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)     

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)     

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 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)     

Learned aversions to copulatory behaviors in male rats.

Used LiCl for an aversive effect on copulatory behavior in adult experienced and inexperienced male hooded rats (Exp I) and in inexperienced adult male Holtzman rats (Exp II). When males received an injection of LiCl immediately after an encounter with an estrous female, the vigor of subsequent copulatory responding was initially unaffected. After 5–20 such pairings, however, males displayed an aversion to copulatory behaviors; they ceased to copulate entirely. These aversions persisted when Ss were tested in a novel environment and extinguished after 4 nonreinforced trials. This multiple-trial adaptation of the conditioned taste aversion paradigm provides a new approach to the aversive control of sexual behavior. (15 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)     

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)     

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)     

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)     

Uterine position and conditioned taste aversion.

Three experiments investigated the influence of uterine position on the performance of female offspring of female Sprague-Dawley and male Long-Evans rats in a conditioned taste aversion paradigm. 49 females that had males caudal to them in the same uterine horn (MF), 48 females with no caudal males (FF), and 24 males that had occupied a variety of different positions in the uterine horn were examined. Exps I and II confirmed a differential behavioral response by males and females during acquisition and extinction of the conditioned taste aversion. However, no differences were found between MF and FF Ss. In Exp III, in which testosterone was administered to females throughout testing, MF females showed an increased sensitivity to testosterone and a more prolonged rate of extinction than FF females. Exposure to testosterone during prenatal development heightened postnatal responsiveness to testosterone in female Ss. Results are discussed in terms of the organizational and activational effects of testosterone on behavior in a conditioned taste aversion situation. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste aversions to mother's milk: The age-related role of nursing in acquisition and expression of a learned association.

Seven experiments examined the development of taste aversion learning to novel cues contained in mother's milk in 176 laboratory and 377 Sprague-Dawley pups. Ss receiving distinctive milk by experimenter-delivered oral infusions followed by toxicosis formed an aversion to the dam's diet. Robust aversions were learned as early as Day 10 and were retained for at least 11 days. When the same distinctive milk was obtained directly from a foster mother through nursing, only weanling-age Ss formed an aversion. X-ray analysis of nipple location in the mouths of suckling Ss suggested that they receive milk at a similar tongue locus between the ages of 10 and 21 days; flavored milk was then delivered at specific time intervals in controlled quantities through tongue cannulas implanted at loci corresponding to the nipple position. Cannulated preweanling Ss that were attached to a nipple during mild delivery failed to associate the taste cue with illness, whereas both preweanlings off the nipple and weanlings on the nipple acquired aversions to the taste cue in the milk. Results suggest that pups of all ages are incapable of expressing a taste aversion in a nursing situation and that preweanling pups in particular are also deficient in acquiring aversions within a suckling context. The inability of preweanling pups to acquire taste aversions in a nursing situation appears to result from a failure to associate taste cues with illness rather than a failure to detect taste cues obtained from a nipple. (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)     

Effects of prior exposure on conditioned taste aversion in the rat: Androgen- and estrogen-dependent events.

Studied the effects of preexposure and gonadal hormone manipulation on the extinction of a conditioned taste aversion in 198 male Sprague-Dawley rats. In Exp I, Ss were given 1 prior exposure to sucrose at some selected time (Days 4, 2, or 1) before a 2nd exposure (Day 0) to sucrose and a LiCl injection, or they were given only a single exposure (Day 0). Under single exposure, castrated Ss extinguished the aversion faster than either testosterone-treated castrated Ss or sham-operated Ss. In Exp II, estradiol, dihydrotestosterone, and testosterone were studied by using only a Day 1 preexposure condition. The testosterone-treated group maintained the aversion for the longest period, followed by dihydrotestosterone-treated, sham, castrated, and estradiol-treated groups. In Exp III, estradiol was administered alone or in combination with 2 doses of dihydrotestosterone. Findings indicate that the outcome of behavior was dependent on the ratio of estradiol to dihydrotestosterone, with variations in this ratio resulting in fast (estrogen effect) to slow (androgen effect) rates of extinction. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Punishment of saccharin drinking by amphetamine in rats and its reversal by chlordiazepoxide.

Demonstrates, in a conditioned taste-aversion paradigm, that doses of dextroamphetamine which are intravenously self-administered by rats may punish saccharin drinking. Ss were male Wistar rats. In Exp I (n = 42), single-trial, dose-related aversion was shown. Aversion was not antagonized by chlorpromazine. Exp II (n = 32) demonstrated dose-related acquisition of taste aversion with repeated administration of very low amphetamine doses. In Exp III (n = 18), drug-induced saccharin aversion was reversed by chlordiazepoxide; this action paralleled the action of chlordiazepoxide in numerous other aversive-conditioning situations. Exp IV (n = 30) ruled out the possibility that depression of saccharin drinking was due to a direct pharmacological action of the drug and not to learned saccharin avoidance. Results indicate that the reinforcing action of amphetamine depends on the response with which its effects are correlated. (20 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ingestional aversion learning in preweanling rats.

In 4 experiments, ingestional aversions were conditioned in 12- and 15-day-old Sprague-Dawley rats by infusing a .5% solution of saccharin into the oral cavity and following this oral infusion by the injection of lithium chloride. At both ages, Ss for which the saccharin exposure was followed by lithium injection within 2–3 min drank less when the saccharin solution was again presented by oral infusion 12 hrs later; such suppressions of intake were not observed in Ss that previously received the saccharin and lithium in an unpaired fashion (Exps I and III). Ingestional aversions were also learned by 12-day-olds when a 30-min interval was introduced between saccharin exposure and lithium toxicosis but not when toxicosis was delayed by 120 min (Exp II). In contrast, 15-day-olds learned aversions with both the 30- and 120-min-delay intervals (Exp III). Despite the absence of long-delay learning in 12-day-olds, ingestional aversions conditioned at 12 days of age were retained for 2 wks (Exp IV). Results provide further evidence of the associative abilities of neonatal rats and illustrate a developmental aspect of long-delay learning. (34 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)     

Conditioned taste aversion in lean and obese rats with ventromedial hypothalamic knife cuts.

Assessed the development of a conditioned taste aversion (CTA) in 60 female Sprague-Dawley rats made hyperphagic with parasagittal knife cuts in the ventromedial hypothalamus (VMH). Ss were water deprived and presented with a .1% saccharin solution paired with injections of either LiCl or NaCl. In Exp I, VMH Ss tested at a nonobese weight level did not differ from sham-operated controls in acquisition and extinction of the CTA. In Exp II, moderately obese VMH Ss displayed a stronger CTA than did sham-operated controls as evidenced by slower extinction. A 2nd group of obese VMH Ss given an amount of LiCl equivalent to that given to the controls also displayed retarded extinction of the CTA. Results reflect an obesity-induced suppression in appetitive motivation. (29 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)