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)     

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)     

Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

24 Long-Evans hooded rats lacking gustatory neocortex and 24 normal rats were familiarized to either hydrochloric acid or quinine hydrochloride solutions during free-drinking trials. Ss were subsequently trained to avoid either the familiar or the novel taste stimulus, using a balanced design, by pairing the to-be-associated taste with ip injections of apomorphine hydrochloride. Balanced, nonpaired presentations of the other taste solution and water were also presented. Normal Ss learned to avoid the novel taste more efficiently than the familiar taste. Ss with gustatory neocortex lesions did not differentiate novel from familiar tastes. They learned aversions to both in a manner highly similar to the aversion learning of familiar tastes by the normal group. Therefore, results demonstrate that Ss lacking gustatory neocortex displayed an associative deficiency only when they were trained on novel stimuli. This suggests that gustatory neocortex lesions disrupt the conditionability of taste stimuli by reducing or eliminating responses to taste novelty. This interpretation is supported by the absence of a "neophobic" response in the lesioned rats to the first presentation of a taste stimulus. (26 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the gustatory neocortex on taste aversion learning in the rat.

In 5 experiments, 110 normal male Long-Evans hooded rats and 125 Ss with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal Ss and 8 Ss with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Ss with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal and GN-lesioned Ss. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normals again learned specific aversions to all 4 solutions, but Ss with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of Ss with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration. It is proposed that the data can be accounted for by postulating a change in the threshold for taste illness associations following GN lesions. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neonatal ablations of the gustatory neocortex in the rat: Taste aversion learning and taste reactivity.

Sprague-Dawley rats sustaining ablations of gustatory neocortex (GN) at 2, 10, 20, or 60 days of age were compared with control-lesion and anesthetized controls (N?=?151) in the acquisition and extinction of a learned taste aversion. Ss were also tested for taste preference across 5 concentrations of NaCl solution (.04, .08, .15, .3, and .6 M). Results indicate that GN ablation disrupted aversion acquisition and extinction regardless of age at surgery. Taste-response functions for solutions shown by all GN Ss mirrored those of controls: preference (relative to water baseline) for middle concentrations and rejection of the strongest concentration. It is suggested that the 20- and 60-day-old GN Ss were hyperresponsive to the suprathreshold concentrations of NaCl (excepting the .6-M concentration). The increased response to NaCl in 20- and 60-day-old GN Ss may have been related to the significant decreases in water consumption relative to that of controls. Water consumption of controls and GN Ss in 2- and 10-day-olds was essentially equal. It is concluded that infant ablation of the GN does not spare normal taste aversion learning and that rats with GN ablations, regardless of age at surgery, respond in a normal manner to the hedonic aspects of NaCl solutions. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustatory detection thresholds after parabrachial nuclei lesions in rats.

Rats with either electrolytic (Experiment 1) or excitotoxic lesions (Experiment 2) that had been electrophysiologically centered in the gustatory zone of the parabrachial nuclei (PBN) were tested for sucrose and NaCl taste detection thresholds in a conditioned avoidance task. With 1 exception, all of these rats had previously shown severe deficits in acquiring an LiCl-based conditioned taste aversion (CTA) to sucrose, NaCl, or alanine. The rats with excitotoxic lesions also had failed to express a depletion-induced sodium appetite. Despite the uniformity of these deficits, the rats with lesions exhibited varied performance in the detectability task. Roughly ? of the rats did not perform competently, ? had elevated thresholds, and ? showed no or only marginal impairments in taste detectability. These findings demonstrate that the elimination of CTA following PBN lesions is not necessarily linked to an impairment in taste signal detection. Thus, PBN-induced deficits on 1 taste-related task do not entirely correspond with impairments on another. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Temporal Coding of Sensation: Mimicking Taste Quality With Electrical Stimulation of the Brain.

Two experiments suggested that the temporal pattern of a taste response in the brain can convey meaningful information. In Experiment 1, rats avoided lick-contingent electrical stimulation of the nucleus of the solitary tract (NTS; the first synaptic relay for taste) when the temporal pattern of pulses mimicked the electrophysiological response to quinine, but not when the temporal pattern was randomized. In Experiment 2, rats avoided lick-contingent electrical stimulation of the NTS that mimicked the temporal pattern of a sucrose response following stimulation-illness pairings. This aversion generalized to sucrose but not to the other tastants; extinction of the aversion to electrical stimulation also extinguished the aversion to sucrose. Results replicate and extend previous findings (P. M. Di Lorenzo & G. S. Hecht, 1993). (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

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)     

Comparison of formation of D2/E2-isoprostanes and F2-isoprostanes in vitro and in vivo--effects of oxygen tension and glutathione

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.     

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)     

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)     

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)     

Sucrose and fructose have qualitatively different flavors to rats

Previous studies suggest that rats might be able to discriminate between sucrose and fructose, but no previous study has examined this possibility in much detail. Rats were conditioned to avoid either sucrose or fructose by injecting them with lithium chloride when they drank these substances. Control rats were given the same injections but were not exposed to either sugar during training. After training, the rats were given a choice of fructose vs. sucrose. Data from control rats provided information about the relative taste intensity of the sugars. If the sugars possess only a single gustatory quality, control rats should prefer the sweeter sugar; under this assumption, sucrose appears to be two-four times sweeter than fructose. The two sugars share a common taste because rats trained to avoid sucrose avoided fructose when the fructose concentration was much greater than the sucrose concentration. Nevertheless, the two sugars are discriminable because, when the apparent sweetness of the sugars was matched, rats showed a greater aversion to the sugar they were trained to avoid. Aversions to sucrose and fructose also generalized to maltodextrins, but sucrose may have a somewhat greater maltodextrin flavor than does fructose. It is proposed that the biological function of maltodextrin taste is to allow animals to sense the ratio of glucose to fructose in foods.     

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)     

Stimulus preexposure reduces generalization of conditioned taste aversions between alcohol and non-alcohol flavors in infant rats.

Results of 3 experiments showed that infant rats (age 13-17 days) generalize conditioned taste aversions between alcohol and non-alcohol tastes such as a mixture of sucrose and quinine, apple cider vinegar, or coffee. Nonreinforced preexposure to those tastes reduced generalized aversions between them. Generalization between alcohol and sucrose-quinine was reduced not only after preexposure to both tastes, but also when only the nonconditioned taste was preexposed, whereas with alcohol and vinegar, both tastes had to be preexposed to obtain that effect. In no case was generalization reduced when only the to-be-conditioned taste was preexposed. Previous experience with alcohol alone, as well as with similar gustatory stimuli, may enhance subjects' ability to differentiate them during infantile stages in rats. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Specificity of acquired aversions to taste qualities in hamsters and rats.

372 golden hamsters and 120 Sprague-Dawley rats tasted 1 of 27 solutions before receiving an ip injection of apomorphine, then were tested for aversions to 4 solutions prototypic of human taste qualities: sucrose, NaCl, HCl, and quinine HCl. With most of the solutions described as sweet employed as CSs, Ss acquired an aversion to sucrose. With CSs described as either salty or sour by humans, Ss acquired an NaCl aversion in the former case or an HCl aversion in the latter case; an aversion to quinine HCl was acquired with 2 of the 3 CSs described as sour. With most of the CSs described as bitter or as having a bitter component, Ss acquired a quinine HCl aversion. Patterns of S activity evoked across 4 classes of peripheral gustatory neurons when the CSs were applied to the tongue were similar to the patterns of aversions across the 4 test stimuli for the CSs. This suggests that 4 neural channels mediate the sensations evoked by the 4 test solutions in rats and hamsters, perhaps even in human beings. (26 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste reactivity to alcohol and basic tastes in outbred mice

The taste reactivity test was used to determine the response of outbred mice to orally infused taste solutions. For the initial measures, mice (n = 10) were tested with 3%, 6%, 9%, and 12% (v/v) alcohol and four taste solutions: sucrose, sodium chloride, hydrochloric acid, and quinine hydrochloride (a single concentration of each). A second group of naive mice (n = 16) was tested with 5%, 10%, 20%, 30%, and 40% alcohol. The final set of measures with naive mice (n = 26) was taken with a range of sucrose concentrations: 0.01 M, 0.05 M, 0.1 M, 0.5 M, and 1.0 M. In general, mice made similar reactivity responses to all solutions tested. A predominant component of the mouse response to all infused fluids was forelimb flailing; gaping was also a common response to all solutions. Despite the large number of aversive-type responses, mice rejected very little fluid via passive drip or fluid expulsion. The single, significant difference in responding to the four taste stimuli was that mice made fewer aversive responses to sucrose. Differential responding to the 5 to 40% alcohol concentrations and sucrose concentrations was observed. Mice increased ingestive responding as the concentration of alcohol and sucrose increased. Aversive responding decreased reliably only with increases in the sucrose concentration. Data provide the first reported taste reactivity responses of mice to orally infused taste solutions. These results can be compared with the extant data available in rats and can also be used as a basis for exploring taste factors in genetically defined mouse populations.     

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)     

Taste avoidance, but not aversion, learning in rats lacking gustatory cortex.

Control rats rapidly learned to avoid drinking either a sucrose solution (Exp 1) or an NaCl solution (Exp 2) when the taste was paired with illness. These rats also produced aversive reactivity to each of these solutions in a taste reactivity test. Rats that lacked gustatory cortex (GC) learned to avoid drinking sucrose and NaCl, albeit at a slower rate than control rats. GC rats failed to display aversive reactivity to these tastes. The GC rats did show normal aversive reactivity to a strong quinine HCl solution during additional tests. It is suggested that the avoidance developed by GC rats did not entail a palatability shift of the conditional stimulus as it did in control rats. This altered learning strategy may account for the consistent learning deficits found in GC rats trained to avoid tastes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustatory functions, sodium appetite, and conditioned taste aversion survive excitotoxic lesions of the thalamic taste area

Rats with bilateral, electrophysiologically guided, ibotenic acid lesions of the gustatory thalamus (THLX) were tested for their ability to perform a variety of taste-guided behaviors. First, in daily 30-min sessions, the rats were given repeated 10-s access periods to a range of concentrations of sucrose, NaCl, or QHCl, plus water. Both the control and the THLX rats exhibited similar concentration-response functions, regardless of hydrational state. Next, on 3 trials, the rats were given 15 min access to 0.3 M l-alanine and then injected with LiCl (0.15 M, 1.33 ml/100 g body weight ip). All rats learned a taste aversion following 1 pairing with LiCl. Finally, on 3 separate occasions, the rats were injected with furosemide, and Na(+)-appetite was evaluated 24 hr later. All rats expressed an equivalent sodium appetite after the first furosemide injection, but only the control rats increased intake of 0.51 M NaCl with repeated sodium depletions. These observations reinforce prior data implying that an intact gustatory thalamus is not necessary for the expression of some taste-guided behaviors.