Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Abstract

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...

Advances in the neurobiological bases for food ‘liking’ versus ‘wanting’

“…Although best known as a visceral/taste sensory relay (Norgren and Leonard, 1971; Di Lorenzo and Monroe, 1997), the PBN has additional functions, including food intake (Wilson et al, 2003; DiPatrizio and Simansky, 2008; Wu et al, 2009; Carter et al, 2013b), establishing a conditioned taste aversion (Yamamoto, 2007; Carter et al, 2013b; Dayawansa et al, 2013), and REM sleep (Quattrochi et al, 1998; Torterolo et al, 2011). …”

Taste Processing: Insights from Animal Models

“…The nucleus of the solitary tract (NTS) is the first brainstem nucleus that receives taste afferents [8][9][10]. From this nucleus, taste information is ipsilaterally sent to another brainstem group of cells, the posteromedial parabrachial nucleus, and then ascending projections reach several brain structures, such as the lateral hypothalamus, the bed nucleus of the stria terminalis, the amygdala and the ventroposteromedial and lateral thalamus [11,12]. Finally, the higher level of taste processing takes place in the gustatory insular cortex [10,13,14].…”

“…The functional connectivity between the parabrachial nucleus and the gustatory insular cortex is selectively involved in the acquisition of CTA but not in the formation of safe taste memories [43]. These pathways and the vagal system involved in the processing of visceral malaise are necessary for the acquisition of CTA and taste aversion memory [10][11][12]14]. Moreover, the role of other brain structures in the neurobiology of CTA, such as the medial prefrontal cortex and the nucleus accumbens, is being elucidated at present [44], together with the functions of the piriform [45] and perirhinal [46] cortices in taste recognition.…”