The role of the lateral hypothalamus in taste-guided behaviors: A comparison with the parabrachial nucleus

Previous data show that the parabrachial nucleus (PBN) is necessary for conditioned taste aversion (CTA) learning and Na+ appetite expression and must be connected with the forebrain for these two tasks. Animals with electrolytic lateral hypothalamus (LH) and PBN lesions demonstrate a similar pattern of taste-guided behavioral deficits. Electrolytic lesions of the LH, however, destroy the intrinsic neurons of the LH as well as passing axons, including those connecting the PBN with other ventral forebrain structures. Thus, the Na+ appetite and CTA deficits in electrolytic LH lesioned animals could be attributed to either destroying the LH itself or interrupting fibers of passage through the LH. In these experiments, ibotenic acid (IBO) lesions of the LH allowed for the assessment of the role the intrinsic neurons of the LH play in Na+ appetite and CTA learning.; These experiments demonstrated that the anterior LH is necessary for rats to increase dH₂O intake when challenged with cellular dehydration. Additionally, rats with LH lesions that destroyed most of the rostrocaudal extent of the LH are unable to express a normal Na+ appetite.; While the anterior LH is involved in compensatory fluid intake, the posterior LH is involved in CTA formation, although the LHX rats were able to remember a preoperatively learned aversion. The nature of the CTA deficit arising from IBO LH lesions was further evaluated. Rats with IBO LH lesions could learn a conditioned flavor preference and could learn conditioned trigeminal or odor aversions, so LHX rats could learn using taste and visceral cues. Thus, it is likely that the CTA deficit in IBO LHX rats results from a specific inability to pair a taste with illness.; Collectively, these data demonstrate that IBO LH lesioned rats have CTA acquisition deficits, although not of the same magnitude as observed in PBNx animals. In addition, the Na+ appetite deficit in LHX rats is more severe than seen previously in PBNx rats. These experiments demonstrate that the deficit pattern following destruction of the intrinsic neurons of the LH, while sparing passing axons, mimic PBN lesion deficits regarding CTA learning and Na+ appetite expression.