Effects of central and basolateral amygdala lesions on conditioned taste aversion and latent inhibition.

[Correction Notice: An erratum for this article was reported in Vol 121(6) of Behavioral Neuroscience (see record 2007-18058-034). Figure 4 on p. 96 (Results and Discussion, Experiment 2: Behavioral section) was incorrect. The correct figure is provided in the erratum.] The present study examined the effects of neurotoxic lesions of the central nucleus (CNA) and basolateral complex (BLA) of the amygdala on conditioned taste aversion (CTA) in a latent inhibition design. In Experiment 1, lesions of the CNA were found to have no affect on CTA acquisition regardless of whether the taste conditioned stimulus (CS) was novel or familiar. Lesions of the BLA, although having no influence on performance when the CS was familiar, retarded CTA acquisition when the CS was novel in Experiment 2. The pattern of results suggests that the CTA deficit in rats with BLA lesions may be a secondary consequence of a disruption of perceived stimulus novelty. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Involvement of the supramammillary nucleus in aversive conditioning.

Mechanisms for the retention and retrieval of conditioned taste aversions (CTAs) have yet to be fully defined. The authors explored relevant subcortical forebrain regions by tracking the expression of immediate early genes, c-fos and zif268. The supramammillary nucleus (SuM) was activated following both viscerally based CTA and somatically based inhibitory avoidance (IA). Excitotoxic lesions of the SuM before conditioning caused no disruption of acquisition but accelerated the extinction of both the CTA and IA. In contrast, lesions after CTA conditioning did not impair retention or retrieval. The present study indicates that the SuM is activated by memory-elicited discomfort during retrieval, suggesting that it plays a role in resisting the extinction of a long-term aversive memory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cooling the area postrema induces conditioned taste aversions in male rats and blocks acquisition of LiCl-induced aversions

The experiments presented in this article were designed to examine whether area postrema (AP) lesions attenuate LiCl-induced conditioned taste aversions (CTAs) by disruption of information about the illness-producing properties of LiCl or by a lesion-induced malaise. Reversible lesioning of the AP caused by cooling induced a CTA in male rats. The cooling-induced CTA could be blocked if males were exposed to cooling for several days before acquisition day. Acquisition of a LiCl-induced CTA was blocked in males if they were exposed to cooling before acquisition day and during LiCl administration on acquisition day was attenuated but not blocked in males if they were exposed to cooling only before acquisition day, and was unchanged in males if they were exposed to cooling only during LiCl administration. Taken together these results indicate that the AP is important for acquisition of LiCl-induced CTAs but that inactivation of this area is so aversive it will induce CTAs that can obscure the attenuation of LiCl-induced aversions.     

"Effects of central and basolateral amygdala lesions on conditioned taste aversion and latent inhibition": Correction to St. Andre and Reilly (2007).

Reports an error in "Effects of Central and Basolateral Amygdala Lesions on Conditioned Taste Aversion and Latent Inhibition" by Justin St. Andre and Steve Reilly (Behavioral Neuroscience, 2007[Feb], Vol 121[1], 90-99). Figure 4 on p. 96 (Results and Discussion, Experiment 2: Behavioral section) was incorrect. The correct figure is provided in the erratum. (The following abstract of the original article appeared in record 2007-02025-008.) The present study examined the effects of neurotoxic lesions of the central nucleus (CNA) and basolateral complex (BLA) of the amygdala on conditioned taste aversion (CTA) in a latent inhibition design. In Experiment 1, lesions of the CNA were found to have no affect on CTA acquisition regardless of whether the taste conditioned stimulus (CS) was novel or familiar. Lesions of the BLA, although having no influence on performance when the CS was familiar, retarded CTA acquisition when the CS was novel in Experiment 2. The pattern of results suggests that the CTA deficit in rats with BLA lesions may be a secondary consequence of a disruption of perceived stimulus novelty. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ibotenic acid lesions of the basolateral, but not the central, amygdala interfere with conditioned taste aversion: Evidence from a combined behavioral and anatomical tract-tracing investigation.

Rats (Rattus norvegicus) with almost complete ibotenic acid lesions (at least 90%) of the basolateral amygdaloid complex (BLA) failed to learn a conditioned taste aversion (CTA; Experiment 1A). In these same BLA rats, the bidirectional parabrachial–insular pathway that courses through the central nucleus of the amygdala (Ce) was shown to be spared (Experiment 1B), indicating that the BLA per se is critical for CTA learning. In contrast to the deleterious effect of BLA lesions on CTA, ibotenic acid lesions of the Ce did not block CTA learning (Experiment 2). Nonreinforced preexposure to the gustatory stimulus attenuated CTA acquisition in normal rats, and, under these conditions, rats with BLA lesions were no longer impaired (Experiment 3). Thus, ibotenic acid lesions centered over the Ce, sparing a considerable extent of the BLA, together with the testing procedure used in previous experiments (e.g., L. T. Dunn & B. J. Everitt, 1988), led to the belief that the CTA deficits reported after electrolytic lesions of the amygdala were the result of incidental damage to fibers of passage. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Forebrain structures specifically activated by conditioned taste aversion.

This study investigates which forebrain structures show Fos protein expression during conditioned taste aversion (CTA) acquisition and whether Fos expression depends on the aversion strength. A novel taste paired with an intraperitoneal injection of a low dose of the malaise-inducing agent lithium chloride (LiCl) induced a weak CTA, whereas associating this novel taste with a high dose of LiCl induced a strong CTA. Increasing the strength of the gastric malaise alone enhanced Fos expression in central, basal, and lateral amygdala nuclei and decreased Fos expression in the nucleus accumbens core. Taste-malaise association induced specific Fos activation in the insular cortex (with both the low and the high doses of LiCl) and the nucleus accumbens shell (with the high LiCl dose only). No significant variation of Fos expression was measured in the perirhinal cortex. Several forebrain areas may be sites of taste-malaise convergence during CTA acquisition depending on the strength of the aversion. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ibotenic acid lesions of the parabrachial nucleus and conditioned taste aversion: Further evidence for an associative deficit in rats.

Rats with extensive ibotenic acid lesions centered in the gustatory zone of the pontine parabrachial nucleus (PBN) failed to acquire a conditioned taste aversion (CTA) induced by lithium chloride (LiCl) toxicosis (Experiments 1 and 4). This deficit cannot be explained as an inability to either perceive or process gustatory information because lesioned rats that failed to acquire a CTA readily acquired a conditioned flavor preference (Experiment 2). Similarly, the CTA deficit cannot be attributed to an inability to experience or process visceral input because PBN-lesioned rats that failed to acquire a CTA successfully learned an aversion to a trigeminal stimulus, capsaicin, when paired with LiCl-induced illness (Experiment 3). This pattern of results supports the view that cell bodies within the PBN are essential for the associative processes that govern CTA learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reduced palatability in lithium- and activity-based, but not in amphetamine-based, taste aversion learning.

Conditioned taste aversions (CTA) based on lithium chloride (Experiment 1), amphetamine (Experiment 2), and wheel running (Experiment 3) were examined using the analysis of the microstructure of licking to measure the palatability of the taste serving as the conditioned stimulus (CS). Pairing saccharin with amphetamine reduced saccharin intake without reducing the size of licking clusters, initial lick rate, or the distribution of inter-lick intervals (ILIs) within a cluster. By contrast, pairing saccharin with lithium or wheel-running reduced saccharin intake as well as lick cluster size, initial lick rate, and the distribution of ILIs within a cluster. As lick cluster size, initial lick rate, and ILI distribution can be used as indices of stimulus palatability, the current results indicate that taste aversions based on either lithium or activity reduced the palatability of the CS. This suggests that aversions based on both lithium and wheel running involve conditioned nausea to the CS taste. The absence of similar changes in licking microstructure with amphetamine-based CTA is consistent with other evidence indicating this does not involve nausea. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of the perirhinal cortex in rats' conditioned taste aversion response memorization.

The role of the perirhinal cortex (PC) in conditioned taste aversion (CTA) learning was investigated in Long-Evans rats. CTA was induced by the intraperitoneal administration of LiCl 60 min after saccharin-sweetened water drinking. The PC was reversibly inactivated by the stereotaxic administration of tetrodotoxin (TTX) 60 min before saccharin drinking, immediately after saccharin drinking (Experiment 1), 6 or 24 hr after LiCl administration (Experiment 2), and 60 min before CTA retrieval testing (Experiment 3). Only pre-saccharin drinking PC inactivation disrupted CTA. Thus, PC integrity is necessary only during the earliest phases of CTA mnemonic processing, that is, taste information acquisition and early gustatory memory elaboration. The results are discussed in relation to PC connectivity and PC temporal involvement in the memorization process of other aversive responses. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cycloheximide impairs reconsolidation of a contextually reactivated memory in a conditioned taste aversion paradigm.

Rats were used to examine the impact of systemic protein synthesis inhibition (PSI) on the reconsolidation of a contextually reactivated memory of conditioned taste aversion (CTA). Rats were administered intraperitoneal injections of saline or lithium chloride (LiCl; .15 M) following exposure to a novel sucrose solution in a unique context. Seven days later, rats were injected subcutaneously with saline or cycloheximide (CXM; 1 mg/kg) and returned to their home cage or placed into the CTA training context in the absence of the target conditioned stimulus to reactivate the training memory. At testing, LiCl-trained rats that had been given CXM at reactivation had significantly greater difference scores (sucrose-water) in comparison with LiCl/CXM rats that had not been given a reactivation treatment and LiCl/saline memory-reactivated rats. These results suggest that context re-exposure effectively reactivates memory of CTA training that may be weakened through PSI. Extinction tests revealed rapid attenuation of taste aversions in all of the LiCl-injected groups. The involvement of taste-potentiated aversions and the role of the context in taste aversion conditioning are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste aversion learning in fyn mutant mice.

Conditioned taste aversion (CTA) learning is a robust form of classical conditioning in which animals rapidly associate a flavor with aversive internal symptoms. The present study assessed CTA learning in transgenic mice deficient in a specific nonreceptor tyrosine kinase (the fyn mutant). Fyn mutants show impaired long-term potentiation and marked deficits in acquisition of spatial learning tasks. To assess whether they are also impaired in CTA learning. fyn mutant and wild-type mice received 2 conditioning trials consisting of access to a flavored solution followed by administration of LiCl. Fyn mutant mice acquired significant CTAs following a single conditioning trial and these aversions were comparable to those seen in wild-type mice. These results indicate that the fyn mutation does not interfere with the acquisition of CTAs and hence that this mutation is not associated with a global learning deficit. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Drug exposure and the acquisition and retention of a conditioned taste aversion

Two experiments examined the effects of preexposure and postexposure to a drug on the acquisition and retention of a conditioned taste aversion induced by that drug. Experiment 1 demonstrated that although drug preexposure attenuated a subsequent conditioned aversion, repeated taste-drug pairings reversed the initial attenuation effect and resulted in nearly complete avoidance of consumption. Experiment 2, however, demonstrated that drug postexposure did not alter a previously established conditioned aversion, although the postexposure experiences were effective in attenuating a conditioned aversion to a second novel solution. It was suggested that conditioned aversions are mediated by ACTH and that preexposure to a drug results in tolerance to that drug, yielding a smaller ACTH response and thereby a weaker aversion.     

Brainstem lesions and gustatory function: III. The role of the nucleus of the solitary tract and the parabrachial nucleus in retention of a conditioned taste aversion in rats.

Bilateral electrolytic lesions of the nucleus of the solitary tract (NST) or ibotenic acid lesions of the pontine parabrachial nuclei (PBN) failed to disrupt retention of a preoperatively acquired conditioned taste aversion (CTA) to 0.3 M alanine. For both sham- and NST-lesioned rats, the CTA persisted following 3 nonreinforced conditioned stimulus (CS) presentations. For PBN-lesioned rats, retention was more labile. The preoperatively acquired CTA was extinguished by the 3rd nonreinforced CS exposure. When assessed postoperatively using a novel CS, NST-lesioned rats acquired a new CTA, although they were rendered anosmic with zinc sulfate (P. S. Grigson et al, see record 199707487-016). Rats with PBN lesions, however, failed to acquire a 2nd CTA postoperatively. Thus, the PBN is essential for the acquisition of a CTA, but neither of the brainstem gustatory nuclei need be intact for the retention of a preoperatively acquired CTA. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thalamocortical relations in taste aversion learning: II. Involvement of the medial ventrobasal thalamic complex in taste aversion learning.

Examined the involvement of the gustatory thalamic nuclei in fundamental taste reactivity, gastrointestinal reactivity, and conditioned taste aversion (CTA) learning. In Exp I, using 72 male Long-Evans rats, bilateral electrolytic lesions were produced in the medial ventrobasal thalamic complex (VBm), including the thalamic gustatory nuclei, in 1 group of Ss. For a 2nd group, at the conclusion of conditioning, lesions were produced in the anterior insular gustatory neocortex (AIGN). Results indicate that destruction of VBm thalamus attenuated taste reactivity to sucrose, citric acid, and quinine hydrochloride. Elimination of VBm thalamus markedly attenuated CTA learning. Results of neocortical lesion manipulations showed that the AIGN contributed to initial CTA learning in Ss lacking a mediodorsal-periventricular thalamus. Whether Ss lacking VBm thalamus used olfactory cues associated with drinking solutions to acquire CTAs was evaluated in Exp II, using 72 male Long-Evans rats. Results demonstrate that Ss lacking VBm thalamus and the olfactory bulbs could not acquire aversions to ingested LiCl following 8 conditioning trials. (54 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The role of the gustatory thalamus in taste-guided behavior

Gustatory thalamus is the functional name for the parvicellular region of the ventroposteromedial nucleus of the thalamus. It is the penultimate nucleus in the thalamocortical pathway of the central gustatory system. Early research encouraged the view that the gustatory thalamus was important for taste detection and recognition. Consistent with this analysis, lesions of the area were found to induce profound deficits of innate taste preferences and aversions, salt appetite, and conditioned taste aversions (CTAs). More recent research using discrete lesions placed with electrophysiological guidance has, however, demonstrated that these deficits were due to damage to structures outside of, rather than within, the boundaries of the gustatory thalamus. In fact, the new data show that the gustatory thalamus is not essential for taste detection, sodium appetite, or CTA learning, but is critical for the preparatory (i.e. food-seeking) rather than the consummatory (i.e. food-eating) aspects of taste-guided behavior.     

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

Three experiments examined the conditioned taste aversion (CTA) deficit that occurs following electrolytic lesions of the parabrachial nucleus (PBN). In Exp 1, lesioned rats failed to avoid either a gustatory or an olfactory stimulus that had been paired with lithium chloride-induced toxicosis. In Exp 2, however, all rats learned a conditioned flavor preference. Finally, in Exp 3, all controls and 7 of the 12 lesioned rats learned a conditioned place aversion. Together, these results demonstrate that the disruption of CTA in lesioned rats cannot be ascribed to an inability to process either gustatory or visceral afferent information per se. Rather, the data suggest that PBN-lesioned rats are unable to form a specific association between gustatory and visceral cues. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cortical substrates of taste aversion learning: Dorsal prepiriform (insular) lesions disrupt taste aversion learning.

The functional relation between restricted damage to ventral primary somatosensory neocortex and the ability of rats to acquire conditioned taste aversions (CTA) was examined by a combination of behavioral and neurohistological techniques. Ss were 84 male Long-Evans hooded rats. Lesions confined exclusively to the established gustatory neocortex (GN) did not disrupt CTA acquisition, nor did lesions confined to suprarhinal cortical areas ventral to the GN. Lesions that encroached on dorsal prepiriform and insular cortices produced CTA acquisition deficits and damaged a large proportion of efferent projections to the prefrontal and precentral neocortex. Lesions of dorsal prepiriform and insular cortices did not modify taste preference–aversion thresholds to any of the 4 taste modalities. It is concluded that ventral somatosensory neocortical fields, including the established GN, do not mediate CTA acquisition and that rhinal cortices ventral and posterior to the GN are preferentially involved in associative learning for tastes and illness. (51 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Brainstem lesions and gustatory function: II. The role of the nucleus of the solitary tract in Na+ appetite, conditioned taste aversion, and conditioned odor aversion in rats.

Rats with lesions of the nucleus of the solitary tract (NST) that demonstrated flat concentration-response functions for NaCl and sucrose (T. Shimura et al, see record 84-21706) expressed a significant (albeit reduced) salt appetite following sodium depletion, and a normal conditioned taste aversion (CTA) for alanine when paired with lithium chloride-induced toxicosis. Rats with lesions of the NST also could acquire a conditioned odor aversion, but the CTA to alanine was not mediated by odor cues because other rats with NST lesions also demonstrated normal CTA learning even when made anosmic with zinc sulfate. Together, the data suggest that the rostral NST is essential for responding appropriately to increasing concentrations of a tastant, but not for the chemical identification necessary for sodium appetite and CTA learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of basolateral amygdala lesions on taste aversions produced by lactose and lithium chloride in the rat.

In Exp I, 24 intact male Lister rats were given either lactose or sucrose solutions. Although on 1st exposure they readily consumed lactose, its ingestion produced a conditioned taste avoidance (CTA) that was partly extinguished by repeated sucrose exposure after lactose conditioning. In Exp II, 8 Ss with large bilateral electrolytic lesions of the basolateral amygdala and 10 with either sham or no operations were given 2 pairings of saline with LiCl injections (upper gastrointestinal tract discomfort) and, in a separate condition, access to high levels of lactose (lower gastrointestinal tract discomfort). CTAs were measured both by 2-bottle tests and by video recordings of orofacial and somatic responses. The lesions attenuated LiCl-induced but not lactose-induced CTA, results demonstrating that a CTA can occur without the basolateral amygdala. Findings suggest that aversions based on distaste can be distinguished from avoidances based on danger, not only in terms of orofacial responses but also in terms of their neuroanatomical substrate. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Boosting cholinergic activity in gustatory cortex enhances the salience of a familiar conditioned stimulus in taste aversion learning.

The cholinergic system is important for learning, memory, and responses to novel stimuli. Exposure to novel, but not familiar, tastes increases extracellular acetylcholine (ACh) levels in insular cortex (IC). To further examine whether cholinergic activation is a critical signal of taste novelty, in these studies carbachol, a direct cholinergic agonist, was infused into IC before conditioned taste aversion (CTA) training with a familiar taste. By mimicking the cholinergic activation generated by novel taste exposure, it was hypothesized that a familiar taste would be treated as novel and therefore a salient target for aversion learning. As predicted, rats infused with the agonist were able to acquire CTAs to familiar saccharin. Effects of carbachol infusion on patterns of neuronal activation during conditioned stimulus–unconditioned stimulus pairing were assessed using Fos-like immunoreactivity (FLI). Familiar taste–illness pairing following carbachol, but not vehicle, induced significant elevations of FLI in amygdala, a region with reciprocal connections to IC that is also important for CTA learning. These results support the view that IC ACh activity provides a critical signal of taste novelty that facilitates CTA acquisition. (PsycINFO Database Record (c) 2010 APA, all rights reserved)