbic system (29). Nevertheless, the intermediate structures and functional relationships remain to be deciphered.The major terminal areas of the PBN in the limbic system: 1) amygdala, 2) bed nucleus of the stria terminalis, and 3) lateral hypothalamus (LH), each influence Na appetite to one degree or another (9,36,42,56). These same areas also are connected to the PBN reciprocally, to one another (3, 21), and to key components in a proposed reward system: the prefrontal cortex, ventral tegmental area, and nucleus accumbens (22,24,47). This anatomical complexity confounds any simple prediction about the mechanisms through which the hedonic sign of parabrachial gustatory activity is altered by body sodium deficit.The conventional approach to such an embarrassment of riches is to damage each of the forebrain targets in turn. As menti...

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Dayawansa S, Ruch S, Norgren R. Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions. Am J Physiol Regul Integr Comp Physiol 306: R190 -R200, 2014. First published November 20, 2013 doi:10.1152/ajpregu.00333.2013.-Rats with bilateral excitotoxic lesions of the parabrachial nuclei (PBN) fail to acquire a conditioned taste aversion (CTA), yet they retain the ability to express a CTA learned prior to incurring the damage. Rats with bilateral electrolytic lesions of the lateral hypothalamus (LH) also have CTA learning deficits. The PBN have reciprocal neural connections with the LH. This suggests that these CTA deficits may be functionally related. Electrolytic lesions damage fibers of passage, as well as intrinsic neurons. Thus, these LH lesions might also interrupt reciprocal connections between the PBN and other ventral forebrain areas, such as the amygdala and bed nucleus of the stria terminalis. To distinguish the source of the LH-lesion deficit, we tested for CTA first after bilateral excitotoxic lesions of LH and subsequently with a second set of animals that had asymmetric excitotoxic PBN and LH lesions. The rats with bilateral excitotoxic LH lesions showed deficits when acquiring a postlesion CTA. The asymmetrical PBN-LH lesions not only slowed acquisition of a CTA but also sped up extinction. This implies that interaction between the two structures, at minimum, facilitates CTA learning and may have a role in its consolidation. conditioned taste aversion; lateral hypothalamus; learning; neural connections; parabrachial nuclei RATS WITH BILATERAL ELECTROLYTIC or excitotoxic lesions of the parabrachial nuclei (PBN) can recall a prelesion conditioned taste aversion (CTA), but postlesion, they are unable to acquire new CTAs (1, 3-5, 9, 28, 37, 44). Rats with bilateral electrolytic lesions of the lateral hypothalamus (LH) exhibit a similar profile. They can retain a CTA learned prior to the lesions but fail to learn new CTAs (4, 34 -36). The PBN has reciprocal neural connections to the LH, central nucleus of the amygdala (CNA), and the bed nucleus of the stria terminalis (BNST) (11,12,14,16,17,(21)(22)(23)(24)43).Electrolytic lesions of the LH can damage the fibers of passage that link the PBN to the CNA and BNST (23,24,33). Thus, the CTA deficits displayed by rats with electrolytic LH lesions (LHx) could be due to the involvement of the intrinsic neurons of the LH or the functional isolation of PBN from the CNA, the BNST, or other anterior forebrain sites.To assess the role of the LH neurons in CTA, we made bilateral lesions using the excitotoxin ibotenic acid to preserve the fibers of passage. These rats were tested for retention of a prelesion CTA and a postlesion CTA acquisition. These experiments can assess the role of LH neurons in CTA, but they cannot demonstrate a functional interaction between the PBN and LH in CTA acquisition.Such an interaction has been demonstrated for salt appetite using rats with asymmetric PBN-LH lesions, i.e., unilateral PBN damage on one s...