Neural Ensemble Coding of Satiety States

Araújo, Ivan E. de; Gutiérrez, Ranier; Oliveira‐Maia, Albino J.; Pereira, Antônio; Nicolelis, Miguel A. L.; Simon, Sidney A.

doi:10.1016/j.neuron.2006.07.009

Cited by 123 publications

(121 citation statements)

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“…Modulation of GC responses by internal states was recently reported at a single cell level (20). By the means of intrinsic imaging, we show that visceral modulations induce a large neuronal ensemble plasticity that signals a shift in tastant hedonic value associated to behavioral shift of the stimulus hedonic value.…”

Section: Discussionsupporting

confidence: 53%

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Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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Primary sensory cortices are remarkably organized in spatial maps according to specific sensory features of the stimuli. These cortical maps can undergo plastic rearrangements after changes in afferent (''bottom-up'') sensory inputs such as peripheral lesions or passive sensory experience. However, much less is known about the influence of ''top-down'' factors on cortical plasticity. Here, we studied the effect of a visceral malaise on taste representations in the gustatory cortex (GC). Using in vivo optical imaging, we showed that inducing conditioned taste aversion (CTA) to a sweet and pleasant stimulus induced plastic rearrangement of its cortical representation, becoming more similar to a bitter and unpleasant taste representation. Using a behavior task, we showed that changes in hedonic perception are directly related to the maps plasticity in the GC. Indeed imaging the animals after CTA extinction indicated that sweet and bitter representations were dissimilar. In conclusion, we showed that an internal state of malaise induces plastic reshaping in the GC associated to behavioral shift of the stimulus hedonic value. We propose that the GC not only encodes taste modality, intensity, and memory but extends its integrative properties to process also the stimulus hedonic value.chemical senses ͉ map plasticity ͉ taste coding

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Section: Discussionsupporting

confidence: 53%

“…We took advantage of the unique features of the central taste system where changes in internal body states, such as satiety (20) or visceral malaise (16,19) have a direct influence on primary GC neuronal responses.…”

Section: Discussionmentioning

confidence: 99%

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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“…That is, in all cases, the animals ingested tastants and water and for this reason we suggest that some of the tuning changes observed in all three protocols arise from evolving differences in the subjects' internals states over the course of each test session, in part due to processes involving feeding (sucrose, salt) and satiety. In this regard it has been shown that chemicals such as insulin [30,57], opiates [31], glucose [32,57] or glucagon [33] that are released throughout the feeding cycle may differentially affect taste responses throughout the gustatory axis.…”

Section: What Are the Possible Origins Of The Observed Changes In Chementioning

confidence: 99%

“…We found that despite differences in behavioral responses in the three protocols tested, we observed similar and extensive inter-sequence variability in chemosensory GC responses. We attribute these chemical tuning changes to differences in areas of the oral cavity that are subjected to the tastants as the animals ingest or reject the tastants, and to changes in tuning properties that occur as a consequence of more central processes resulting from changes in the state of the animal [22] and to compounds that are released upon ingestion that can affect gustatory responses [30][31][32][33]57]. The experiment-wide probability of eliciting appetitive responses in each trial (solid lines) was plotted for both PRE and POST sequences (grey and black, respectively).…”

Section: What Are the Possible Origins Of The Observed Changes In Chementioning

confidence: 99%

Behavioral and neural responses to gustatory stimuli delivered non-contingently through intra-oral cannulas

Soares

Stapleton

Rodríguez

et al. 2007

Physiology & Behavior

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The act of eating requires a decision by an animal to place food in its mouth. The reasons to eat are varied and include hunger as well as the food's expected reward value. Previous studies of tastant processing in the rat primary gustatory cortex (GC) have used either anesthetized or awake behaving preparations that yield somewhat different results. Here we have developed a new preparation in which we explore the influences of intra-oral and non-contingent tastant delivery on rats' behavior and on their GC neural responses. We recorded single unit activity in the rat GC during two sequences of tastant deliveries, PRE and POST, which were separated by a waiting period. Six tastants ranging in hedonic value from sucrose to quinine were delivered in the first two protocols called 4TW and L-S. In the third one, the App L-S protocol, only hedonically positive tastants were used. In the 4TW protocol, tastants were delivered in blocks whereas in the two L-S protocols tastants were randomly interleaved.In the 4TW and L-S protocols the probability of ingesting tastants in the PRE sequence decreased exponentially with the trial number. Moreover, in both protocols this decrease was greater in the POST than in the PRE sequence likely because the subjects learned that unpleasant tastants were to be delivered. In the App L-S protocol the decrease in ingestion was markedly slower than in the other protocols, thus supporting the hypothesis that the decrease in appetitive behavior arises from the noncontingent intra-oral delivery of negatively hedonic tastants like quinine.Although neuronal responses in the three protocols displayed similar variability levels, significant differences existed between the protocols in the way the variability was partitioned between chemosensory and non-chemosensory neurons. While in the 4TW and L-S protocols the former population displayed more changes than the latter, in the App L-S protocol variability was homogeneously distributed between the two populations. We posit that these tuning changes arise,

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“…22 De Araujo and Simon have found that the multimodal sensory features of foods in the mouth are encoded by neuronal ensembles within the insula, and that the activity within these ensembles is hunger/satiety dependent. 32 They have also recently shown that transgenic mice that lack the trpm5 taste receptor, and are hence unable to sense sweet taste, can still learn to prefer a sucrose-containing solution because of the post-ingestive effects of sucrose. 33 Insular lesions disrupt this phenomenon.…”

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confidence: 99%

The neurobiology of appetite: hunger as addiction

Dagher

2009

Int J Obes

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Obesity is now being recognized as a neurobehavioral disorder. Although the view of appetite as an addiction to food is controversial, there are useful lessons to be learned from the neuroscience of addiction for understanding obesity. The speakers in this symposium all addressed different aspects of the neurobiology of feeding and obesity. In this overview and the associated reviews, the behavioral, genetic and neural factors that promote over-eating in animals and humans are discussed. International Journal of Obesity (2009) 33, S30-S33; doi:10.1038/ijo.2009 Keywords: dopamine; striatum; amygdala; insula; orbitofrontal cortexIn 1949, Donald Hebb 1 suggested that hunger could be viewed as an addiction, an idea he attributes to the physiologist AJ Carlson in 1916. Hebb proposed that hunger was a learned behavior, in which eating is initially reinforcing because it reverses an unpleasant bodily signal (change in nutrient levels in blood, hunger hormones and stomach contractions). With time the behavior becomes organized and food cues, such as the sight and smell of food, develop the ability to induce craving, approach and consumption, much as drug-associated cues do. Later, Roy Wise 2 showed that dopamine receptor blockade with a neuroleptic attenuated the reinforcing effects food, as it did for stimulant drugs and electrical brain stimulation, leading him to conclude that addictive drugs act on brain circuitry that controls feeding. The notion of hunger as addiction has been criticized in the media, 3 and for seemingly contradictory reasons: referring to the obese as 'addicts' either unfairly stigmatizes them or undeservedly exculpates them. (Note that even the view of drug addiction as a brain disease is still rejected by some.) On the other hand, some governments are sold on the analogy, having mandated cigarette-style health warnings on food advertisements. 4 It must be admitted, however, that opponents of the addiction model are correct in pointing out the paradox of ascribing energy intake, the most basic survival behavior, to aberrant function of neurobiological systems. Nonetheless, evidence of parallels between addiction and feeding behavior continues to accumulate at the neurobiological and behavioral levels (for example, see Grigson 5 for a review). Perhaps a less controversial position could be that we have much to learn about obesity from the neuroscience of addiction. 6 Neural systems implicated in feeding are depicted in Figure 1. According to this model four heavily interconnected structures (shown in gray in the figure), the amygdala/hippocampus, insula, orbitofrontal cortex (OFC), and striatum are the central elements in the control of appetitive behavior. Although a specific role for each node within the network can be differentiated, as a group these structures are involved in (1) learning about (food) rewards; (2) allocating attention and effort towards (food) rewards; (3) setting the incentive value of stimuli in the environment; (4) integrating homeostatic information about energy stores an...

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Neural Ensemble Coding of Satiety States

Cited by 123 publications

References 39 publications

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Behavioral and neural responses to gustatory stimuli delivered non-contingently through intra-oral cannulas

The neurobiology of appetite: hunger as addiction

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