Taste-potentiated odor aversion learning: Role of the amygdaloid basolateral complex and central nucleus.

Examined the relative contributions of the amygdaloid basolateral complex (ABL) and central nucleus (CN) to taste-potentiated odor aversion (TPOA) learning, an associative learning task that is dependent on information processing in 2 sensory modalities. In Exp 1, rats with neurotoxic lesions of these systems were trained on the TPOA task by presenting a compound taste–odor conditioned stimulus (CS), which was followed by LiCl administration. Results showed that ABL damage caused an impairment in potentiated odor aversion learning but no deficit in the conditioned taste aversion. In contrast, rats with CN damage learned both tasks. Exp 2 examined the effects of ABL damage on TPOA and odor discrimination learning. The odor discrimination procedure used a place preference task to demonstrate normal processing of olfactory information. Results indicated that although ABL-lesioned animals were impaired on TPOA, there was no deficit in odor discrimination learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

N-methyl-D-aspartate antagonist D-APV selectively disrupts taste-potentiated odor aversion learning.

Examined in 2 experiments the effects of the competitive N-methyl-{d}-aspartate (NMDA) antagonist {d}-APV ({d}-2-amino-5-phosphonovalerate) on rats' ability to acquire potentiated aversions to the odor element of a taste–odor compound. In Exp 1, pretreatment with {d}-APV (2.5 μg/side icv) caused stereospecific deficits in potentiated odor aversion learning but left simple taste and odor aversion learning intact. In Exp 2, pretreatment with {d}-APV had no effect on rats' acquisition of an illness-based odor discrimination task. These results parallel those previously obtained using a noncompetitive NMDA antagonist (G. S. Robinson et al, 1989) and show that interference with NMDA receptors can selectively impair potentiated odor aversion learning. These results suggest that NMDA receptors play a critical role in some, but not all, forms of learning and memory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure to show modification of male golden hamster mating behavior through taste/odor aversion learning

This research investigated whether the dependence of mating behavior in the male hamster on olfactory and gustatory stimuli could be used with the taste/odor conditioning paradigm to alter sexual behavior. Preliminary experiments established the effectiveness of lithium chloride and methyl-atropine nitrate in forming aversions to a saccharin solution. These same agents failed to modify mating behavior when the conditional stimulus was an estrous female hamster. Animals made ill after an exposure to a cotton swab containing phenylacetic acid later showed increased latencies in the initiation of mating with an estrous female swabbed with phenylacetic acid. Animals given three punished exposures to phenylacetic acid also showed increased latency to initiate mating and decreased anogenital sniff-licking with a phenylacetic acid-swabbed estrous female. However, no other measures of mating behavior were altered.     

Effects of brain lesions on taste-potentiated odor aversion in rats.

Rats failed to acquire aversions to odor stimulus, which was followed 30 min later by an unconditioned stimulus (US). However, when the odor stimulus was accompanied by a taste stimulus, they acquired odor aversions as well as taste aversions. In this phenomenon, referred to as a taste-potentiated odor aversion, lesions of the amygdala disrupted both taste and odor aversions, whereas lesions of the parvicellular part of ventroposteromedial thalamic nucleus (VPMpc) or insular cortex (IC) disrupted taste aversion but attenuated only odor aversion. These results suggest that both taste and odor stimuli are associated with US in the amygdala and that taste inputs delivered to the amygdala through the IC and/or VPMpc play an important role in potentiation of odor aversion. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste-potentiated odor conditioning: Impairment produced by infusion of an N-methyl-D-aspartate antagonist into basolateral amygdala.

Two experiments examined the effects of infusing an N-methyl-D-aspartate (NMDA) receptor antagonist, d-2-amino-5-phosphonovalerate(d-APV), on taste-potentiated odor conditioning: a form of learning that is dependent on information processing in 2 sensory modalities. In Experiment 1, rats infused with d-APV were impaired in their acquisition of the potentiated learning to an odor cue. Expression of this learning and acquisition of a simple taste aversion remained intact following drug treatment. In Experiment 2, dose dependence and stereoselectivity were demonstrated for the antagonist compound. These results are consistent with previous studies demonstrating that either basolateral amygdala lesions, or treatment with NMDA antagonists, by other routes (systemic or intraventricular) produce selective deficits in taste-potentiated odor conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Unilateral conditioning of an odor aversion in 6-day-old rat pups.

In young rats, several forms of olfactory memory can be functionally localized to one side of the brain by restricting training stimuli to one naris and corresponding olfactory bulb. In this experiment, the analysis of lateralized olfactory learning in 6-day-old rat pups was extended by an evaluation of the consequences of aversive reinforcers in a unilateral olfactory conditioning paradigm. An olfactory aversion was conditioned by delivering a mild footshock to animals in the presence of a novel odor. Olfactory stimulation was confined to one naris and corresponding olfactory bulb by inserting a soft rubber plug into the opposite naris. This lateralization in processing resulted in unilateral memory for the odor aversion that was only expressed when the trained naris was open during an odor preference test. The hypothesis that the hedonic value (or valence) component of conditioning is represented in structures that are unilaterally accessed during training and testing is discussed. (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)     

Ingestional aversion learning in preweanling rats.

In 4 experiments, ingestional aversions were conditioned in 12- and 15-day-old Sprague-Dawley rats by infusing a .5% solution of saccharin into the oral cavity and following this oral infusion by the injection of lithium chloride. At both ages, Ss for which the saccharin exposure was followed by lithium injection within 2–3 min drank less when the saccharin solution was again presented by oral infusion 12 hrs later; such suppressions of intake were not observed in Ss that previously received the saccharin and lithium in an unpaired fashion (Exps I and III). Ingestional aversions were also learned by 12-day-olds when a 30-min interval was introduced between saccharin exposure and lithium toxicosis but not when toxicosis was delayed by 120 min (Exp II). In contrast, 15-day-olds learned aversions with both the 30- and 120-min-delay intervals (Exp III). Despite the absence of long-delay learning in 12-day-olds, ingestional aversions conditioned at 12 days of age were retained for 2 wks (Exp IV). Results provide further evidence of the associative abilities of neonatal rats and illustrate a developmental aspect of long-delay learning. (34 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Facilitation of conditioned odor aversion by entorhinal cortex lesions in the rat.

This study examined the role of the entorhinal cortex (EC) in conditioned odor aversion learning (COA). Lateral EC lesions did not impair but rather facilitated COA. In the experiments the delay separating the odor cue presentation from the subsequent toxicosis was varied during acquisition. EC-lesioned rats demonstrated COA for delays up to 2 hr, whereas sham-operated rats displayed COA only if toxicosis immediately followed the odor cue. This facilitation was not dependent on the intensity of the odor and corresponded to a facilitated long-delay learning. EC lesion did not affect conditioned taste aversion, confirming that the facilitation effect does not correspond to a general facilitation of conditioned aversion learning. Taken together, these results indicate that the removal of the EC may allow odor-toxicosis associations across longer delays by extending the duration of the olfactory trace. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Age-related differences in short-term retention of separable elements of an odor aversion.

The rate of forgetting over short intervals was tested in preweanling rats, 8, 12, or 18 days postnatal, using procedures that may have analytical advantages over other tests of short-term retention. Separate tests of retention were conducted for the simple occurrence of an odor and for the occurrence of an odor paired with a mild footshock. Forgetting of odors with either of two histories, incidental or target, was more rapid the younger the preweanling, over intervals of less than an hour. There was some indication of more rapid forgetting for incidental than target odors. Finally, although exposure to a CS– (conditioned stimulus [an odor not paired with footshock]) was necessary for conditioning of the CS+ (an odor paired with footshock) in rats 8 or 12 days of age, exposure to a CS– had no influence on conditioning of the CS+ in preweanlings 18 days of age. The age-related differences in forgetting over intervals less than an hour long suggest that substantial age-related differences in forgetting can occur that, it is likely, are not accounted for by differential growth. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Importance of retronasal and orthonasal olfaction for odor aversion memory in rats.

The role of odors in food memory formation, especially for aversions, has long been considered secondary to taste. However, the importance of odor ingestion in conditioned odor aversion (COA) has recently challenged this assumption (B. M. Slotnick, F. Westbrook, & F. M. C. Darling, 1997). The aim of the present study was to evaluate the respective role of orthonasal and retronasal olfactory experience in COA acquisition, long-term retention, extinction, and spontaneous recovery. To this end, the odor was presented either close to the drinking spout (orthonasal stimulation) or close to and mixed with the drinking water (eliciting both orthonasal and retronasal stimulation). The authors brought evidence that odor ingestion was crucial for COA acquisition, especially when odor presentation and gastric malaise were separated by long delays. On the contrary, once formed, a distal (orthonasal) odor recognition was sufficient for COA to be retrieved. COA was odor specific and long lasting (more than 50 days). Moreover, results brought evidence for a spontaneous recovery of odor aversion tested 57 days after its extinction. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Thalamocortical relations in taste aversion learning: I. Involvement of gustatory thalamocortical projections in taste aversion learning.

Examined the involvement of presumed gustatory thalamocortical projections in conditioned taste aversion (CTA) learning, using 108 male Long-Evans rats in 4 experiments. Neuroanatomical and neurobehavioral manipulations in the ventrolateral neostriatum were used. Findings demonstrate that projections from posterior ventromedial thalamic nuclei, parvicellular division (VPMpc), and thalamus to the anterior insular gustatory neocortex (AIGN) were essential for normal CTA learning. Because both VPMpc thalamus and the AIGN each have been implicated as functional substrates of CTA learning, the present results suggest that the gustatory thalamocortical relay per se is necessary for normal taste-illness learning. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cortical substrates of taste aversion learning: Involvement of dorsolateral amygdaloid nuclei and temporal neocortex in taste aversion learning.

Examined the involvement of the central (CE), lateral (LA), and basolateral (BL) amygdaloid nuclei and the temporal neocortices (area 20) in conditioned taste-aversion (CTA) learning. 40 adult male Long-Evans hooded rats received bilateral electrolytic lesion placements in the CE, LA, BL, or the temporal neocortices. 16 controls received scalp and meningeal incisions only. Following recovery, Ss were habituated to a restricted drinking schedule with distilled water. Animals then received CTA conditioning, with LiCl used both as the CS and as the UCS. Anterograde degeneration histologies were performed on all brain tissue to evaluate relations between CTA learning deficits and axonal pathology induced by lesion placements. Results indicate that destruction of the CE, LA, or temporal neocortex impaired CTA acquisition, but damage induced to the BL amygdaloid nucleus did not. Anatomical observations indicated that degeneration of amygdalofugal and/or corticofugal projections to the convolutions of the olfactory tubercle (medial), subthalamic nucleus, and the parabrachial complex was correlated with CTA learning deficits. Findings suggest that destruction of the dorsolateral amygdaloid nuclei and/or the temporal neocortices may produce CTA learning deficits by affecting olfactory, gustatory, and/or gastrointestinal processing in various portions of the forebrain. (51 ref) (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 parabrachial nucleus is essential for acquisition of a conditioned odor aversion in rats.

Rats with bilateral ibotenic acid lesions of the gustatory zone of the parabrachial nuclei (PBN) failed to acquire a conditioned taste aversion (CTA) in Exp 1. They also failed to acquire a conditioned odor aversion (COA) when the olfactory cue was presented on an odor disk in Exp 2 or when it was presented in water in Exp 3. The failure to acquire the COA was not due to an inability to detect or use olfactory stimuli because the lesioned rats displayed neophobia to a novel odor in Exp 3 and used an olfactory cue to predict the availability of an aversive capsaicin solution in Exp 4. Together, the results demonstrate that, as with CTA learning, PBN cell bodies are essential for the establishment of a specific association between an olfactory conditioned stimulus and a lithium chloride unconditioned stimulus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste aversion learning in young and adult rats.

Compared a total of 159 male Long-Evans rat pups and adults on their ability to learn taste aversions with 1- and 2-bottle tests, 2 different illness-inducing agents and flavors, and varying taste–illness delays. Rat pups learned taste aversions with either 1- or 2-bottle tests, but only with short taste–illness delays. Delays of 60 min were sufficient to block taste aversion learning in pups. Pups also failed to demonstrate neophobia to a novel taste. These findings suggest that pups forget taste information more rapidly than adults, perhaps because taste information is not so salient for pups as for adults. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the bed nucleus of the stria terminalis, lateral hypothalamus, or insular cortex on conditioned taste aversion and conditioned odor aversion.

The effects of permanent forebrain lesions on conditioned taste aversions (CTAs) and conditioned odor aversions (COAs) were examined in 3 experiments. In Experiment 1, lesions of the bed nucleus of the stria terminalis had no influence on CTA or COA acquisition. Although lesions of the lateral hypothalamus induced severe hypodipsia in Experiment 2, they did not prevent the acquisition of CTAs or COAs. Finally, in Experiment 3, lesions of the insular cortex retarded CTA acquisition but had no influence on COA acquisition. The implications of these findings are discussed with regard to the forebrain influence on parabrachial nucleus function during CTA acquisition. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Within-compound learning with US presentation in taste aversion.

Determined whether the presentation of a LiCl unconditioned stimulus/stimuli (UCS) disrupts within-compound learning in a taste aversion preparation, using 30 male and 32 female rats in 3 experiments. In Exp I, Ss showed stronger associations between 2 solutions presented in a compound when the compound was followed by LiCl. Exp II showed that an immediate LiCl injection produced stronger flavor–flavor association than a delayed injection. Exp III provided a comparison with Ss that did not receive the treatment to enhance consumption of salty solutions. Results indicate that the effects of Exp II depended on the treatment that altered consumption of 1 component. (French abstract) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Area postrema lesions impair flavor-toxin aversion learning but not flavor-nutrient preference learning.

Rats with lesions of the area postrema. (APX) or sham lesions were trained to associate flavored solutions with positive or negative postingestive consequences. The APX rats were similar to controls in learning preferences for flavors paired with concurrent intragastric infusions of maltodextrin or corn oil and for a flavor paired with delayed maltodextrin infusions. In contrast, the APX rats displayed impaired aversion learning for flavors paired with toxic drug treatments (lithium chloride infusion or methylscopolamine injection). The aversion learning deficit ranged from mild to total, depending on training procedures. These findings confirm the important role of the area postrema in flavor-toxin learning but provide no evidence for its involvement in flavor-nutrient conditioning. (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)