Carbohydrate-conditioned odor preferences in rats.

The effectiveness of odor cues to support nutrient-conditioned flavor preferences in rats was studied. When the rats drank fluid, the CS+ odor was paired with intragastric (IG) infusions of Polycose, and the CS– odor with IG water. In Experiment 1, rats trained with almond and anise odors presented with plain drinking water failed to acquire a CS+ odor preference. In contrast, rats in Experiment 2 formed a strong aversion to anise (or almond) paired with lithium chloride, which indicated that the odors were distinguishable to the rats. Experiment 3 showed that providing unique tastes (bitter or sour) in combination with the odors during training potentiated odor conditioning. The rats displayed a strong preference for the odor?+?taste CS+ and for the odor component alone. Experiment 4 showed that with another pair of odors (peppermint and vanilla), CS+ preferences could be conditioned in the absence of taste cues during training. These results demonstrate that rats can acquire strong nutrient-conditioned odor preferences. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste preconditioning augments odor-aversion learning.

On the basis of previous work that has shown a taste can potentiate odor-aversion conditioning in AX+ conditioning, 6 experiments used rats to examine the effects of pairing a preconditioned taste (A) with a novel odor cue (X) in an A+/AX+ aversion conditioning design. Experiments 1A and 1B demonstrated that a preconditioned taste produced a robust odor aversion that was significantly stronger than a potentiated odor aversion. The results of Experiment 2 showed that the robust odor aversion produced by A+/AX+ conditioning was not the result of the potentiated odor aversion summating with generalization from the taste aversion. The augmented odor aversion was produced only when the taste and odor stimuli were presented simultaneously (Experiment 3) and the preconditioned taste aversion was intact at compound conditioning (Experiment 4). Pairing a novel odor with a preconditioned taste was not sufficient to condition an aversion to odor (Experiment 5), although other results implicated a role for an association between odor and taste in the odor augmentation effect (Experiment 6). The present results have implications for current models of taste + odor interactions in flavor-aversion conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Alcohol aversion generalization in rats: Specific disruption of taste and odor cues with gustatory neocortex or olfactory bulb ablations.

Rats with ablations of the gustatory neocortex (Experiment 1) and rats with olfactory bulb ablations (Experiment 2) were compared with normal rats for aversion generalization to both single taste solutions (sucrose, sodium chloride, quinine hydrochloride, hydrochloric acid) and compound taste solutions (pairs of the four single tastants) following alcohol aversion training. All rats acquired equal and strong alcohol aversions. Control rats showed consistent aversion generalization to both the sucrose plus quinine and the sucrose plus hydrochloric acid solutions; no significant generalization occurred to the single tastants except a weak generalization to sucrose in Experiment 2. Rats with gustatory neocortical ablations failed to show aversion generalization to any of the taste solutions. Rats with olfactory bulbectomies displayed the same aversion generalization functions as control rats but exhibited significantly faster extinction of the alcohol aversion than did the trained control rats. Results from the present experiments suggest that during alcohol aversion learning, rats lacking gustatory neocortex use odor cues (no taste generalization), whereas rats lacking olfactory bulbs utilize taste cues (normal taste generalization). (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Augmentation of taste conditioning by a preconditioned odor.

Five experiments explored facilitated taste-aversion conditioning (odor-mediated taste augmentation), using rats that experienced odor (A) and taste (X) in an A+/AX+ design. Augmentation occurred when the stimuli were presented simultaneously during AX+ conditioning, and significantly weaker conditioning occurred after a sequential presentation (Exp 1). Exps 2 and 3 demonstrated that augmented conditioning decreased if the odor aversion was reduced through preexposure or extinction following A+ conditioning. A second-order conditioning explanation was not supported by the results of Exp 4. Exp 5 showed that extinction of the odor aversion after AX + conditioning did not alter the strength of the augmented taste aversion. Odor-mediated taste augmentation is similar to potentiation, in which odor and taste cues operate in a synergistic, not competitive, manner. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Odor of Taste Stimuli in Conditioned "Taste" Aversion Learning.

The present research addresses whether rats can express odor aversions to the odor of taste stimuli. In Experiment 1, saccharin or salt were either mixed in distilled water, so the rats could taste and smell them, or presented on disks attached to the tubes' metal spouts so the rats could only smell them. Aversions were established to taste stimuli under both conditions. The results of Experiment 2 indicate that conditioning was to the odor of the tastes when they were presented on disks in Experiment 1, hence both taste and odor aversions were established by means of "taste" stimuli. Taste aversion learning thus may more properly be termed flavor aversion learning, with flavor referring to both taste and odor components. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste potentiation of poisoned odor by temporal contiguity.

Investigated the synergistic interaction between odor and taste in flavor-toxicosis conditioning in 2 experiments with 85 male Sprague-Dawley rats, in which the temporal interval between a 2-min odor and a 2-min taste was varied for thirsty Ss licking at a water spout. In Exp I (34 Ss), taste was presented at 0 min, and odor was presented at –20, –2, 0, 1, and 10 min to independent groups in a simple compartment. In Exp II (51 Ss), taste was presented at 0 min, and odor was presented at –5, –2, and 0 min in a wind-tunnel apparatus. Results indicate that odor alone was an ineffective CS for a toxic UCS under the conditions of the present experiments. Simultaneous (0-min) presentation of odor with taste potentiated the odor component so that it became more effective than the taste component. A 2-min interval between odor and taste attenuated potentiation, and a 5-min interval disrupted the effect. The interaction was asymmetrical; odor had no systematic effect on the conditioning of taste. (25 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)     

Taste-potentiated odor aversion learning based on amphetamine

This study sought to determine whether a taste can potentiate a conditioned odor aversion based on amphetamine as well as those based on lithium. A taste-potentiated odor aversion (TPOA) based on lithium was obtained in Experiment 1 only with a low concentration of an almond odor. This concentration was used in Experiment 2 where the taste, 0.1% saccharin, potentiated an odor aversion based on 1 mg/kg d-amphetamine. This was replicated in Experiment 3 where potentiation was found with doses of both 1 and 3 mg/kg amphetamine, and no effect of dose was detected. It was concluded that TPOA learning is not restricted to drugs such as lithium that produce conditioned unpalatability as well as conditioned aversions to a taste, because amphetamine does not produce conditioned unpalatability at the doses used here. Furthermore, because in Experiment 3 postconditioning extinction of the saccharin aversion removed the potentiation effect, it appears that this form of TPOA may depend on an association between the odor and taste, as proposed by within-compound theory.     

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)     

Gustatory thalamus lesions in the rat: II. Aversive and appetitive taste conditioning.

The learning capacities of rats with electrolytic lesions of the gustatory thalamus (GT) were investigated in 3 experiments. In Experiment 1, the presence of a taste cue failed to overshadow odor aversion learning in the lesioned rats, yet these same animals acquired normal taste and odor aversions. Thalamic lesions had no discernible effect on the acquisition of a conditioned flavor preference in Experiment 2. Finally, GT lesions completely reversed the anticipatory contrast effect shown by control subjects in Experiment 3. These results suggest that damage to the GT spares taste detection and recognition and simple associative learning but interferes with learning that involves more complex gustatory information processing. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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)     

Potentiation of odor by taste in rats: Tests of some nonassociative factors.

Three experiments with 94 male Sprague-Dawley rats tested the contribution of nonassociative neophobia and sensitization to the potentiation of odor by taste. In Exp I, neophobia for almond odor (O), saccharin taste (T), and odor-taste compound (OT) cues was tested before and after noncontingent LiCl poisoning and compared with conditioned aversions produced by OT–LiCl temporal pairing. The OT compound potentiated unconditioned neophobia, but there was no evidence of poison-enhanced neophobia, disinhibition of neophobia, or sensitization by noncontingent LiCl; temporal pairing produced aversions for the compound and its elements. In Exp II, generalization to a novel odor was tested after O–LiCl or compound OT–LiCl pairing. The potentiated odor aversion did not generalize to the novel odor; it was specific to the odor paired with taste and LiCl. In Exp III, potentiation of the odor component by a discriminant or nondiscriminant taste component was tested. Potentiation was evident only when a novel discriminant taste was in compound with odor prior to LiCl poisoning. Results from all experiments support an associative "indexing" hypothesis of the potentiation effect in rats. (14 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Flavor-illness aversions: Potentiation of odor by taste with toxin but not shock in rats.

Paired almond odor or saccharin taste as a single CS or as a compound CS for both a footshock UCS and a toxin UCS (LiCl) to test the generality of potentiation in male Sprague-Dawley rats. Extinction tests with the almond and saccharin components were then given. In single CS–toxin experiments, taste was more effective than odor, and after compound conditioning, the taste component potentiated the odor component. Conversely, in single CS–shock experiments, odor was more effective than taste, and after compound conditioning, no potentiation was observed. Instead, interference effects were observed. In Exps I and II, the addition of taste disrupted odor CS–shock conditioning, and in Exp III, odor interfered with taste CS–shock conditioning. Visceral feedback was apparently a necessary UCS for the potentiation of odor by taste. Data support the neural convergence and gating hypothesis of flavor aversion conditioning. (33 ref) (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)     

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)     

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)     

Flavor-illness aversions: Gustatory neocortex ablations disrupt taste but not taste-potentiated odor cues.

Two studies evaluated the contribution of the gustatory neocortex (GN) to the potentiation of odor by taste during illness-induced aversions in 130 male Sprague-Dawley rats. In Exp I, Ss lacking GN and controls were given an odor, a taste, or an odor–taste compound cue followed by intragastric gavage of LiCl. Prior to conditioning, neophobia for flavored solutions was absent in Ss with GN lesions. After pairing with LiCl, GN Ss developed normal conditioned odor aversions, whereas conditioned taste aversions were attenuated or totally blocked. Potentiation of odor by taste after compound conditioning was evident in both control and GN Ss. In Exp II, normal Ss were given compound conditioning to induce potentiated odor aversions and then given GN lesions prior to tests with the odor and taste components. Taste aversion retention was totally disrupted by GN ablation; potentiated odor aversions were retained by both groups, although the GN group extinguished faster. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Basolateral amygdala NMDA receptors are selectively involved in the acquisition of taste-potentiated odor aversion in the rat.

In the taste-potentiated odor aversion (TPOA) paradigm, animals acquire a strong aversion to an odor that is followed by delayed intoxication only if a gustatory stimulus is presented with the odor during conditioning. Although previous work has shown that N-methyl-D-aspartate (NMDA) receptors in the basolateral nucleus of the amygdala (BLA) play a role in the acquisition of TPOA, the present study aimed at.describing the process in which NMDA receptors in the BLA are involved during acquisition of TPOA. Male Long-Evans rats received intra-BLA infusions of the competitive NMDA receptor antagonist {d},{l}-2-2-amino-5-phosphonovalerate ({d}-APV; 0.05 and 0.50 μg) immediately before or after the odor–taste conditioned stimulus (CS) presentation, or immediately before the test. Results showed that {d}-APV impaired acquisition of TPOA when infused before, but not after, the CS presentation, but did not affect retrieval. These results suggest that NMDA receptors of the BLA are involved in the formation of potentiation—by taste—of the olfactory memory trace, but not in the maintenance of this process. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste agnosia following gustatory neocortex ablation: Dissociation from odor and generality across taste qualities.

In Exp I, 18 male Long-Evans hooded rats trained to avoid drinking in the presence of a compound odor (benzyl acetate) and taste (sucrose) CS lost the taste habit but retained the odor habit following gustatory neocortex (GN) ablation. Conversely, olfactory bulb ablation resulted in loss of the odor habit but retention of the taste habit. In Exp II, with 60 Ss, Ss lacking GN did not retain preoperatively instated learned aversions to a suprathreshold quinine hydrochloride (bitter) taste solution that had been employed as a CS. However, Ss with GN lesions that were virtually identical to those of the bitter-trained group retained a preoperatively learned aversion to a hydrochloric acid (sour) CS. Exp III, with 60 Ss, demonstrated that reliable agnosia for an acid CS could be produced by lesions that extended more deeply into perirhinal areas near the claustrum at the level of the GN. It is concluded that the agnosia following GN ablation is relatively specific to gustation and that agnosia for preoperatively acquired tasted aversion habits occurs for all 4 basic gustatory stimuli following anterolateral cortex ablations centered on the GN. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Conditioned taste and taste-potentiated odor aversions in the Syracuse high- and low-avoidance (SHA/Bru and SLA/Bru) strains of rats (Rattus norvegicus).

SHA/Bru and SLA/Bru rats were selectively bred for good and poor active-avoidance learning. However, SLA/Bru animals are superior to SHA/Bru rats in conditioned suppression and passive avoidance learning. In this experiment, saccharin taste and almond odor were the components of a compound CS (flavor) in an illness-induced aversive conditioning paradigm. SLA/Bru rats (n?=?17) showed stronger conditioned flavor, taste, and odor aversion than did SHA/Bru animals (n?=?18). Unselected Long-Evans rats (n?=?18) were intermediate between the selected strains. SLA/Bru and Long-Evans rats showed taste-potentiated odor aversion in this experiment, whereas SHA/Bru animals did not. The results provide evidence that genetic factors, as exemplified by the different strains, are importantly involved in the mechanisms underlying interoceptive and exteroceptive aversive conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)