Taste Memory Research Articles

Souvenirs gastronômicos na percepção do turista: o caso do queijo minas artesanal do serro

Este estudo teve como objetivo analisar o queijo minas artesanal como souvenir gastronômico, sob a percepção do turista. A justificativa do tema refere-se ao fato de que os souvenirs carregam diversos significados para o turista e também servem à divulgação do destino. Os souvenirs gastronômicos permitem uma memória gustativa e um compartilhamento da vivência diferenciado. A escolha do queijo minas artesanal do Serro como souvenir gastronômico deu-se pelo fato desse produto ser componente da cultura do estado de Minas Gerais (Brasil) e detém registro de patrimônio imaterial e de indicação geográfica. A abordagem da pesquisa foi quanti-qualitativa e optou-se pela metodologia de questionário aplicado online a pessoas que viajaram à região produtora. Obteve-se 129 respostas, das quais 103 consideradas válidas. Também foi realizada observação direta em locais de comercialização durante pesquisa de campo. Sua originalidade decorre dos escassos trabalhos sobre souvenirs gastronômicos e mais especificamente sobre produtos com registro de indicação geográfica como souvenirs dessa categoria. Os resultados apontam fragilidades na comercialização do produto como souvenir gastronômico. Entretanto, os respondentes demonstraram atitude favorável a questões relacionadas a identidade diferenciadora, identificação da origem, embalagem adequada e transporte facilitado. Os achados são congruentes com a proposta de Horodyski et al. (2014).

Molecular mechanisms involved in taste learning and memory

Taste learning, and particularly conditioned taste aversion (CTA), is an adaptive learning involving complex brain mechanisms and molecular pathways. Taste learning and CTA are critical behaviors for survival, and the knowledge of the molecular bases involved in the acquisition, retention and extinction of CTA can help to understand the brain mechanisms of normal and altered taste learning. The aim of this review is to describe recent findings on the molecular mechanisms of taste learning, from the genetic, receptors, and intracellular and extracellular signaling biological levels. We can conclude that some molecular pathways and processes for the acquisition of taste learning and the formation of taste memories are well identified. However, new molecular, neurobiological and behavioral studies are needed to thoroughly elucidate the complexity of the taste system and the neural mechanisms of CTA.

P.1.g.075 - Psilocybin-induced psychosis in humans and in rats − translational quantitative EEG study

The medial prefrontal cortex (mPFC) has reciprocal projections with many cerebral structures that are crucial in the control of food ingestion behavior and reward processing; Thus the mPFC has an important function in taste memory recognition. Previous results indicate that long-term consumption of sugar produces changes in appetitive re-learning and suggest that this could trigger an escalating consumption due to the inability to learn new negative consequences related to the same taste. Further evidence suggests that general identity reward value could be encoded in the mPFC. Therefore, the purpose of this study was to evaluate in rats whether after 21 days of sugar consumption the increase in sweet taste preference and latent inhibition of conditioned taste aversion (CTA) were affected differentially by pharmacological activation or blockage of dopaminergic and β-adrenergic receptors, in the mPFC, during CTA acquisition. Results showed that after long-term sugar exposure, mPFC activation of β-adrenergic receptors with clenbuterol delayed aversive memory extinction, but the blockade with propranolol or activation of dopaminergic receptors with apomorphine increased CTA latent inhibition and accelerated aversive memory extinction only after acute sugar exposure. Only dopaminergic blockade with haloperidol prevented sweet taste preference expression after long-term sugar consumption, increased CTA latent inhibition and accelerated extinction after acute sugar exposure. Taken together, the present data provide evidence that catecholaminergic receptors in the mPFC after prolonged sugar consumption underwent functional changes related to re-learning and new aversive taste learning.

Brain Potentials Highlight Stronger Implicit Food Memory for Taste than Health and Context Associations.

Increasingly consumption of healthy foods is advised to improve population health. Reasons people give for choosing one food over another suggest that non-sensory features like health aspects are appreciated as of lower importance than taste. However, many food choices are made in the absence of the actual perception of a food’s sensory properties, and therefore highly rely on previous experiences of similar consumptions stored in memory. In this study we assessed the differential strength of food associations implicitly stored in memory, using an associative priming paradigm. Participants (N = 30) were exposed to a forced-choice picture-categorization task, in which the food or non-food target images were primed with either non-sensory or sensory related words. We observed a smaller N400 amplitude at the parietal electrodes when categorizing food as compared to non-food images. While this effect was enhanced by the presentation of a food-related word prime during food trials, the primes had no effect in the non-food trials. More specifically, we found that sensory associations are stronger implicitly represented in memory as compared to non-sensory associations. Thus, this study highlights the neuronal mechanisms underlying previous observations that sensory associations are important features of food memory, and therefore a primary motive in food choice.

The differential role of cortical protein synthesis in taste memory formation and persistence.

The current dogma suggests that the formation of long-term memory (LTM) is dependent on protein synthesis but persistence of the memory trace is not. However, many of the studies examining the effect of protein synthesis inhibitors (PSIs) on LTM persistence were performed in the hippocampus, which is known to have a time-dependent role in memory storage, rather than the cortex, which is considered to be the main structure to store long-term memories. Here we studied the effect of PSIs on LTM formation and persistence in male Wistar Hola (n⩾5) rats by infusing the protein synthesis inhibitor, anisomycin (100 μg, 1 μl), into the gustatory cortex (GC) during LTM formation and persistence in conditioned taste aversion (CTA). We found that local anisomycin infusion to the GC before memory acquisition impaired LTM formation (P=8.9E−5), but had no effect on LTM persistence when infused 3 days post acquisition (P=0.94). However, when we extended the time interval between treatment with anisomycin and testing from 3 days to 14 days, LTM persistence was enhanced (P=0.01). The enhancement was on the background of stable and non-declining memory, and was not recapitulated by another amnesic agent, APV (10 μg, 1 μl), an N-methyl-D-aspartate receptor antagonist (P=0.54). In conclusion, CTA LTM remains sensitive to the action of PSIs in the GC even 3 days following memory acquisition. This sensitivity is differentially expressed between the formation and persistence of LTM, suggesting that increased cortical protein synthesis promotes LTM formation, whereas decreased protein synthesis promotes LTM persistence.

Rich man's food, poor man's food in "The mansions and the shanties": A narrative review of the book written by Gilberto Freyre

This article aims to perform a narrative review of the book "The mansions and the shanties" written by the Brazilian sociologist Gilberto Freyre, published for the first time in 1936. The study analyzed Gilberto Freyre's contribution to the process of interpreting the formation and modification of the eating habits and patterns of the Brazilian society. The analysis is limited to a review, from a dietician's perspective, of text clippings where Freyre seeks to reconstruct and interpret the process of formation and modification of eating habits and patterns in the context of a patriarchal society. The text will try to answer the questions: what, how much, how, when, where, and with whom were the dwellers of mansions and shanties eating? Comparison of the eating habits of the rural patriarchal society with those of the emerging urban patriarchal society has shown Freyre's clear trend of aversion to the "Europeanization" of eating habits and his affection for traditional culinary values. The new eating habits of mansions and plantation houses were portrayed with disdain, denoting an author who remained stuck to the culinary traditions of a rural patriarchal society, to taste memories, especially of the sweets, cakes, and desserts created, adapted, and savored in Pernambuco state sugar mills.

Sweet and bitter taste perception in anorexia nervosa: A functional MRI study

IntroductionTaste perception is a complex phenomenon modulated by different factors, such as taste receptors and memory brain circuits. The palatability of the food, that activates the central reward pathways, also plays an important role in taste perception. It means that taste is able to influence the choice of food and then eating behaviour.ObjectivesIt is well known that people with anorexia nervosa (AN) have a lower sensitivity to reward stimuli and recent studies suggested that altered function of taste neural circuitry may contribute to restricted eating in AN.AimsThe aim of this study was to evaluate, in patients suffering from AN, the activation of brain areas involved in taste perception and in central reward mechanisms to both pleasant and aversive taste stimuli and to correlate gustatory neurocircuitry activity with eating behaviours, temperament measures and/or sensitivity to reward and to punishment.MethodsFifteen underweight female AN patients and sixteen normal-weight healthy women underwent a functional MRI to measure brain areas activation to repeated stimuli of a pleasant taste (sucrose solution), alternated with an aversive taste (bitter solution), and water taste.ResultsCompared to healthy controls, patients with AN showed a significantly reduced activation of left insula and left dorsolateral prefrontal cortex to sweet stimulus and reduced activation of right parietal cortex to bitter stimulus.ConclusionsThese results, if confirmed in future studies, may improve our knowledge about the pathophysiological mechanisms of AN.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Opposing Roles of Cholinergic and GABAergic Activity in the Insular Cortex and Nucleus Basalis Magnocellularis during Novel Recognition and Familiar Taste Memory Retrieval.

During learning and recall, several brain structures act together. This work demonstrates interactions between cortical cholinergic and GABAergic systems during taste learning and memory retrieval. We found that the neuroactivity pattern during novel taste exposure is opposite that which occurs during familiar taste recognition. GABAA receptors must be inactive during novel tasting to enable new memory formation, but must be active and inhibiting acetylcholine release in the cortex to allow memory retrieval. These findings indicate that GABA inhibition modulates cholinergic transmission and that cholinergic-GABAergic system interactions are important during the transition from novel to familiar memory.

Fluid consumption and taste novelty determines transcription temporal dynamics in the gustatory cortex.

BackgroundNovel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the gustatory cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.ResultsHere, we report that transcription in the GC is necessary for taste learning in rats, and that drinking and its consequences, as well as the novel taste experience, affect transcription in the GC during taste memory consolidation. We show differential effects of learning on temporal dynamics in set of genes in the GC, including Arc/Arg3.1, known to regulate the homeostasis of excitatory synapses.ConclusionsWe demonstrate that in taste learning, transcription programs were activated following the physiological responses (i.e., fluid consumption following a water restriction regime, reward, arousal of the animal, etc.) and the specific information about a given taste (i.e., taste novelty). Moreover, the cortical differential prolonged kinetics of mRNA following novel versus familiar taste learning may represent additional novelty related molecular response, where not only the total amount, but also the temporal dynamics of transcription is modulated by sensory experience of novel information.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-016-0188-4) contains supplementary material, which is available to authorized users.

NMDAR-dependent proteasome activity in the gustatory cortex is necessary for conditioned taste aversion

Taste information is processed in different brain structures in the mammalian brain, including the gustatory cortex (GC), which resides within the insular cortex. N-methyl-d-aspartate receptor (NMDAR) activity in the GC is necessary for the acquisition of conditioned taste aversion (CTA) but not positive novel taste learning. Previous studies have shown that taste memory consolidation requires intact protein synthesis in the GC. In addition, the direct involvement of translation initiation and elongation factors was documented in the GC during taste learning. However, protein expression is defined by protein synthesis, degradation, and localization. Protein degradation is critical for the consolidation and reconsolidation of other forms of learning, such as fear learning and addiction behavior, but its role in cortical-dependent learning is not clear. Here, we show for the first time that proteasome activity is specifically increased in the GC 4h following experiencing of a novel taste. This increase in proteasome activity was abolished by local administration to the GC of the NMDA antagonist, APV, as well as a CaMKII inhibitor, at the time of acquisition. In addition, local application of lactacystin, a proteasome inhibitor, resulted in impaired CTA, but not novel taste learning. These results suggest that NMDAR-dependent proteasome activity in the GC participates in the association process between novel taste experience and negative visceral sensation.

Insights on consciousness from taste memory research

Taste research in rodents supports the relevance of memory in order to determine the content of consciousness by modifying both taste perception and later action. Associated with this issue is the fact that taste and visual modalities share anatomical circuits traditionally related to conscious memory. This challenges the view of taste memory as a type of non-declarative unconscious memory.

Increased N-Ethylmaleimide-Sensitive Factor Expression in Amygdala and Perirhinal Cortex during Habituation of Taste Neophobia.

Interactions between GluR2 and N-ethylmaleimide-sensitive factor (NSF) mediate AMPA receptors trafficking. This might be linked with molecular mechanisms related with memory formation. Previous research has shown basolateral amygdala (BLA) dependent activity changes in the perirhinal cortex (PRh) during the formation of taste memory. In the present experiments we investigate both the behavioral performance and the expression profile of NSF and GluR2 genes in several brain areas, including PRh, BLA, and hippocampus. Twenty-one naïve male Wistar rats were exposed to a saccharin solution (0.4%) during the first (novel), the second (Familiar I), and the sixth presentation (Familiar II). Total RNA was extracted and gene expression was measured by quantitative PCR (qPCR) using TaqMan gene expression assays. In addition the expression of the synaptic plasticity related immediate early genes, Homer 1 and Narp, was also assessed. We have found increased expression of NSF gene in BLA and PRh in Group Familiar I in comparison with Familiar II. No changes in the expression of GluR2, Homer 1, and Narp genes were found. The results suggest the relevance of a potential network in the temporal lobe for taste recognition memory and open new possibilities for understanding the molecular mechanisms mediating the impact of sensory experience on brain circuit function.

A Dopamine-Modulated Neural Circuit Regulating Aversive Taste Memory in Drosophila

Taste memories allow animals to modulate feeding behavior in accordance with past experience and avoid the consumption of potentially harmful food [1]. We have developed a single-fly taste memory assay to functionally interrogate the neural circuitry encoding taste memories [2]. Here, we screen a collection of Split-GAL4 lines that label small populations of neurons associated with the fly memory center-the mushroom bodies (MBs) [3]. Genetic silencing of PPL1 dopamine neurons disrupts conditioned, but not naive, feeding behavior, suggesting these neurons are selectively involved in the conditioned taste response. We identify two PPL1 subpopulations that innervate the MB α lobe and are essential for aversive taste memory. Thermogenetic activation of these dopamine neurons during training induces memory, indicating these neurons are sufficient for the reinforcing properties of bitter tastant to the MBs. Silencing of either the intrinsic MB neurons or the output neurons from the α lobe disrupts taste conditioning. Thermogenetic manipulation of these output neurons alters naive feeding response, suggesting that dopamine neurons modulate the threshold of response to appetitive tastants. Taken together, these findings detail a neural mechanism underlying the formation of taste memory and provide a functional model for dopamine-dependent plasticity in Drosophila.

Pleasant and Aversive Taste Perception in Anorexia Nervosa: a Functional MRI Study

Introduction Taste perception is a complex phenomenon modulated by different factors, such as taste receptors and memory brain circuitry. The palatability of the food, that activates central reward pathways, also plays an important role in taste perception. It means that taste is able to influence the choice of food and then the eating behavior. Objectives It's well known that people with anorexia nervosa (AN) have lower sensitivity to reward stimuli and recent studies have shown that altered function of taste neural circuitry may contribute to restricted eating in AN. Aims The aim of this study is to evaluate, in patients suffering from AN, the activation of the brain areas involved in taste perception and in central reward mechanisms to both pleasant and aversive taste stimuli and to correlate gustatory neural circuitry activity with eating behaviors, temperament measures and/or sensitivity to reward and to punishment. Methods 12 underweight AN patients and 12 normal-weight healthy subjects underwent a functional MRI to measure brain areas activation to repeated stimuli of a pleasant taste, a sucrose solution, alternated with an aversive taste, a bitter solution, and a water taste. Results Preliminary results showed, in patients with AN, a dysfunctional activation of brain areas involved in both taste perception and reward mechanisms following both the pleasant and aversive stimulus. Conclusions These results, if confirmed in future analyses, may improve our knowledge about the pathophysiological mechanism of AN.

Microglial activation enhances associative taste memory through purinergic modulation of glutamatergic neurotransmission.

The cerebral innate immune system is able to modulate brain functioning and cognitive processes. During activation of the cerebral innate immune system, inflammatory factors produced by microglia, such as cytokines and adenosine triphosphate (ATP), have been directly linked to modulation of glutamatergic system on one hand and learning and memory functions on the other hand. However, the cellular mechanisms by which microglial activation modulates cognitive processes are still unclear. Here, we used taste memory tasks, highly dependent on glutamatergic transmission in the insular cortex, to investigate the behavioral and cellular impacts of an inflammation restricted to this cortical area in rats. We first show that intrainsular infusion of the endotoxin lipopolysaccharide induces a local inflammation and increases glutamatergic AMPA, but not NMDA, receptor expression at the synaptic level. This cortical inflammation also enhances associative, but not incidental, taste memory through increase of glutamatergic AMPA receptor trafficking. Moreover, we demonstrate that ATP, but not proinflammatory cytokines, is responsible for inflammation-induced enhancement of both associative taste memory and AMPA receptor expression in insular cortex. In conclusion, we propose that inflammation restricted to the insular cortex enhances associative taste memory through a purinergic-dependent increase of glutamatergic AMPA receptor expression at the synapse.

Effects of glutamate and its metabotropic receptors class 1 antagonist in appetitive taste memory formation

Cortical glutamatergic activity is known to be important for memory formation in different learning tasks. For example, glutamate activity in the insular cortex plays an important role in aversive taste memory formation by signaling the unconditioned stimulus. However, the role of glutamate in the insular cortex in appetitive taste learning has remained poorly studied. Therefore, we considered the function of glutamate in attenuation of neophobia, a model of appetitive taste recognition memory. For this purpose, we performed infusions of vehicle, glutamate, a specific mGluR1 antagonist (AIDA) or a combination of glutamate and AIDA at 0 or 30min, and glutamate or vehicle at 60min after novel saccharin consumption. Glutamate infusion impaired appetitive taste recognition memory when infused at 0 or 30min, whereas, AIDA infusions produced enhanced appetitive memory at the same infusion times. Furthermore, when glutamate and AIDA were infused together no effect on attenuation of neophobia was observed. As opposed to shorter infusion times, the administration of glutamate 60min after the presentation of the saccharin consumption was ineffective in the impairment of the appetitive taste memory. These results are discussed in view of the effect of glutamate and its mGluR1 during the appetitive taste recognition memory formation in the insular cortex.

Differential contribution of perirhinal cortex and hippocampus to taste neophobia: Effect of neurotoxic lesions

Although the perirhinal cortex (Prh) has been extensively related to recognition memory, little is known about its specific role in taste memories. The main aim of the present series was therefore to examine the effect of neurotoxic lesions of the Prh on taste neophobia, a phenomenon consisting of a low intake of a novel food until its postingestive consequences are determined. The results showed that Prh-lesioned rats consumed significantly more novel saccharin in trial 1 than control subjects when a saccharin solution of 0.3% (expt. 1a) and 0.5% (expt. 1b) was presented. However, when the saccharin concentration was high and qualitatively more aversive, Prh lesions did not affect the neophobic response (0.7%, expt. 1c) and the lesioned and control animals consumed a similar amount of the fluid during the first and subsequent test trials. In all three experiments, Prh-lesioned and control rats showed a comparable intake at asymptote. Experiment 2 and 3 showed that neurotoxic lesions to the dorsal hippocampus prior to or 24h after the intake of the novel taste (0.3% saccharin) had no effect on the initial occurrence of the neophobic response or on the consolidation of safe taste memory, respectively. These findings support a dissociation of functions between the Prh and the hippocampus in taste neophobia. Also, the data suggests that the Prh plays an essential role in detecting the novelty of the new tastant.

Gustatory insular cortex, aversive taste memory and taste neophobia

Prior research indicates a role for the gustatory insular cortex (GC) in taste neophobia. Rats with lesions of the GC show much weaker avoidance to a novel and potentially dangerous taste than do neurologically intact animals. The current study used the retention of conditioned taste aversion (CTA) as a tool to determine whether the GC modulates neophobia by processing taste novelty or taste danger. The results show that GC lesions attenuate CTA retention (Experiment 1) and impair taste neophobia (Experiment 2). Given that normal CTA retention does not involve the processing of taste novelty, the pattern of results suggests that the GC is involved in taste neophobia via its function in processing the danger conveyed by a taste stimulus.

CREB Regulates Memory Allocation in the Insular Cortex

The molecular and cellular mechanisms of memory storage have attracted a great deal of attention. By comparison, little is known about memory allocation, the process that determines which specific neurons in a neural network will store a given memory. Previous studies demonstrated that memory allocation is not random in the amygdala; these studies showed that amygdala neurons with higher levels of the cyclic-AMP-response-element-binding protein (CREB) are more likely to be recruited into encoding and storing fear memory. To determine whether specific mechanisms also regulate memory allocation in other brain regions and whether CREB also has a role in this process, we studied insular cortical memory representations for conditioned taste aversion (CTA). In this task, an animal learns to associate a taste (conditioned stimulus [CS]) with the experience of malaise (such as that induced by LiCl; unconditioned stimulus [US]). The insular cortex is required for CTA memory formation and retrieval. CTA learning activates a subpopulation of neurons in this structure, and the insular cortex and the basolateral amygdala (BLA) interact during CTA formation. Here, we used a combination of approaches, including viral vector transfections of insular cortex, arc fluorescence in situ hybridization (FISH), and designer receptors exclusively activated by designer drugs (DREADD) system, to show that CREB levels determine which insular cortical neurons go on to encode a given conditioned taste memory.

Differential role of insular cortex muscarinic and NMDA receptors in one-trial appetitive taste learning

Our current understanding of the neurobiology of taste learning and memory has been greatly facilitated by the use of a reliable behavioural model, conditioned taste aversion (CTA). This model has revealed that the insular cortex (IC), specifically muscarinic and N-methyl-d-aspartate (NMDA) receptor activation in the IC, is critical for the formation of aversive taste memories. In contrast, current models of appetitive taste learning are less adequate, relying on the use of neophobic tastes (attenuation of neophobia) or on the integration of appetitive and aversive taste memories (latent inhibition of CTA). While these models have implicated IC muscarinic receptors, the involvement of NMDA receptors in the IC remains unclear. Here, we examined the role of both muscarinic and NMDA receptors in appetitive taste learning using a simple paradigm that is independent of neophobic and aversive components. First, we demonstrated that a single exposure to a novel taste, saccharin 0.1%, is sufficient to promote an appetitive taste memory as revealed by an increase in saccharin consumption during the second presentation. This increase was blocked by bilateral infusion in the IC of the muscarinic receptor antagonist, scopolamine. In contrast, infusion of the NMDA receptor antagonist, AP5, did not block appetitive taste learning but did abolish CTA. Therefore, common and distinct molecular substrates within the IC mediate appetitive versus aversive learning about the same taste.