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)     

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)     

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)     

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)     

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)     

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)     

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)     

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)     

Effects of basolateral amygdala lesions on neophobia, learned taste aversions, and sodium appetite in rats.

Reports results of 8 experiments with a total of 327 male Sprague-Dawley rats. Lesions to the basolateral amygdala produced permanent impairment in Ss' ability to learn a taste aversion. When lesions were administered after Ss had already learned an aversion, there was complete loss of the aversion. Ss with amygdala lesions also had a diminished neophobic response when presented with a novel solution and showed a more generalized aversion to water after a sucrose-sickness trial. Whether a solution was novel or familiar affected the learning of an aversion for controls more than it did for Ss with amygdala lesions. Ss with amygdala damage also showed less sodium appetite than normals in response to desoxycorticosterone acetate injections. These results indicate that rats with amygdala lesions have deficits in recognizing the significance of stimuli. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mapping Conditioned Taste Aversion Associations Using c-Fos Reveals a Dynamic Role for Insular Cortex.

Novel tastes are more effective than familiar tastes as conditioned stimuli (CSs) in taste aversion learning. Parallel to this, a novel CS-unconditioned stimulus (US) pairing induced stronger Fos-like immunoreactivity (FLI) in insular cortex (IC), amygdala, and brainstem than familiar CS-US pairing, suggesting a large circuit is recruited for acquisition. To better define the role of IC, the authors combined immunostaining with lesion or reversible inactivation of IC. Lesions abolished FLI increases to novel taste pairing in amygdala, suggesting a role in novelty detection. Reversible inactivation during taste preexposure increased FLI to familiar taste pairing in amygdala and brainstem. The difference between temporary inactivation, which blocked establishment of "safe" taste memory, and lesions points to a dual role for IC in taste learning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Perceptual characteristics of the amiloride-suppressed sodium chloride taste response in the rat.

Assessed the contribution of amiloride-sensitive membrane components to the perception of NaCl taste using a conditioned taste aversion procedure with 8 groups of adult rats conditioned to avoid either 0.1M NaCl, 0.5M NaCl, 0.1M NH?Cl, or 1.0M sucrose while their tongues were exposed either to water or to amiloride hydrochloride. Differences in the acquisition of taste aversions between the amiloride- and nonamiloride-treated groups were not apparent when the conditioned stimulus (CS) was 0.5M NaCl, 0.1M NH?Cl, or 1.0M sucrose. Although the magnitude of the 0.5M NaCl aversion was similar between amiloride- and nonamiloride-treated Ss, the perceptual characteristics of the CS differed between groups. Amiloride-treated Ss avoided monochloride salts after conditioning to 0.5M NaCl but not nonsodium salts or nonsalt stimuli. Ss not treated with amiloride only generalized the 0.5M NaCl aversion to sodium salts. The "salty" taste of NaCl is related to the amiloride-sensitive portion of the functional taste response in rats. The portion of the NaCl response insensitive to amiloride has "sour-salty" perceptual characteristics and is not perceived as being salty. (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)     

Bait-shyness acquisition is impaired by VMH lesions that produce obesity.

Lesioned Carworth CFE female rats in the area of the ventromedial nucleus of the hypothalamus (VMH) before or after avoidance learning. Prelesioned Ss learned to avoid familiar saccharin-sweetened water associated with apomorphine less rapidly, and during extinction lost the avoidance more rapidly than controls. Ss lesioned after avoidance learning continued to avoid, and during extinction lost the avoidance at the same rate as controls. When given ad-lib food and water, lesioned Ss became obese. 1 tentative interpretation is that VMH-lesioned rats overrespond to environmental stimuli, including their food. This interferes with gustatory-visceral associations needed for satiety and bait-shyness acquisition. Another possibility is that overresponding to environmental stimuli and impaired gustatory-visceral associations are both direct consequences of VMH lesions. (32 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)     

Improved large-scale isolation of breeder porcine islets: possibility of harvesting from nonheart-beating donor

Previous studies of the effect of carbonation on taste perception have suggested that it may be negligible, manifesting primarily in increases in the perceived intensity of weak salt and sour stimuli. Assuming CO2 solutions in the mouth stimulate only trigeminal nerve endings, this result is not altogether surprising; however, there are neurophysiological data indicating that CO2 stimulates gustatory as well as trigeminal fibers. In that case, carbonation might alter the quality profile of a stimulus without producing substantial changes in overall taste intensity--much as occurs when qualitatively different taste stimuli are mixed. To address this possibility, subjects were asked to rate the total taste intensity of moderate concentrations of stimuli representing each of the basic tastes and their binary combinations, with an without added carbonation. They then subdivided total taste intensity into the proportions of sweetness, saltiness, sourness, bitterness and 'other taste qualities' they perceived. The addition of carbonation produced only small increases in ratings of total taste intensity. However, rather dramatic alterations in the quality profiles of stimuli were observed, particularly for sweet and salty tastes. The nature of the interaction is consistent with a direct effect of carbonation/CO2 on the gustatory system, although the possibility that at least some of the observed effects reflect trigeminal-gustatory interactions cannot be ruled out.     

Dissociation between learning and remembering in rats with lesions in the lateral hypothalamus.

10 female Sprague-Dawley albino rats which had recovered regulatory feeding after lesions in the lateral hypothalamus (LH) were tested for retention of a taste aversion acquired prior to the lesions. All 10 Ss retained the aversion. 2 of these Ss provided evidence that preoperative memory can be lost following lesions but subsequently recovers. The same 10 recovered LH-lesioned Ss were exposed to a taste-aversion training procedure identical to that used prior to the lesion, but with novel flavors. 7 of the 10 failed to acquire the new taste aversion. 3 additional Ss served as unoperated controls. It is concluded that rats with lateral hypothalamic damage are thus capable of remembering previously learned taste aversions but unable to learn new ones. (17 ref) (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.     

Parabrachial gustatory lesions impair taste aversion learning in rats.

Lesions in the gustatory zone of the parabrachial nuclei (PBN) severely impair acquisition of a conditioned taste aversion (CTA) in rats. To test whether this deficit has a memorial basis, 15 intact rats and 10 rats with PBN lesions (PBNX) received 7 intraoral taste stimulus infusions (30 sec, 0.5 ml) distributed over a 30.5-min period after either LiCl or NaCl injection. This task measures the rapid formation of a CTA and has minimum demands on memory. LiCl-injected intact rats progressively changed their oromotor response profiles from one of ingestion to one of aversion. NaCl-injected intact rats did not change their ingestive pattern of responding. In contrast, there was no difference between LiCl- and NaCl-injected PBNX rats. These same PBNX rats failed to avoid licking the taste stimulus when tested in a different paradigm. A simple impairment in a memorial process is not likely the basis for the CTA deficit. (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)     

Visual sampling after lesions of the superior colliculus in rats.

In 2 experiments with 20 male black-hooded rats, Ss with bilateral lesions of the superior colliculus showed significantly poorer relearning of a horizontal/vertical stripe discrimination than control Ss. In Exp I, all Ss showed disruption of performance when a stimulus–response (S–R) separation was introduced by raising the stimuli above the site of responding. However, colliculectomized Ss were much more disturbed by the S–R separation than were control Ss. In Exp II, all Ss showed lower performance levels when conflicting patterns were introduced into the upper portion of the stimulus doors, but this time Ss with collicular lesions were less disturbed than controls. It is suggested (a) that when the stimulus and response sites are discontinuous, rats must make an appropriate orienting response to effectively sample the visual stimuli and (b) that lesions of the superior colliculus alter performance by interfering with this orienting behavior. The impairment in relearning is attributed to the absence of preoperative overtraining on the discrimination task. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)