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K C Berridge

Publications and source records attributed to K C Berridge.

54 records · Page 3Linked to original sources

Taste reactivity analysis of 6-hydroxydopamine-induced aphagia: implications for arousal and anhedonia hypotheses of dopamine function.

The deficits in feeding and drinking that result from 6-hydroxydopamine (6-OHDA) lesions of the mesostriatal dopamine system are often explained using either sensorimotor arousal or anhedonia hypotheses. Sensorimotor arousal hypotheses posit that dopamine systems facilitate the capacity of sensory stimuli to activate any motor output. The anhedonia hypothesis suggests that dopamine systems amplify the hedonic impact of positive reinforcers. Natural palatability-dependent ingestive and aversive actions, which are emitted by rats to tastes, provide a sensitive test that can discriminate between these hypotheses: A reduction of sensorimotor arousal should diminish the ability of tastes to elicit any actions, whereas anhedonia should shift the balance between positive and aversive actions. To directly compare these two hypotheses, taste reactivity was examined in rats made aphagic by intranigral 6-OHDA injections. The results did not support either of these predictions: Taste reactivity was essentially unchanged. The persistence of normal taste reactivity argues against both an anhedonia and a global sensorimotor arousal interpretation and provides further evidence that the capacity for hedonics can be neurologically dissociated from motivated appetitive behavior. An incentive attribution hypothesis that can account for the results is discussed, along with its implications for a wide range of phenomena associated with dopamine depletion.

Animals↗

Palatability shift of a salt-associated incentive during sodium depletion.

Previous studies of natural palatability-sensitive reactions, elicited from rats by tastes, have indicated that the taste of concentrated NaCl becomes more palatable during states of body sodium depletion. A training procedure based upon "sensory preconditioning" or "irrelevant incentive" designs was used here to establish gustatory conditioned labels (quinine or citric acid) for either NaCl or fructose while rats were in a normal physiological state. Experiment 1 replicated demonstrations by others that gustatory conditioned labels for salt can attract and act as independent incentives during the salt appetite induced by sodium depletion. Experiment 2 used the taste reactivity measure to show that the enhanced palatability of the taste of NaCl transfers to produce enhanced palatability of the taste of the isolated conditioned label for salt in a state-dependent fashion. These results offer further support for the proposition that conditioned incentives not only predict hedonic events to follow, but themselves become attributed with the hedonic properties of their reinforcers.

Animals↗

Brainstem systems mediate the enhancement of palatability by chlordiazepoxide.

Previous studies have indicated that the benzodiazepine receptor complex is involved in enhancing taste palatability after chlordiazepoxide (CDP) administration. Positive, palatability-dependent ingestive reactions elicited by orally infused tastes are facilitated in rats by CDP (10 mg/kg), and this effect is reversible by benzodiazepine antagonists. In contrast, the rats' more neutral or aversive reactions are not facilitated by CDP. Because benzodiazepine receptors exist in highest density in the forebrain, it has seemed plausible to posit forebrain structures as the locus of CDP action. However, benzodiazepine receptors do exist in the caudal brainstem (albeit in lesser density), and the isolated decerebrate brainstem has been demonstrated to possess considerable taste processing and response capacity. The present study examined the effects of CDP on taste reactivity in chronic mesencephalic decerebrate rats. The results show that CDP can act on the subdiencephalic brainstem to enhance positive ingestive reactions even in the absence of communications with the forebrain. This indicates that both the relevant benzodiazepine receptors and the minimal neural circuit needed to modulate taste reactivity exist within or below the mesencephalon.

Animals↗

A triggered hyperkinesia induced in rats by lesions of the corpus striatum.

The role of the corpus striatum (caudate, putamen, and globus pallidus) in movement control has been suggested to involve the modulation of sensory traffic to downstream motor mechanisms. We report that kainic acid lesions of the posterior corpus striatum, which preferentially spare fibers of passage while destroying striatopallidal neurons, produce a stimulus-sensitive movement pattern in rats that has a highly specific sensory trigger. The triggered choreic movement pattern is not a motor pathology per se, nor a response to diffuse states of arousal or stress, but rather is activated specifically in response to oral sensory stimulation. This sensory-specific hyperkinesia may be relevant to certain human sensorimotor pathologies.

Animals↗

The direct enhancement of positive palatability by chlordiazepoxide is antagonized by Ro 15-1788 and CGS 8216.

In a previous study, it was found that positive, palatability-dependent consummatory reactions in rats to intraorally infused tastes were facilitated by chlordiazepoxide (10 mg/kg). In contrast, the rats' more neutral or aversive reactions to these tastes were not facilitated by chlordiazepoxide. This suggested that chlordiazepoxide might selectively enhance the positive palatability of tastes. This effect was replicated in the present experiment, and in addition, the benzodiazepine antagonists Ro 15-1788 and CGS 8216 were found to counteract the enhancement of positive ingestive reactions produced by chlordiazepoxide. These antagonist effects generally suggest that the benzodiazepine receptor complex may be involved in making tastes more palatable after chlordiazepoxide administration.

Animals↗

Natural syntax rules control action sequence of rats.

Knowledge of the principles by which behavioral sequences are generated is essential to progress in our understanding of neural mechanisms. We describe here a set of natural principles or syntax rules that organize the components of grooming and feeding. The behavioral stream of facial grooming or of taste-elicited ingestive/aversive consummatory actions of rats can be viewed as a long series of individual movements linked together to form functional sequences. In order to ascertain the syntax rules that determine how these actions are linked together, many thousands of spontaneous grooming and elicited ingestive/aversive actions were videotaped and scored with a microcomputer. Techniques of information analysis of sequential stereotypy, tabulation of the sequential transitions between single actions and between action groups, and visual inspection for linear action chains, were employed to expose underlying rules of behavioral sequencing. These analyses revealed two global patterns: action perserveration and transitional reciprocation between sequential pairs and triplets, which together account for approximately 75% of all sequential transitions during grooming and ingestion/aversion. The pattern of transitional reciprocation could be divided further into patterns of alternation between individual actions on the one hand, and between perseverating bouts of actions on the other. Global syntax rules applied equally to actions emitted during grooming or during taste-elicited ingestion/aversion. In addition, a specific rule of linear chaining was found to apply only to facial grooming. These natural rules of action syntax provide insight into the sequential structure of behavior, and lend themselves well to analyses of neural mechanisms.

Animals↗

Deafferentation does not disrupt natural rules of action syntax.

Natural rules of action syntax control the sequential order of grooming and ingestive/aversive actions emitted by rats. Grooming and ingestive actions share a common feature in that all are performed with or directed towards the mouth, tongue, and face. This study examined the role of orofacial somatosensory cues and feedback in the generation of natural action syntax. Bilateral deafferentation of the mandibular and maxillary branches of the trigeminal nerve was used to eliminate tactile sensation from the rostral face and mouth while preserving motor function. Neither the overall degree of sequential stereotypy (H) of grooming or ingestive sequences, nor the generation of particular natural sequencing rules were affected by trigeminal deafferentation. These natural rules appear to be specified by the brain without need of somatosensory feedback.

Afferent Pathways↗

Chlordiazepoxide directly enhances positive ingestive reactions in rats.

Benzodiazepines such as chlordiazepoxide (CDP) promote feeding in a number of species. This effect has been interpreted generally to be an indirect consequence of benzodiazepine anti-anxiety action, although some have questioned whether it might not reflect instead a direct action upon the reinforcing properties of foods. The present study employed a behavioral measure that can discriminate between these possibilities: palatability-dependent consummatory actions elicited in rats by tastes. The results suggest that chlordiazepoxide enhances the positive palatability of tastes selectively while having little or no effect on aversive palatability. The net effect is to make tastes more reinforcing following CDP administration.

Animals↗

Pre- and postabsorptive insulin secretion in chronic decerebrate rats.

Basal, taste-stimulated (preabsorptive), and postabsorptive insulin secretion and plasma glucose responses were studied in chronic decerebrate rats and their pair-fed neurologically intact controls. In experiment 1, preabsorptive insulin responses (PIR) elicited by oral infusions of glucose solution was measured in chronic decerebrate rats. Oral glucose was ingested and led to a significant short-latency elevation in plasma insulin levels. Plasma glucose levels remained constant during this time. These data show that caudal brain stem mechanisms, in isolation of the forebrain, are sufficient for the neurally mediated PIR elicited by oral glucose stimulation. In experiment 2, effects of decerebration on postabsorptive insulin secretion were measured. During the 3 h immediately after transection there was no effect of decerebration on peripheral plasma insulin or glucose levels. Thereafter, however, basal plasma insulin levels of decerebrate rats were at least twice that of control rats. Plasma glucose levels of both groups remained identical despite the hyperinsulinemia in decerebrate rats. Atropine treatment decreased, and phentolamine administration elicited a greater absolute and percent change increase in insulin levels of decerebrate rats. These data indicate that altered autonomic tone contributes to maintaining the basal hyperinsulinemia in the decerebrate rat. In response to intragastric meals and glucose and intravenous glucose administration, insulin secretion was greater in decerebrate than in control rats. Percent change in insulin levels from base line was similar in both groups after intragastric meals and intravenous glucose. In response to intragastric glucose, however, percent increase in insulin levels was greater in decerebrate rats. Decerebrate rats demonstrated mild glucose intolerance after intragastric and intravenous treatments. These results are contrasted with the known effects of ventromedial hypothalamic lesions on insulin secretion and glucose homeostasis.

Animals↗

Control of fluid palatability by exteroceptive Pavlovian signals.

Tastes elicit a set of palatability-dependent orofacial and somatic responses in rats. We investigated whether discrete auditory conditioned stimuli that signal the availability or onset of unconditioned taste stimuli (sucrose, quinine) can control orofacial responses in the absence of those unconditioned stimuli. In Experiment 1, one auditory stimulus (CS+) was paired with the delivery of a sucrose solution to the magazine floor, and another auditory stimulus (CS-) was never followed by sucrose. Following conditioning, oral infusions of water that were preceded by the CS+ were found to elicit more ingestive (sucrose-typical) orofacial responses than did water alone or water preceded by the CS-. In Experiment 2, the conditioned ingestive reactions to a signal for sucrose observed in Experiment 1 again occurred, and conditioned aversive (quinine-typical) orofacial responses occurred in response to water infusions preceded by a former signal for quinine. These data suggest that perceived palatability may be influenced by Pavlovian associations involving exteroceptive conditioned stimuli. Further, they illustrate the importance of supporting stimuli in modulating the effects of Pavlovian associations upon behavior.

Animals↗

Contextual control of trigeminal sensorimotor function.

Simple actions, such as rhythmic tongue protrusions, forelimb facial strokes, and forelimb flails, are emitted by rats both during taste-elicited ingestion/aversion and during postprandial grooming. This study combined peripheral trigeminal deafferentation with a computer-assisted video analysis of action form to examine the use of cutaneous feedback from the face in action production. Changes in action form after deafferentation were found to be context-dependent: Deformations characterized rhythmic tongue protrusions when emitted in ingestive but not in grooming contexts. The opposite was true for alterations in forelimb action. Further, postprandial grooming as a whole was found to comprise distinct sequentially defined phases. Actions occurring in one highly stereotyped sequence phase were protected from deafferentation effects, although the same actions occurring outside of this phase were not. The results suggest that behavioral context (e.g., grooming versus ingestive set, sequence phase) can shift the integration of sensory guided and endogenous mechanisms that pattern simple actions.

Animals↗

Trigeminal-taste interaction in palatability processing.

Peripheral transection of the sensory branches of the trigeminal nerve in rats unbalanced palatability, selectively reducing the ingestive actions elicited by preferred tastes but leaving unchanged the aversive actions elicited by unpreferred tastes. The reduction in the number of positive ingestive actions occurred even though the capacity to emit these actions remained unimpaired. These findings show that there is an interaction between somatosensation and gustation in the processing of palatability.

Animals↗

Rats learn to like the taste of morphine.

When rats are forced to drink a morphine solution as their only source of fluid, they eventually reverse their initial preference and drink more morphine than water in a two-bottle preference test. The cause of this shift in preference was examined with the taste reactivity test which involves the analysis of fixed action patterns elicited by taste solutions infused into rats' mouths. Three morphine concentrations and two levels of motivation were studied. A greater percentage of ingestive taste reactivity responses occurred to the oral morphine infusion in morphine-raised rats than in water-raised rats. These data argue against the idea that enhanced morphine ingestion is caused by anticipation of positive consequences. Instead, they support the idea that rats come to "like" the flavor of the morphine solution; in other words, the palatability evaluation of the morphine changes, possibly through an association between the flavor and the hedonically positive effects of the morphine.

Animals↗

Isohedonic tastes support a two-dimensional hypothesis of palatability.

The hypothesis that tastes activate two systems of palatability processing was tested by examining the ingestive and aversive fixed-action patterns (FAPs) elicited by equally preferred tastes. Berridge and Grill (1983) reported that the probability of occurrence of aversive FAPs could be increased without producing a reciprocal reduction in the probability of ingestive responses. This independence of ingestion and aversion was confirmed, and it was shown that the effect extends to measures of the actual quantity, as well as the probability, of the FAPs. It was further shown that ingestive and aversive FAPs could be increased together by simultaneously increasing the sucrose and quinine concentration of a taste. Equal preference between tastes may therefore need not imply identical hedonic evaluations, but rather simply an equivalent balance between ingestive and aversive systems. These data provide support for a two-dimensional hypothesis of palatability processing.

Animals↗

Sodium depletion enhances salt palatability in rats.

Sterotyped fixed action patterns (FAPs) are elicited in rats by oral infusions of taste solutions. These taste-elicited FAPs can be classified as either ingestive or aversive. They reflect the palatability of the taste and can be modified by learning and by the physiological state of the animal. These studies demonstrated that when the physiological state of the rat is altered by sodium depletion, the pattern of FAPs elicited by oral infusions of 0.5 M NaCl shifts from a mixture of ingestive and aversive components (while sodium replete) to exclusively ingestive ones (while sodium deplete). This shift in taste reactivity occurred the first time the rats were made sodium deplete. A similar shift was not observed to accompany infusions of 0.01 M HCl, a taste solution that also elicited mixed ingestive and aversive FAPs. This result suggests that the shift in response to NaCl is not due to a general change in ingestive bias or to a general taste deficit. On the basis of the change in FAPs, it is concluded that the palatability of highly concentrated salt solutions increases in sodium-deplete rats. Such a shift in salt palatability may be instrumental in directing the appetitive behavior of the animal.

Animals↗

Oral glucose is the prime elicitor of preabsorptive insulin secretion.

Seven sugars, two sugar alcohols, and a nonnutritive sweetener were orally administered to naive rats with and without gastric drainage fistulas. Although all taste solutions were ingested, only glucose evoked a statistically significant elevation of insulin levels. This rise was independent of a rise in glycemia. The preeminence of oral glucose as an elicitor of preabsorptive insulin secretion is especially striking, considering that glucose is neither the most intense (as measured electrophysiologically) nor the most palatable (as measured by behavioral preference tests) taste stimulus tested. These results suggest the existence of a gustatory and/or gastrointestinal chemoreceptor that is most responsive to glucose.

Administration, Oral↗

Alternating ingestive and aversive consummatory responses suggest a two-dimensional analysis of palatability in rats.

The hedonic response to a taste is typically regarded to be the product of a central integration of gustatory afferent information, which ends in a single decision about the nature and intensity of the response to be given. This hedonic response is often characterized as a point lying along a single dimension of palatability, stretching from strongly positive to strongly negative. The present analysis of species-specific consummatory responses suggests that the final response is not made on the basis of a single central analysis of taste information but rather is the result of a competition between two separate systems that are activated by tastes. A single oral infusion of a taste solution may elicit rapid alternation between ingestive and aversive consummatory responses. Such alternation is better interpreted as due to a simultaneous activation of two palatability dimensions than as a reflection of neutral palatability. When increases in the magnitude of aversive responses are produced by taste mixtures, there is not necessarily a reciprocal decrease in ingestive responses. This asymmetry supports the hypothesis of independent palatability dimensions.

Animals↗

The neural basis of drug craving: an incentive-sensitization theory of addiction.

This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.

Adaptation, Physiological↗