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)     

The parabrachial nucleus is essential for acquisition of a conditioned odor aversion in rats.

Rats with bilateral ibotenic acid lesions of the gustatory zone of the parabrachial nuclei (PBN) failed to acquire a conditioned taste aversion (CTA) in Exp 1. They also failed to acquire a conditioned odor aversion (COA) when the olfactory cue was presented on an odor disk in Exp 2 or when it was presented in water in Exp 3. The failure to acquire the COA was not due to an inability to detect or use olfactory stimuli because the lesioned rats displayed neophobia to a novel odor in Exp 3 and used an olfactory cue to predict the availability of an aversive capsaicin solution in Exp 4. Together, the results demonstrate that, as with CTA learning, PBN cell bodies are essential for the establishment of a specific association between an olfactory conditioned stimulus and a lithium chloride unconditioned stimulus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Electrolytic lesions of the parabrachial nuclei (PBN) disrupt conditioned taste aversion (CTA) in the rat, but it is not known whether this effect is due to damaging axons of passage or to destruction of intrinsic neurons. We tested 10 rats with electrophysiologically guided, ibotenic acid lesions of the PBN (PBNx) to determine whether they could acquire an LiCl-induced CTA to l-alanine (0.3 M) or demonstrate a sodium appetite following furosemide treatment and overnight access to sodium deficient chow. Vehicle-treated and nonsurgical controls were included in the design. PBNx rats failed to develop a CTA, even after 3 conditioning trials. Moreover, more than 8 months later, a subset of the PBNx rats were again unable to learn a CTA using NaCl as the conditional stimulus (CS). After the furosemide treatment, the control rats drank an average of 20.3 ml of strong salt in 24 hr. The PBNx rats drank virtually no NaCl during the first 2 hr and averaged only 4.0 ml in 24 hr. In the PBN, damage to neuronal somata is more critical than interrupting fibers of passage for producing deficits in taste-guided behaviors. (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.     

The parabrachial nucleus: A brain stem substrate critical for mediating the aversive motivational effects of morphine.

Bilateral ibotenic acid lesions of the lateral, but not the medial, parabrachial nucleus (PBN) blocked conditioned taste aversion (CTA) induced by morphine but not conditioned place preference induced by morphine. The same lateral PBN lesions also blocked conditioned place aversion produced by low intraperitoneal doses of morphine (shown to produce aversion, instead of preference, due to a restricted action on gut opiate receptors). Lateral PBN lesions did not block CTA produced by LiCl. Cerebral peduncle lesions that destroyed the direct descending projections from the visceral cortex to the PBN did not block CTA induced by morphine, nor did ibotenic acid lesions of the tegmental pedunculopontine nuclei (shown to block place preference produced by even high morphine doses). It is suggested that the lateral PBN is a critical link in the neural pathway carrying the aversive motivational effects of opiates from the gut into the CNS, independent of the neural pathway carrying the rewarding motivational effects of morphine. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustatory detection thresholds after parabrachial nuclei lesions in rats.

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

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)     

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)     

Reflex facilitation of the nictitating membrane response remains after cerebellar lesions.

Reflex facilitation and associated properties were investigated during classical conditioning of the nictitating membrane (NM) response in rabbit. In the first experiment, the role of the cerebellum was examined by comparing the unconditioned responses of animals with bilateral lesions of the deep cerebellar nuclei with those of operated controls during counterbalanced tone/light (T/L) discrimination training. Both T and L facilitated unconditioned NM responses when used as the CS+ (conditioned stimulus), but neither facilitated when used as the CS–. There were no significant differences in the amount of reflex facilitation exhibited by animals with lesions compared with control animals. Animals with lesions, however, failed to acquire conditioned responses after 10 days of training, whereas all control animals met acquisition criterion within 4 days. In the second experiment, reflex facilitation was shown to decrement in a stimulus-specific manner when nonreinforced presentations of an auditory stimulus were given. The discussion of results focuses on the relation between reflex facilitation and classical conditioning in terms of behavioral properties and underlying neural systems. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Involvement of the supramammillary nucleus in aversive conditioning.

Mechanisms for the retention and retrieval of conditioned taste aversions (CTAs) have yet to be fully defined. The authors explored relevant subcortical forebrain regions by tracking the expression of immediate early genes, c-fos and zif268. The supramammillary nucleus (SuM) was activated following both viscerally based CTA and somatically based inhibitory avoidance (IA). Excitotoxic lesions of the SuM before conditioning caused no disruption of acquisition but accelerated the extinction of both the CTA and IA. In contrast, lesions after CTA conditioning did not impair retention or retrieval. The present study indicates that the SuM is activated by memory-elicited discomfort during retrieval, suggesting that it plays a role in resisting the extinction of a long-term aversive memory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of central and basolateral amygdala lesions on conditioned taste aversion and latent inhibition.

[Correction Notice: An erratum for this article was reported in Vol 121(6) of Behavioral Neuroscience (see record 2007-18058-034). Figure 4 on p. 96 (Results and Discussion, Experiment 2: Behavioral section) was incorrect. The correct figure is provided in the erratum.] The present study examined the effects of neurotoxic lesions of the central nucleus (CNA) and basolateral complex (BLA) of the amygdala on conditioned taste aversion (CTA) in a latent inhibition design. In Experiment 1, lesions of the CNA were found to have no affect on CTA acquisition regardless of whether the taste conditioned stimulus (CS) was novel or familiar. Lesions of the BLA, although having no influence on performance when the CS was familiar, retarded CTA acquisition when the CS was novel in Experiment 2. The pattern of results suggests that the CTA deficit in rats with BLA lesions may be a secondary consequence of a disruption of perceived stimulus novelty. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gustatory parabrachial lesions disrupt taste-guided quinine responsiveness in rats.

This study examined the effects of electrophysiologically placed electrolytic lesions in the gustatory zone of the parabrachial nuclei (PBN) on the rat's taste-guided unconditioned licking of quinine hydrochloride during repeated 10-sec trials. Concentration–response functions measured in water-deprived rats before and after surgery significantly shifted to the right as a result of the bilaterally placed lesions. These same rats were tested on their ability to acquire a lithium chloride (LiCl)-based conditioned taste aversion (CTA) to 0.1 M sucrose. Although the largest lesions severely affected performance in both tasks, there was only a modest correlation (r?=?–.447) between the extent of the lesion-induced shift in the quinine concentration–response curves and the degree of sucrose intake suppression after the first CTA conditioning trial. Thus, PBN lesions can disrupt performance on both tasks, but it appears that the neural processes governing unconditioned responsiveness to quinine may be to some extent dissociable from those subserving acquisition of a sucrose–LiCl-based CTA. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Lesions of the amygdala central nucleus abolish lipoprivic-enhanced responding during oil-predicting conditioned stimuli.

T. L. Davidson, A. M. Altizer, S. C. Benoit, E. K. Walls, and T. L. Powley (see record 1997-43076-013) reported that rats show facilitated responding to conditioned stimuli (CSs) that predict oil, after administration of the lipoprivic agent, Na-2-mercaptoacetate (MA). This facilitation was blocked by vagal deafferentation. The present article extends that investigation to another structure, the amygdala central nucleus (CN). The CN receives inputs from dorsal vagal nuclei, and neurotoxic lesions of this nucleus are reported to abolish feeding in response to lipoprivic challenges. In Experiment 1, rats with ibotenic acid (IBO) lesions of the CN failed to show enhanced appetitive responding during oil-predicting CSs after administration of MA. Experiment 2 used a conditioned taste-aversion procedure to establish that rats with IBO lesions of the CN were able to discriminate the tastes of sucrose and peanut oil and had intact CS–US representations. It is concluded that the amygdala CN is a necessary structure for the detection of lipoprivic challenges. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Learning- and cerebellum-dependent neuronal activity in the lateral pontine nucleus.

The effects of inactivation of cerebellar deep nuclei and the lateral pontine nucleus on classical eyeblink conditioning with tone or lateral reticular nucleus (LRN) stimulation as conditioned stimuli (CSs) were examined. Inactivation of cerebellar deep nuclei abolished eyeblink conditioned responses (CRs) when the CS was either a tone or LRN stimulation. Inactivation of the lateral pontine nucleus prevented only the acquisition and retention of tone-evoked eyeblink CRs. Multiple-unit recording demonstrated that when LRN stimulation was used as the CS, inactivation of the interpositus nucleus abolished learning-related neuronal activity in the lateral pontine nucleus, whereas inactivation of pontine nucleus had little effect on similar activity in the interpositus nucleus. Thus, the learning-induced neuronal activity in the lateral pontine nucleus was most likely driven by the cerebellar interpositus nucleus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of selective excitotoxic lesions of the nucleus accumbens core, anterior cingulate cortex, and central nucleus of the amygdala on autoshaping performance in rats.

The nucleus accumbens core (AcbC), anterior cingulate cortex (ACC), and central nucleus of the amygdala (CeA) are required for normal acquisition of tasks based on stimulus-reward associations. However, it is not known whether they are involved purely in the learning process or are required for behavioral expression of a learned response. Rats were trained preoperatively on a Pavlovian autoshaping task in which pairing a visual conditioned stimulus (CS+) with food causes subjects to approach the CS+ while not approaching an impaired stimulus (CS-). Subjects then received lesions of the AcbC, ACC, or CeA before being retested. AcbC lesions severely impaired performance; lesioned subjects approached the CS + significantly less often than controls, failing to discriminate between the CS + and CS-. ACC lesions also impaired performance but did not abolish discrimination entirely. CeA lesions had no effect on performance. Thus, the CeA is required for learning, but not expression, of a conditioned approach response, implying that it makes a specific contribution to the learning of stimulus-reward associations. (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)     

Dissociable effects of cingulate and medial frontal cortex lesions on stimulus-reward learning using a novel Pavlovian autoshaping procedure for the rat: Implications for the neurobiology of emotion.

The effects of quinolinic acid-induced lesions of the anterior cingulate, posterior cingulate, and medial frontal cortices on stimulus-reward learning were investigated with a novel Pavlovian autoshaping procedure in an apparatus allowing for the automated presentation of computer-graphic stimuli to rats (T. J. Bussey, J. L. Muir, & T. W. Robbins, 1994). White vertical rectangles were presented on the left or the right of a computer screen. One of these conditioned stimuli (the CS+) was always followed by the presentation of a sucrose pellet; the other, the CS–, was never followed by reward. With training, rats came to approach the CS+ more often than the CS–. Anterior cingulate cortex-lesioned rats failed to demonstrate normal discriminated approach, making significantly more approaches to the CS– than did sham-operated controls. Medial frontal cortex-lesioned rats acquired the task normally but had longer overall approach latencies. Posterior cingulate cortex lesions did not affect acquisition. (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)     

Disturbances of neophobia and taste-aversion learning after bilateral kainate microlesions in the rat pallidum.

These experiments aimed to elucidate feeding-associated behavioral roles of globus pallidus (GP) neurons in gustatory functions: The effects of bilateral microiontophoretic kainate (KA) lesions of the ventromedial pallidal (vmGP) region on neophobia and conditioned taste aversion (CTA) were studied. Lesioned rats displayed strong and persistent neophobia to a mild citric acid solution. Neuron-specific damage to the vmGP also prevented rats from proper acquisition of CTA. Rats that previously showed normal neophobia and successfully learned CTA demonstrated difficulties in CTA retention after GP lesions. KA-lesioned rats, in addition, exhibited deficits in orientation reactions but did not have aphagia, adipsia, or motor disturbances seen after larger pallidal lesions. These findings suggest that neurons of the GP are significant in acquisition, memory storage, and retrieval mechanisms of feeding-associated taste information. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Importance of trials versus accumulating time across trials in partially reinforced appetitive conditioning.

Four experiments with rats examined partial reinforcement in appetitive conditioning. In Experiment 1, adding nonreinforced trials to a continuous reinforcement schedule slowed acquisition, whereas deleting reinforcers did not. Trial massing suppressed performance and learning. In Experiment 2, conditioning with a short conditioned stimulus (CS) was rapid, and partial reinforcement with a short CS was as effective as continuous reinforcement with equal accumulated time in the CS. In Experiment 3, conditioning was nevertheless influenced by the probability of reinforcement. In Experiments 3 and 4, conditioning was especially disrupted when nonreinforced trials preceded reinforced trials closely in time. The results underscore the importance of temporal variables in conditioning but are more consistent with trial-based accounts than time-accumulation accounts of conditioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)