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)     

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)     

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)     

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 responses to a taste conditioned stimulus paired with lithium chloride administration.

The present experiments examined whether behavioral conditioned responses (CRs) develop to lithium chloride (LiCl)-paired tastes and whether these CRs are similar to the behaviors that follow administration of the drug. Rats were exposed to a saccharin solution via intraoral infusions before being injected with either LiCl or saline. CRs were assessed after conditioning when the saccharin conditioned stimulus (CS) was delivered alone. The unconditioned response (UCR) to LiCl delivery is a very distinctive posture that has been termed "lying-on-belly." The present study indicates that this behavior pattern also occurs after the delivery of a LiCl-paired taste solution. The similarity between these unconditioned and conditioned behaviors is consistent with the hypothesis that responses are conditioned during taste aversion acquisition and that CRs are similar to those that are generated by the drugs used in conditioning. (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)     

Functional decortication by cortical spreading depression does not prevent forced extinction of conditioned saccharin aversion in rats.

In 2 experiments conditioned taste aversion established in Druckrey hooded rats by association of saccharin drinking with subsequent lithium chloride intoxication decreased saccharin intake to 22% of normal consumption. Force-feeding saccharin to intact and functionally decorticate trained Ss returned saccharin consumption on the next day to 62% (n = 18) and 77% (n = 19), respectively. Overtrained conditioned saccharin aversion was affected by forced extinction in a similar way (saccharin intake increased from 28% to 50% and 63%, respectively). Intact-brain Ss refused to swallow saccharin during forced feeding, while functionally decorticate Ss showed no signs of aversion; extinction was almost equal in both cases. Application of lithium chloride after forced feeding of saccharin in functionally decorticate Ss neither prevented extinction of conditioned taste aversion nor reestablished the aversion habit extinguished earlier with intact brain. It is concluded that acquisition of the conditioned taste aversion requires cortical input to a short-term memory file, whereas decorticate extinction can be induced by subcortical gustatory processing analogous to the mechanism controlling feeding behavior during the preweaning period. (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)     

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)     

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)     

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)     

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)     

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)     

Effects of hypothermia on the acquisition of conditioned taste aversion in rats.

Analyzed the mechanism of conditioned taste aversion (CTA) by subjecting 131 male and hooded rats in 5 experiments to reduced body temperature during various phases of CTA acquisition. A 15-min access to .1% saccharin served as the CS, and an ip injection of LiCl (.15 M, 4% of body weight) given 30 min later served as the UCS. Hypothermia (cooling to 20-22°C colonic temperature) alone or combined with anesthesia (Nembutal 20 or 40 mg/kg) did not prevent CTA acquisition when applied during the CS-UCS interval. Hypothermia induced immediately after LiCl administration to anesthetized or unanesthetized Ss failed to disrupt CTA or to increase neophobic rejection of saccharin. On the other hand, hypothermic Ss were not able to form the short-term gustatory trace when the CS (2% saccharin, 1% of body weight) was injected ip, although this procedure yielded significant CTA in euthermic Ss. It is concluded that the most vulnerable link of CTA acquisition is the formation of the short-term gustatory trace. Persistence of the short-term trace, its association with poisoning, and consolidation of the permanent CTA engram are accomplished by mechanisms that are resistant to hypothermia and/or anesthesia. (39 ref) (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)     

Area postrema mediates the formation of rapid, conditioned palatability shifts in lithium-treated rats.

The rapid acquisition and subsequent retention of lithium-induced conditioned changes in taste reactivity responses to sucrose were examined in rats with the area postrema (AP) either ablated or intact. On 2 conditioning days, a series of brief intraoral sucrose infusions was paired with the effects of LiCl or NaCl injections. Repeated associations of the sucrose taste with the effects of lithium significantly reduced ingestive responses and increased aversive responses only in the AP-intact group. AP-ablated rats treated with LiCl and rats injected with NaCl displayed an ingestive pattern of responses. Only the AP-intact rats, previously injected with LiCl, subsequently displayed evidence of a conditioned taste aversion. We conclude that toxin activation of the AP is required to produce the conditioned shift in taste reactivity responses and subsequent expression of a taste aversion in rats treated with lithium. (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)     

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

Paired almond odor or saccharin taste as a single CS or as a compound CS for both a footshock UCS and a toxin UCS (LiCl) to test the generality of potentiation in male Sprague-Dawley rats. Extinction tests with the almond and saccharin components were then given. In single CS–toxin experiments, taste was more effective than odor, and after compound conditioning, the taste component potentiated the odor component. Conversely, in single CS–shock experiments, odor was more effective than taste, and after compound conditioning, no potentiation was observed. Instead, interference effects were observed. In Exps I and II, the addition of taste disrupted odor CS–shock conditioning, and in Exp III, odor interfered with taste CS–shock conditioning. Visceral feedback was apparently a necessary UCS for the potentiation of odor by taste. Data support the neural convergence and gating hypothesis of flavor aversion conditioning. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A comparison of taste aversions induced by radiation and lithium chloride in CS-US and US-CS paradigms.

Describes 3 experiments with a total of 454 albino male Charles-River rats. Conditioned taste aversions induced by ionizing radiation and lithium chloride (LiCl) were compared with both forward (CS-UCS, conditioned stimulus-unconditioned stimulus) and backward (UCS-CS) conditioning paradigms. Taste aversions were produced when a saccharin CS preceded or followed a 100-r radiation UCS by as much as 6 hrs, but a 2%-of-body-weight, .15-mol LiCl UCS was effective only in CS-UCS pairings. It is argued that the ineffectiveness of an LiCl stimulus in UCS-CS pairings was not attributable to differences in the "strength" of the respective LiCl and radiation doses in that these doses yielded comparable aversions in forward pairings. These results are related to inadequacies of a "sickness" model of taste aversion conditioning. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Rationale for en bloc vein resection in the treatment of pancreatic adenocarcinoma adherent to the superior mesenteric-portal vein confluence. Pancreatic Tumor Study Group

The enzymatic activity of protein kinase C (PKC) was measured in the cytosol and particulate fraction of parabrachial nucleus, the presumed site of conditioned taste aversion (CTA) engrams. At various time intervals after acquisition of the task (pairing saccharin consumption with subsequent LiCl poisoning) the nucleus was dissected from the frozen coronal sections. An increase (+40%) in the cytosol PKC activity was found 48 h after that pairing in comparison with controls (saline injection instead of LiCl). Particulate enzyme activity virtual did not change (-5%). Thus the total PKC activity increased significantly (21%). Qualitatively similar but less markedly expressed PKC shifts (+18% in cytosol) ere found 24 h following CTA. Twelve hours and 5 days after CTA acquisition the activity and distribution of PKC was similar to that seen in normal rats. The control experiments revealed that 6 h after LiCl injection alone (without previous saccharin consumption) translocation of PKC from the cytosol to the membrane fraction (found previously 1 h after LiCl injection alone) still persisted but did not differ from that found 6 h after its pairing with saccharin drinking (CTA). It is concluded that acquisition of conditioned taste aversion may be followed by synthesis of PKC rather than by its translocation or downregulation.