Parabrachial nucleus lesions and conditioned taste aversion: Evidence supporting an associative deficit.

Reilly, Steve; Grigson, Patricia S.; Norgren, Ralph

doi:10.1037/0735-7044.107.6.1005

Cited by 129 publications

(164 citation statements)

References 49 publications

(77 reference statements)

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“…By way of indirect support, a great deal of data suggest that drugs of abuse are rewarding and that drug-induced suppression of CS intake is not like that induced by LiCl. Specifically, drugs of abuse are readily self-administered [for review, see 27] and they support the development of conditioned place preferences [41][42][43][44]. Unlike drugs of abuse that support a reduction in CS intake, but an increase in instrumental responding (as described above), LiCl suppresses both consummatory and instrumental responding [24, 28 , 29 ].…”

Section: The Model: Experimenter Delivered Drugmentioning

confidence: 99%

Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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In the words of the late Charles Flaherty, reward comparison is commonplace. Rats and man, it appears, compare all rewards and this capacity likely contributes to our ability to select the most appropriate reward/behavior (food, water, salt, sex), at the most ideal level (e.g., a certain sweetness), at any given time. A second advantage of our predisposition for reward comparison is that the availability of rich alternative rewards can protect against our becoming addicted to any single reward/behavior. Thus, the potential protective effects of natural rewards/enrichment are addressed. Despite this, behavior can become inflexible when, through the development of addiction, stress, drug, or cues elicit craving, withdrawal, and ultimately, drug-seeking. Drug-seeking corresponds with a 'window of inopportunity', when even potent natural rewards have little or no impact on behavior. During this time, there is a unitary solution to the need state, and that solution is drug. The present animal model explores this 'window of inopportunity' when natural rewards are devalued and drug-seeking is engaged and considers a mode of possible intervention.

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Section: The Model: Experimenter Delivered Drugmentioning

confidence: 99%

Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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“…Although the neural basis of CTA is unknown, previous research demonstrated that lesions of the parabrachial nucleus (PBN) in rodents can cause deficits in CTA (Dilorenzo, 1988;Flynn et al, 1991;Reilly et al, 1993;Grigson et al, 1998). However, because the PBN contains subpopulations of neurons that regulate multiple functions including both taste (Rosen et al, 2011;Tokita and Boughter, 2012;Tokita et al, 2012) and appetite suppression (Becskei et al, 2007;DiPatrizio and Simansky, 2008;Wu et al, 2009;Carter et al, 2013), the molecular identity of neurons that underlie these effects is unknown.…”

Section: Introductionmentioning

confidence: 99%

Parabrachial Calcitonin Gene-Related Peptide Neurons Mediate Conditioned Taste Aversion

2015

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Conditioned taste aversion (CTA) is a phenomenon in which an individual forms an association between a novel tastant and toxininduced gastrointestinal malaise. Previous studies showed that the parabrachial nucleus (PBN) contains neurons that are necessary for the acquisition of CTA, but the specific neuronal populations involved are unknown. Previously, we identified calcitonin gene-related peptide (CGRP)-expressing neurons in the external lateral subdivision of the PBN (PBel) as being sufficient to suppress appetite and necessary for the anorexigenic effects of appetite-suppressing substances including lithium chloride (LiCl), a compound often used to induce CTA. Here, we test the hypothesis that PBel CGRP neurons are sufficient and necessary for CTA acquisition in mice. We show that optogenetic activation of these neurons is sufficient to induce CTA in the absence of anorexigenic substances, whereas genetically induced silencing of these neurons attenuates acquisition of CTA upon exposure to LiCl. Together, these results demonstrate that PBel CGRP neurons mediate a gastrointestinal distress signal required to establish CTA.

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“…The LH lesions were positioned stereotaxically at Ϫ3.0 mm from ␤, 2.0 mm lateral, and 8.8 mm deep into the skull surface, and the lesion procedure was identical to that described in experiment 1, except that it was unilateral. The parabrachial lesions were placed under electrophysiological guidance using procedures detailed elsewhere (2,24,28,35). Once a PBN gustatory response was located, the recording electrode was replaced with a micropipette glued to the shaft of a 1.0-l syringe and filled with ibotenic acid (20 g/l in PBS, pH ϭ 7.4).…”

Section: Methodsmentioning

confidence: 99%

Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Dayawansa

Ruch

Norgren

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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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...

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Parabrachial nucleus lesions and conditioned taste aversion: Evidence supporting an associative deficit.

Cited by 129 publications

References 49 publications

Reward comparison: the Achilles’ heel and hope for addiction

Reward comparison: the Achilles’ heel and hope for addiction

Parabrachial Calcitonin Gene-Related Peptide Neurons Mediate Conditioned Taste Aversion

Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

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