Taste-potentiated Odor Aversion Research Articles

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

Two experiments examined 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 Experiment 1, pretreatment with D-APV (2.5 micrograms/side icv) caused stereospecific deficits in potentiated odor aversion learning but left simple taste and odor aversion learning intact. In Experiment 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 (Robinson, Crooks, Shinkman, & Gallagher, 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.

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

Two experiments examined 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 Experiment 1, pretreatment with D-APV (2.5 micrograms/side icv) caused stereospecific deficits in potentiated odor aversion learning but left simple taste and odor aversion learning intact. In Experiment 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 (Robinson, Crooks, Shinkman, & Gallagher, 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.

The conditioned stimulus^unconditioned stimulus^feedback feeding sequence: Reply to Ellins, von Kluge, and Cramer (1990).

Taste-potentiated noise aversions have been demonstrated in rats (Ellins, Cramer, & Whitmore, 1985; Ellins & von Kluge, 1987; Holder, Bermudez-Rattoni, & Garcia, 1988). However, these aversions are apparently less readily established than taste-potentiated odor aversions suggesting that all exteroceptive stimuli are not equally well potentiated by taste (Holder et al., 1988). Despite the claims of Ellins, von Kluge, and Cramer (1990), we replicated their findings and see no inconsistency between our findings and theirs. Both sets of results are explained by a common theory of conditioning (Garcia, 1989; Garcia & Holder, 1985).

Effect of taste preexposure on taste and odor aversions

Thirsty Sprague-Dawley rats drank flavored water in a wind tunnel prior to lithium-induced toxicosis. Flavors were presented for 5 min; 30 min later a toxin, lithium chloride, was injected. After the rats had recovered, subsequent aversions to the taste and the odor were assessed separately. In Experiment 1, extensive preexposure to the taste component of the flavor attenuated neophobia to the flavor and the subsequent taste aversion. However, the subsequent odor aversion was unaffected. Experiment 2 partially replicated the results of Experiment 1 and showed that, in a situation in which only taste-potentiated odor aversions are usually found, nonpotentiated aversions were evident. Experiment 3 found that, in addition to attenuating taste aversions, taste preexposure enhances the capacity of rats to learn nonpotentiated odor aversions. The results are interpreted with a neural-based model of conditioned flavor aversions.

Role of temporal order and odor intensity in taste-potentiated odor aversions.

The role of the temporal order of odor and taste was studied in two experiments, and a third experiment studied the role of odor intensity in flavor-toxicosis conditioning with thirsty rats licking water spouts in a "wind tunnel." In all experiments, odors and tastes were presented for 2 min to rats, and 30 min later, a toxin (lithium chloride) was intubated. In Experiment 1, an odor was presented 90 s before, during, or 90 s after a taste to independent groups. Experiment 2 was a within-subjects partial replication of the first. Each rat was presented with one odor, then a taste, then a second odor with each stimulus separated by 45 s. The results of Experiments 1 and 2 indicated that (a) odor alone is not associated with illness under our conditions, (b) presenting an odor and a taste at the same time potentiates the odor component so that it is associated with illness, (c) 45-s and 90-s intervals between odor and taste eliminate potentiation, and (d) taste and odor interact asymetrically; that is, odor has little affect on the development of taste-illness associations. In Experiment 3, an odor and a taste were presented simultaneously, and odor intensity varied. As odor intensity increased, the strength of the taste-potentiated odor aversion increased, whereas the aversion to the taste remained constant. However, even at the highest intensity, odor presented in the absence of taste did not result in odor aversions.

Role of temporal order and odor intensity in taste-potentiated odor aversions.

Role of temporal order and odor intensity in taste-potentiated odor aversions.

Flavor-illness aversions: The role of the amygdala in the acquisition of taste-potentiated odor aversions

In the present experiments the role of the amygdaloid complex and its specific nuclei were tested in the conditioning of taste potentiated odor aversions. In the first experiment two groups of rats were given either large electrolytic lesions in the amygdala (AMX) or sham operations (SH). Postoperatively, these rats were trained to avoid either a taste, an odor, or a taste-odor compound using LiCl illness. Subsequent tests with odor and taste alone showed that the SH group developed strong taste and odor aversions; however, the AMX group failed to display either an odor or taste aversion. In the second experiment, another four groups of rats received either lesions in the medial and basomedial nuclei (M), central nuclei (C), lateral and basolateral (L), or sham operations (SH). The results from postoperative conditioning showed that all groups had strong taste and odor aversions, except group L which displayed a significant disruption of odor aversion learning. In conclusion, these data indicate that the amygdala is involved in the acquisition of taste, odor and potentiated odor aversions learning. Moreover, it is demonstrated that the lateral and/or basolateral nuclei are particularly involved in the development of potentiated odor aversions learning.

Involvement of the anterior insular gustatory neocortex in taste-potentiated odor aversion learning

When an odor conditioned stimulus (CS) precedes illness (unconditioned stimulus; UCS), rats acquire relatively weak odor aversions. Conversely, when a compound odor-taste (flavor) CS precedes illness, rats acquire robust aversions both to the odor and to the taste components of a compound flavor CS. Thus, tastes potentiate odor-illness aversions during toxiphobic conditioning. Such conditioning effects have been referred to as taste-potentiated odor aversion learning (POA). Previous neurobehavioral experiments have shown that the anterior insular gustatory neocortex contributes to conditioned taste aversion (CTA) learning. The present experiment examined the involvement of the anterior insular gustatory neocortex in CTA learning and POA learning. To that end, four distinct groups of rats received bilateral electrolytic lesion placements in the orbitofrontal neocortex, the “somatic” gustatory neocortex, the anterior insular gustatory neocortex or the posterior insular neocortex. Control animals received anesthesia only. Subgroups of animals thereafter received aversion conditioning using either an odor (almond) CS or a compound odor-taste (almond-saccharin) CS. Aversions to the almond odorant and/or saccharin tastant were evaluated during extinciton. Results indicated that animals lacking orbitofrontal neocortex or posterior insular neocortex acquired normal CTAs and POAs. Animals lacking somatic gustatory neocortex exhibited impaired CTA learning, yet those animals showed normal POA learning. Lesions centered in the anterior insular neocortex impaired both CTA learning and POA learning. These results demonstrate that the insular gustatory neocortex is uniquely involved in the higher-order integration of odors, tastes and illness.