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)     

Role of the hippocampus in blocking and conditioned inhibition of the rabbit's nictitating membrane response.

In Exp I, bilateral aspiration of the dorsal hippocampus produced a disruption of blocking of 30 New Zealand rabbits' nictitating membrane response in L. J. Kamin's (1968, 1969) 2-stage paradigm, but had no effect on the formation of a Pavlovian conditioned inhibitor in Exp II (27 Ss). Results of Exp I indicate that normal Ss and those with cortical lesions given conditioning to a light-plus-tone CS gave CRs to both light and tone during nonreinforced presentations of each (test phase). If, however, compound conditioning was preceded by tone acquisition, only the tone elicited a CR during testing; that is, blocking was observed. In Ss with hippocampal lesions, however, CRs were given to both light and tone during testing whether or not compound conditioning was preceded by tone acquisition. Data from Exp II show that Ss with hippocampal lesions could discriminate as well as normal Ss and those with cortical lesions between a light (CS+) and light plus tone (CS-). In addition, when the inhibitory tone was subsequently paired with the UCS in retardation testing, Ss in all 3 lesion conditions acquired the CR at the same rate. Thus, it appears that hippocampal lesions do not disrupt conditioned inhibition. Results are taken as support for the view that the hippocampus is responsible for "tuning out" stimuli that have no adaptive value to the organism. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Conditioned aversion to distinct environmental stimuli resulting from gastrointestinal distress.

In Exp I, 40 male Sprague-Dawley-derived rats subjected to apomorphine-induced malaise following a 2-min placement in a black compartment avoided this black compartment significantly more than 10 controls in a choice situation. The degree of aversion, however, was substantially reduced when Ss were provided water (or saccharin) in the black compartment during conditioning and testing. Ss learned to suppress consumption of fluid in the black compartment. In Exp II, 10 Ss were made ill in the black compartment. Later, when drinking saccharin (or saline) preceded placement in the black compartment, Ss learned to suppress consumption of that fluid. The black compartment had become a conditioned reinforcer for taste aversion. (19 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Selective hippocampal lesions abolish the contextual specificity of latent inhibition and conditioning.

The contextual specificity of the CR and latent inhibition (LI) was examined in rats with selective hippocampal lesions. Acquisition of the CR to a novel CS was equally rapid in control and hippocampal rats (Exps 1 and 2), and CS preexposure disrupted acquisition (i.e., produced LI) to an equal extent in both groups (Exp 2). In control Ss, however, the CR established in one context transferred incompletely to a 2nd context (Exp 1), and LI was attenuated when CS preexposure and conditioning occurred in different contexts (Exp 3). This context specificity of the CR and LI was not apparent in hippocampal rats; the CR and LI transferred readily from one context to another. In addition, hippocampal rats were impaired in a spatial learning task (Exp 2) but were unimpaired in learning a Pavlovian contextual discrimination (Exp 3). Results suggest that a common contextual retrieval process underlies the contextual dependence of the CR and of LI and that this process is mediated by the hippocampus. (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)     

Disruption of conditioned taste aversion in the rat by stimulation of amygdala: A conditioning effect, not amnesia.

Conducted 2 experiments with a total of 143 male Wistar rats to determine whether the disruption of conditioned taste aversion by amygdaloid brain stimulation (BST) during conditioning could be attributed to the stimulus properties of the BST. In Exp I, Ss receiving BST (a) while drinking saccharin, (b) during the onset of LiCl toxicosis, or (c) in the interval between taste exposure and toxicosis drank significantly more saccharin solution during a 48-hr retest than implanted or unoperated controls receiving similar taste–toxicosis pairings. In contrast, Ss receiving BST during both conditioning and retention trials developed a strong conditioned aversion. Exp II confirmed that BST formed a compound with the taste of the saccharin solution. A small but significant aversion was displayed by groups exposed to BST plus taste during conditioning and to either taste alone or BST alone during the retest. Again, the group presented with BST and taste prior to and following LiCl toxicosis displayed a strong conditioned aversion. Results suggest that disruption of conditioned taste aversion with amygdaloid BST represents a conditioning effect, not amnesia. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

ACTH and ACTH4–20 modification of neophobia and taste aversion responses in the rat.

A series of 6 experiments assessed the effects of ACTH and the ACTH analog ACTH4–20 on drinking in conditioned taste aversion and neophobic situations using a total of 168 male Sprague-Dawley rats as Ss. Both substances delayed the extinction of a conditioned taste aversion established by a single pairing of lithium chloride with milk (Exp I). However, in this situation, the ACTH parent peptide was more potent behaviorally. ACTH supressed milk consumption in Ss with no toxicosis experience (Exp II). This effect was apparently not due to the conditioning of a taste aversion (Exp III) with ACTH serving as a weak aversive UCS. Exogenous ACTH (Exp IV) or ACTH4–20 (Exp V) did not enhance neophobia; however, repeated injections of ACTH suppressed drinking. This ACTH suppression was related to the familiarity/novelty of the substance being consumed. The neophobic response to milk was not accompanied by pituitary-adrenal activation (Exp VI). Both neophobic and conditioned taste aversion situations appear to be useful for assessing peptide effects on consummatory behavior. (36 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)     

Lithium chloride and avoidance of novel places.

In Exp I, 40 male hooded rats were exposed to a distinctive chamber (Chamber A, part of a 2-chamber apparatus) that was novel for half of the Ss but familiar for the other half. Each S was subsequently injected with lithium chloride or saline. In a test trial conducted 24 hrs later, all Ss were given a choice between Chamber A and Chamber B, which was novel for all Ss. The group made familiar with Chamber A and then given lithium showed a significant preference for that side or an avoidance of the novel side, a "spatial neophobia." Exp II, with 40 Ss, confirmed the spatial neophobia effect and demonstrated that it did not depend on the particular conditioning procedure used in the 1st experiment. The spatial neophobia effect was related to similar effects in the taste aversion literature and to the results of research on lithium-induced decreases in exploratory behavior. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ibotenate lesions of the hippocampus enhance latent inhibition in conditioned taste aversion and increase resistance to extinction in conditioned taste preference.

In 2 experiments, the effects of axon-sparing lesions of the hippocampus on performance in aversive and appetitive taste conditioning tasks were investigated. In Exp 1, hippocampally lesioned rats showed no impairment of conditioned taste aversion learning relative to controls, but they did display an increased sensitivity to latent inhibition (LI). In Exp 2, the same hippocampectomized rats acquired a conditioned taste preference but failed to show any evidence of extinction. The influence of the neurotoxic lesion on LI is in the opposite direction to the effect typically found following hippocampal damage induced by traditional methods. Accordingly, the data present challenges for most current theories of hippocampal function. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Dorsal hippocampal lesions impair blocking but not latent inhibition of taste aversion learning in rats.

The aim of the present experiments was to study the effect of nonselective electrolytic lesions of the rat dorsal hippocampus on 2 learning phenomena: the L. J. Kamin (1969) blocking effect and latent inhibition of taste aversion learning. Bilateral dorsal hippocampal lesions selectively impaired blocking induced by 1 saccharin-lithium chloride pairing previous to 1 serial compound (saccharin–cider vinegar)–lithium pairing, but lesions had no effect on latent inhibition of a saline aversion, induced by 6 saline preexposures, in the same group of animals. Moreover, dorsal hippocampal lesions did not affect latent inhibition of saccharin-conditioned aversion induced by 1 or 6 preexposures. It is argued that blocking and latent inhibition of taste aversion learning do not share a common neural mechanism. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Vagotomy facilitates extinction of conditioned taste aversions in rats.

Results from 3 experiments indicate that severing the subdiaphragmatic vagus in male Sprague-Dawley rats increased the rate of extinction of learned taste aversions. In Exp I, when the illness-inducing agent was the blood-borne toxin apomorphine, vagotomized Ss tended to consume more saccharin than controls during repeated extinction tests. In Exp II, vagotomy disrupted retention and increased extinction of a preoperatively acquired saccharin aversion. Disruptions were found when the taste aversion was induced by copper sulfate, a local gastric irritant, or apomorphine. Exp III demonstrated that vagotomy did not affect retention or extinction of a shock-induced conditioned emotional response to noise. It is concluded that integrity of the vagus is not necessary for acquisition of a learned taste aversion when a blood-borne toxin is used as the illness-inducing agent. However, the vagus apparently mediates an integral portion of the CR following taste–illness acquisition. (24 ref) (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)     

Patterned (single) alternation in infant rats after combined or separate lesions of hippocampus and amygdala.

The role of the developing hippocampus and the amygdala on patterned (single) alternation (PA) in the infant rat was investigated in 4 experiments. In Exps 1 and 2, Ss were given 2 bilateral electrolytic hippocampal lesions or sham surgeries at 10 or 11 days of age and were trained 6 days later in a straight runway. In Exp 1, there were 120 trials in 1 day, with an 8-, a 15-, or a 30-s intertrial interval (ITI). PA learning occurred in lesion and sham Ss at the 8- and 15-s ITIs. In Exp 2, training was extended to 240 trials over 2 days, with a 30- or 60-s ITI. Sham and lesion Ss showed PA at the 30-s ITI, but the emergence of PA was delayed in the lesion pups at the 60-s ITI. In Exp 3, amygdaloid lesions had no effect on PA learning at the 8-s ITI. However, when Ss with hippocampal and amygdaloid lesions were trained at the 8-s ITI, the emergence of PA was delayed, and its size was reduced (Exp 4). Results argue for a role of the hippocampus in PA learning at long ITIs and suggest that, even in 16-day-old Ss exposed to an 8-s ITI, the combined hippocampal and amygdaloid lesion produces a deficit greater than either the hippocampal or the amygdaloid lesion. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Acquisition and extended retention of a conditioned taste aversion in preweanling rats.

Four experiments employed a taste aversion conditioning procedure appropriate for both neonatal and adult rats to investigate the ontogeny of extended retention. In Exp I, 200 outbred albino rats trained at 1, 10, 20, or 60 days of age were tested for retention of the taste aversion 25 days later. At testing, only those Ss conditioned when 20 or 60 days old demonstrated significant taste aversions. Exps II and III, with 190 Ss, established that Ss 14–25 days old and older were able to retain significant taste aversions following a 25-day retention interval. 80 younger Ss did, however, acquire and retain the aversion for several days and showed a gradual retention loss over progressively longer retention intervals (Exp IV). Findings suggest that preweanling rats demonstrate initial consolidation, storage, and retrieval of conditioned taste aversions. It is only after this initial period that retention deficits become evident. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Learned taste aversions over long delays in rats: The role of learned safety.

Tested the proposal that learned safety accounts for the delay gradient in learned taste aversions in 4 experiments. In Exp I and II, 132 female Sprague-Dawley rats drank a small quantity of a nontoxic solution toward which they had a mild aversion. It was found, in support of the learned safety concept, that the intake in a 2nd test was a function of the delay time between tests. Exp III with 72 Ss demonstrated that no additional curve of learned safety would occur when Ss had previously received extensive experience with the solution. Exp IV with 81 Ss found, however, that learned safety was not a sufficient explanation for the delay gradient in learned taste aversions by showing that the gradient still persisted even when the experimental procedure minimized the effects of learned safety. (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)     

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)     

Taste reactivity as a dependent measure of the rapid formation of conditioned taste aversion: A tool for the neural analysis of taste-visceral associations.

Investigated the ability of animals to form taste aversions following neural manipulations. In Exp 1, 10 rats received intraoral infusions of sucrose every 5 min starting immediately after the injection of LiCl. 12 controls were injected with NaCl. Oromotor and somatic taste reactivity behaviors were videotaped and analyzed. Lithium-injected Ss decreased their ingestive taste reactivity over time; aversive behavior increased. Controls maintained high levels of ingestive responding and demonstrated virtually no aversive behavior following sodium injection. Ss were tested several days later for a conditioned taste aversion (CTA). Rats previously injected with lithium demonstrated significantly more aversive behavior than controls. Exp 3 revealed that when similarly treated rats were tested for a CTA while in a lithium-induced state, difference in the ingestive behavior was observed. In Exp 2, naive rats were injected with NaCl or LiCl but did not receive their 1st sucrose infusion for 20 min. Ss also received infusions at 25 and 30 min postinjection. There were no differences in the task reactivity behavior displayed. Rats dramatically changed their oromotor responses to sucrose during the period following LiCl administration, provided the infusions started immediately after injection, a change attributable to associative processes. (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)