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Gustatory cortex

The gustatory cortex (GC), also known as the primary gustatory cortex, is a specialized region of the cerebral cortex dedicated to the initial processing and perception of taste sensations, integrating gustatory inputs with multisensory cues to contribute to flavor recognition and hedonic evaluation.^[1] Located primarily within the anterior insula and adjacent frontal operculum in humans—deep within the Sylvian fissure—this area receives direct projections from the gustatory nucleus in the brainstem via the thalamus, enabling the decoding of basic taste qualities such as sweet, sour, salty, bitter, and umami.^[2] In addition to pure gustatory processing, the GC exhibits multimodal responsiveness, with neurons that respond to somatosensory inputs (e.g., texture and viscosity), olfactory signals (especially retronasal), thermal sensations, and even visual or cognitive factors like expectation and satiety, thereby playing a key role in the holistic experience of flavor rather than isolated taste detection.^[3]^[2] Structurally, the GC is divided into primary and secondary zones, with the core primary area in the insular-opercular region handling basic sensory representation and the secondary gustatory cortex extending into the caudolateral orbitofrontal cortex for higher-order integration and affective processing, such as linking tastes to reward or aversion.^[2] Functional imaging studies in humans, including fMRI, have confirmed GC activation not only by prototypical tastants (e.g., glucose or NaCl solutions) but also by non-gustatory stimuli like fat emulsions or viscous solutions that mimic mouthfeel, underscoring its role beyond mere chemosensation.^[2] In animal models, such as rodents and primates, electrophysiological recordings reveal that a small proportion of GC neurons (approximately 6.5% in primates) respond exclusively to taste, while most are modulated by behavioral context, including learning processes like conditioned taste aversion or neophobia, where novel flavors trigger avoidance.^[3]^[2] Lesions to the GC typically spare basic taste identification but impair nuanced discrimination, multisensory flavor perception, and taste-related memory, highlighting its essential yet non-absolute role in gustatory function.^[3] The GC's development and plasticity further emphasize its adaptive significance; it matures early in ontogeny to support feeding behaviors and exhibits experience-dependent changes, such as enhanced responsiveness following dietary exposure or sensory training.^[4] Ongoing research continues to elucidate its contributions to disorders like anorexia, obesity, or chemosensory loss, where GC dysfunction may underlie altered taste preferences or aversions, positioning it as a critical node in sensory-affective neural circuits.^[5]^[6]

Anatomy and Location

Primary Gustatory Cortex

The primary gustatory cortex serves as the initial cortical processing site for gustatory information in primates and humans, located primarily in the anterior insular cortex and the adjacent frontal operculum within the inferior frontal gyrus of the frontal lobe. This region is situated deep within the Sylvian fissure (lateral sulcus), rendering it hidden beneath the overlapping frontal, parietal, and temporal opercula, which contributes to its relative inaccessibility in early anatomical studies.^[3]^[7] Cytoarchitecturally, the primary gustatory cortex corresponds to the dysgranular portion of the insular cortex, characterized by a transitional structure between granular and agranular regions, with distinct layering across II-VI that supports integration of sensory inputs. Layer IV, though less dense in granule cells compared to purely granular cortices, receives thalamocortical afferents, while layers II/III and V/VI exhibit pyramidal neurons suited for intra- and extracortical projections. This organization corresponds to Brodmann area 13 in the anterior insula and area 43 in the adjacent operculum, emphasizing its role in basic sensory relay rather than higher associative functions.^[8]^[9] The cortex receives direct, predominantly ipsilateral projections from the parvocellular division of the ventral posteromedial thalamic nucleus (VPMpc), which acts as the key relay for ascending gustatory signals. These connections terminate primarily in the middle layers, establishing the primary gustatory cortex as the thalamic target zone for taste-specific processing.^[2]^[10] Historically, the primary gustatory cortex was first delineated in primates through lesion studies by Benjamin in 1963, which revealed significant taste perception deficits following targeted damage to the insular region, confirming its necessity for gustatory function.^[11]

Secondary and Higher-Order Areas

The secondary gustatory cortex is situated in the caudolateral orbitofrontal cortex (OFC), a region that receives direct projections from the primary gustatory cortex in the insula and frontal operculum to enable advanced processing of taste signals.^[12] This area integrates gustatory inputs with olfactory and somatosensory information, contributing to flavor perception and affective evaluation.^[13] Extensions of this secondary cortex into the agranular insula, located in the anterior portion adjoining the caudal OFC, further support multimodal integration by processing visceral and interoceptive signals alongside taste.^[2] Higher-order gustatory projections from the secondary cortex target the agranular insula and caudal OFC, forming a network that links to the amygdala and ventral striatum to facilitate reward valuation of gustatory stimuli.^[14] The agranular insula provides dense inputs to the caudal ventral striatum, where these signals converge with amygdalar projections to encode the motivational and hedonic value of tastes, influencing feeding behaviors and decision-making.^[15] These connections underscore the role of secondary areas in associating sensory taste qualities with emotional and reinforcement outcomes.^[16] Gustatory processing in the secondary and higher-order areas occurs bilaterally across hemispheres but exhibits asymmetry, with greater right-hemisphere activation linked to the hedonic evaluation of tastes.^[17] For instance, right caudolateral OFC and anterior temporal regions show heightened responses to taste stimuli associated with pleasantness or quality recognition, supporting specialized right-sided dominance in affective processing.^[18] Recent anatomical mapping through anterograde tracing in rodents has delineated OFC subregions, such as the dorsolateral orbital area, with taste-specific projections from the insula, aligning with human fMRI evidence of activation gradients in caudal OFC during gustatory tasks.^[14] These studies confirm functional specialization within OFC subregions for taste-related processing, including weaker interhemispheric connectivity in the OFC under taste stimulation in certain conditions.^[19]

Neural Pathways

Peripheral Input and Ascending Projections

Taste buds, the peripheral sensory organs responsible for detecting chemical stimuli, are primarily located on the tongue's fungiform, foliate, and circumvallate papillae, as well as the soft palate and epiglottis.^[20] These structures are innervated by three cranial nerves: the facial nerve (cranial nerve VII) via its chorda tympani branch supplies the anterior two-thirds of the tongue, including fungiform and foliate papillae, while the greater petrosal nerve branch innervates taste buds on the soft palate; the glossopharyngeal nerve (cranial nerve IX) innervates the posterior third of the tongue, including circumvallate and foliate papillae; and the vagus nerve (cranial nerve X) provides innervation to taste buds in the epiglottis and oropharyngeal region.^[21]^[20] The cell bodies of these first-order gustatory afferent neurons reside in the geniculate ganglion for CN VII, the petrosal ganglion for CN IX, and the nodose ganglion for CN X.^[21]^[20] These peripheral afferents convey gustatory signals centrally, synapsing onto second-order neurons in the nucleus of the solitary tract (NTS) within the medulla oblongata, specifically in its rostral subdivision dedicated to gustation.^[21] The NTS serves as the primary central relay for taste information, integrating inputs from all three cranial nerves before further ascending transmission.^[22] From the rostral NTS, gustatory projections ascend differently across species: in rodents, up to 80% of taste-responsive NTS neurons project ipsilaterally to the parabrachial nucleus (PBN) in the pons, forming a key relay station.^[22] In primates, including humans, these projections bypass the PBN and terminate directly in the parvocellular division of the ventroposteromedial thalamic nucleus (VPMpc).^[21]^[22] This brainstem organization ensures that all gustatory signals must traverse the NTS as a prerequisite for reaching higher centers, including the thalamic relay that ultimately projects to the gustatory cortex.^[21]

Thalamic Relay and Cortical Termination

The parvocellular portion of the ventral posteromedial nucleus of the thalamus (VPMpc) serves as the primary thalamic relay nucleus for gustatory information, receiving direct projections from the nucleus of the solitary tract (NTS) in primates and relaying signals to the gustatory cortex located in the insular and opercular regions.^[23]^[24] In this role, the VPMpc integrates ascending gustatory inputs and forwards them via thalamocortical afferents, forming a critical gateway that filters and refines sensory signals before cortical processing.^[25] These projections primarily target the ipsilateral insular-opercular cortex, adjacent to the superior limiting sulcus, with dense terminations in the middle layers to support initial sensory representation.^[26] Within the VPMpc, individual neurons often respond to multiple taste qualities and modalities, including thermal and tactile cues.^[24] Thalamocortical afferents from the VPMpc terminate densely in layer IV of the primary gustatory cortex, where they form strong synaptic connections primarily with excitatory neurons, enabling efficient relay of sensory input as the primary recipient layer for thalamic signals.^[10] In contrast, projections to layers II and III are sparser, supporting intracortical integration and modulation through short-term synaptic facilitation at lower frequencies, which contributes to higher-order processing without overwhelming superficial layers.^[10] Species differences in these pathways highlight evolutionary variations: rodents predominantly rely on an obligatory relay through the parabrachial nucleus (PBN) before reaching the VPMpc, whereas primates feature direct NTS-to-VPMpc connections, streamlining the ascending route and potentially enhancing processing speed for taste signals.^[24] Recent comparative reviews confirm these distinctions, noting that the direct pathway in primates may allow for more integrated multisensory handling in the thalamus.^[25]

Core Functions

Taste Perception and Basic Coding

The gustatory cortex processes the five basic tastes—sweet, sour, salty, bitter, and umami—through neurons that are predominantly broadly tuned, meaning individual cells respond to multiple taste qualities rather than being specialized for a single one.^[27] This broad tuning allows for flexible representation of taste stimuli, with studies in primates showing that many taste-responsive neurons react to two or more basic tastants.^[28] For instance, a neuron might fire in response to both sucrose (sweet) and sodium chloride (salty), integrating signals from diverse chemical inputs to form initial perceptual categories.^[29] Taste quality is encoded via across-fiber pattern or population coding, where ensembles of neurons collectively distinguish between tastes through their distributed activity patterns, rather than a strict gustotopic map organizing the cortex by taste type.^[30] In this scheme, no dedicated regions exist solely for sweet or bitter; instead, overlapping activations across the population convey identity, as evidenced by multivariate analyses of neural ensembles in awake animals that accurately decode taste modalities from collective firing rates.^[31] This population-level strategy supports robust perception even with variable neuronal responses, emphasizing integration over segregation in early cortical processing.^[27] Electrical microstimulation of the gustatory cortex, particularly in the insular region, can elicit specific taste sensations in humans, such as perceptions of sweetness or other basic qualities, confirming its role in generating conscious taste experiences.^[32] These effects occur when stimulating the mid-dorsal insula, where gustatory representations are concentrated, and demonstrate that targeted activation mimics natural taste input.^[32] As the primary cortical endpoint of the ascending gustatory pathway, the gustatory cortex enables conscious perception of taste by integrating quality and initial intensity signals from thalamic relays, transforming subconscious brainstem processing into subjective awareness.^[27] This integration occurs rapidly, within hundreds of milliseconds of stimulus onset, allowing for immediate behavioral relevance like acceptance or rejection of food.^[30]

Intensity and Concentration Encoding

In the gustatory cortex, taste intensity is primarily encoded through variations in neuronal firing rates that scale with the concentration of tastants. Single-unit recordings in awake rats reveal that many neurons exhibit monotonic increases in firing rates as tastant concentration rises, allowing the cortex to represent stimulus strength quantitatively. For instance, in the primary gustatory cortex (posterior insular cortex), neuronal responses to sucrose show progressive elevation in spike rates across concentrations from approximately 0.09 M to 0.53 M (equivalent to 3–18% w/v), with intensity-selective neurons comprising about 15% of the recorded population and contributing disproportionately to decoding accuracy.^[33] This scaling supports the discrimination of subtle intensity differences, as neurometric functions derived from these firing rates closely match rats' behavioral performance in sucrose concentration tasks.^[33] Neuronal responses often display broad tuning, where individual cells respond to multiple tastant types in a concentration-dependent fashion, rather than being narrowly selective for one quality. In electrophysiological studies of rats, gustatory cortical neurons tested with NaCl, quinine, and other stimuli at varying concentrations showed that many cells modulated their activity across different tastants as concentration increased, facilitating a distributed representation of intensity irrespective of specific taste identity.^[34] Such broad tuning enables the cortex to integrate intensity signals from diverse chemical stimuli, with firing rates adjusting dynamically during active licking behaviors.^[34] Some neurons exhibit non-linear responses, including saturation at higher concentrations, which mirrors the compressive nature of perceived taste intensity in behavioral paradigms. For example, sigmoid-shaped response curves in gustatory cortical populations fit observed perceptual scaling, where incremental concentration changes yield diminishing returns in neural activation beyond moderate levels (e.g., above 0.5 M for sucrose).^[33] Experimental evidence from single-unit recordings in rats demonstrates firing rate modulations in response to concentration shifts in tastants like NaCl and quinine, highlighting the cortex's sensitivity to intensity gradients.^[34] These mechanisms ensure robust encoding of concentration without overwhelming the system at extreme intensities.

Neuronal Mechanisms

Chemosensory Neuron Properties

In the primary gustatory cortex, approximately 34% of recorded units are chemosensitive neurons responsive to chemical tastants such as sucrose, quinine, monosodium glutamate, sodium chloride, and citric acid.^[34] These neurons are classified based on their preferential responses: sweet-preferring (often termed sucrose-best), which show maximal firing to sucrose; bitter-preferring (quinine-best), with strongest activation by quinine hydrochloride; and multi-tastant responsive (broadly tuned), which react to multiple tastants without a dominant preference.^[35] This classification highlights the diversity in tuning specificity, enabling differential processing of basic taste qualities. Chemosensory neurons in the gustatory cortex display characteristic phasic-tonic firing patterns in response to taste stimuli, featuring an initial high-frequency phasic burst followed by a sustained lower-rate tonic phase that persists during stimulus presence. Response latencies typically range from 70 to 120 ms post-stimulus onset, varying with tastant concentration and allowing rapid encoding of taste onset.^[36] These temporal dynamics facilitate precise temporal coding of taste events, distinct from slower tonic adaptations in lower brainstem relays. At the molecular level, chemosensory processing in the gustatory cortex involves modulation by inhibitory mechanisms. The cortex features a mix of excitatory pyramidal neurons, which propagate taste signals forward, and inhibitory interneurons, including parvalbumin-expressing subtypes, that regulate network activity and selectivity.^[37] Recent optogenetic studies have identified specialized subsets of gustatory cortical neurons tuned to umami stimuli.^[38] These findings underscore the role of targeted circuit dissection in revealing taste-specific cellular diversity.

Population Coding and Multimodal Responses

In the gustatory cortex (GC), taste information is encoded through population coding rather than strict labeled-line mechanisms, where ensembles of neurons collectively represent taste qualities via distributed activity patterns. Analysis of multi-neuron firing rates has demonstrated that these population-level representations distinguish between basic tastes, such as sweet, salty, sour, and bitter, more accurately than the responses of individual neurons. This ensemble approach allows for robust discrimination of complex stimuli, as shown in studies where population vectors—constructed from weighted average firing rates across neurons—enable decoding of taste identity with temporal precision on the order of milliseconds.^[39] Support for population coding over labeled-line theory in the GC arises from the substantial overlap in projections from peripheral gustatory nerves, such as the chorda tympani and glossopharyngeal, which precludes strict segregation of taste-specific pathways into the insular cortex. Anatomical tracing reveals that these inputs converge broadly within the GC, leading to combinatorial representations where no single neuron or fiber line exclusively signals a particular taste quality. Electrophysiological recordings confirm this overlap, with neurons often responding broadly to multiple tastants, further emphasizing distributed coding.^[40] A key feature of GC population coding is its multimodality, where approximately 20-30% of neurons integrate taste with non-chemical inputs like touch or temperature, enhancing flavor perception. For instance, about 23% of GC neurons in primates respond to somatosensory stimuli such as tongue or jaw movements alongside taste, while thermal stimuli evoke responses in a similar proportion, indicating convergent processing of intra-oral sensations.^[2] Evidence from cross-modal priming studies supports this integration, showing that visual or tactile cues preceding taste delivery modulate GC firing rates, with population activity shifting to reflect anticipated multisensory flavor profiles rather than isolated taste qualities.^[2] Recent investigations using functional near-infrared spectroscopy (fNIRS) and calcium imaging have illuminated population dynamics in the GC for distinguishing flavor from pure taste. A 2023 study employing two-photon calcium imaging in mice revealed that learning enhances ensemble representations during taste-guided mixture discrimination tasks, with population activity trajectories separating flavor mixtures (taste + odor) from single tastes more distinctly post-training, achieving decoding accuracies up to 90%.^[41] These findings underscore the GC's role in dynamic, context-dependent coding that supports behavioral decisions in naturalistic feeding scenarios. As of 2025, ongoing research continues to explore advanced imaging techniques for finer resolution of these ensemble dynamics.

Modulation and Plasticity

Adaptation to Concentration Changes

Neurons in the gustatory cortex exhibit habituation to sustained tastant stimulation, characterized by a phasic-tonic response profile where firing rates initially surge in a brief phasic phase (lasting 0.3–2 seconds) before declining in the subsequent tonic phase to a level above spontaneous activity. This adaptation enables the cortex to filter out constant sensory input while preserving responsiveness to novel or changing stimuli, as demonstrated in recordings from awake rats during intraoral delivery of tastants like NaCl rinses. For instance, prolonged exposure to NaCl leads to a progressive decrease in neuronal firing rates, typically by 20–40% after 5–10 seconds of constant stimulation, reflecting central mechanisms that prevent overstimulation from steady-state inputs.^[42] Sensitivity to dynamic concentration shifts further highlights the cortex's role in detecting temporal variations rather than static levels alone. Gustatory cortical neurons show robust on-responses—sharp increases in firing rate—to rapid elevations in tastant concentration, such as stepwise rises in NaCl or sucrose, with latencies as short as 70–120 ms and response magnitudes scaling with the change's steepness. In contrast, responses to concentration decreases are weaker or absent in most neurons, though a subset exhibits off-responses, such as transient firing upon stimulus offset or dilution, potentially influenced by carryover excitation from lower brainstem relays like the nucleus of the solitary tract.^[43] In the context of tastant mixtures, adaptation manifests as suppression effects, where neuronal responses to binary combinations are diminished compared to individual components at equivalent concentrations. For example, in awake rat preparations, binary mixtures like sucrose-citric acid or sucrose-NaCl (at 100 mM each) elicit firing rates in the gustatory cortex that match or fall below the dominant single tastant, rather than summing additively, with suppression evident in 53–65% of taste-specific neurons during early response windows (100–350 ms post-delivery). This mixture suppression is transient, fading after about 600 ms as responses shift toward palatability coding, but it illustrates how competitive interactions among tastants lead to attenuated cortical output during complex, dynamic oral exposures.^[44]

Effects of Familiarity and Learning

Repeated exposure to taste stimuli modulates activity in the gustatory cortex (GC), enhancing the specificity of neural responses to familiar tastes. In rodent models, familiarity leads to a reduction in the number of active and taste-responsive neurons in the GC, with approximately a 23% decrease in active cells after five days of exposure, suggesting a sparsening of the population code that may improve efficiency in processing known stimuli.^[45] This process is accompanied by increased magnitude of excitatory responses (from 11.59 to 13.35 normalized spikes) and reduced suppression, contributing to sharper discrimination of familiar versus novel inputs over time.^[45] Synaptic plasticity in the GC underlies these effects of familiarity and learning, particularly through long-term potentiation (LTP) at thalamocortical synapses within the insular cortex. LTP in the rat insular cortex is induced during conditioned taste aversion learning, with spatiotemporal dynamics showing enhanced synaptic strength that persists for hours post-training, facilitating the consolidation of taste memories.^[46] Dopamine release from the ventral tegmental area (VTA) to the GC plays a key role in this plasticity, as optogenetic stimulation of VTA dopaminergic terminals in the insular cortex promotes the consolidation of conditioned taste aversion memories via D1-like receptors, linking reward prediction and sensory adaptation.^[47] Taste neophobia, the innate aversion to novel flavors, is reflected in broader neural activation patterns in the GC, which narrow with repeated exposure and familiarity. In awake rats, novel tastes initially recruit a wider ensemble of GC neurons, but familiarity induces a specific late-phase increase in firing rates (from 7 to 8.3 spikes per phase) that is tastant-selective, reducing the breadth of activation and attenuating neophobic responses over sessions.^[48] Rodent lesion studies confirm the GC's role, as bilateral damage impairs neophobia by weakening avoidance of novel tastes on first exposure.^[49] Recent research highlights how familiarity influences value coding in taste processing networks, extending to downstream areas like the orbitofrontal cortex (OFC). In 2024 mouse studies using two-photon imaging, learning through repeated taste discrimination tasks enhanced decision-related selectivity in the GC, increasing categorical responses from 11.6% to 21.5% in delay periods, which supports refined value assignments for familiar safe foods over novel ones.^[50] This plasticity alters OFC integration of gustatory signals, prioritizing hedonic value for familiar stimuli in feeding decisions.^[51]

Clinical and Advanced Aspects

Associated Disorders and Dysfunctions

Impairment of the gustatory cortex, primarily located in the insular region, is implicated in various taste disorders, notably ageusia (complete loss of taste) and hemiageusia (unilateral loss). Insular strokes, particularly those affecting the anterior insula, can lead to bilateral or contralateral ageusia as a rare but documented consequence, often presenting as the sole clinical manifestation in acute cases.^[52] Unilateral damage to the insula typically results in contralateral hemiageusia due to the somatotopic organization of taste representation, with lesions disrupting central processing of gustatory signals from the contralateral tongue and oral cavity.^[53] In neurodegenerative conditions, gustatory cortex dysfunction contributes to taste deficits. A 2023 systematic review and meta-analysis of 18 studies demonstrated a significant association between dementia, including Alzheimer's disease (AD), and gustatory impairments, with AD patients exhibiting worse taste detection thresholds (mean difference = 3.28, p = 0.004) and identification scores (mean difference = -2.26, p = 0.05) compared to controls.^[54] Similarly, reduced volume in the bilateral insular cortex, a key component of the gustatory cortex, has been observed in Parkinson's disease (PD) patients using structural MRI, correlating with disease progression and sensory alterations beyond motor symptoms.^[55] Recovery from gustatory lesions, such as those from insular infarcts, often involves neural plasticity, with high recovery rates reported in transient cases; for instance, taste function improves in a majority of patients through reorganization of contralateral or perilesional cortical areas, though permanent deficits persist in severe bilateral involvement.^[56] Therapeutic interventions targeting the insula, such as deep brain stimulation (DBS) for refractory epilepsy, can modulate gustatory functions incidentally, as insular stimulation during epilepsy mapping evokes or alters taste perceptions in responsive patients, highlighting potential for sensory restoration in comorbid disorders.^[57]

Role in Multisensory Integration and Decision-Making

The gustatory cortex (GC) plays a pivotal role in multisensory integration, particularly by combining gustatory signals with olfactory inputs to form coherent flavor perceptions, with further processing in the orbitofrontal cortex (OFC). In the OFC, which receives projections from the GC, a substantial proportion of neurons exhibit multimodal responses, integrating taste and retronasal olfaction to encode flavor identity and reward value.^[58] This integration enhances the distinct representation of odor-taste mixtures, as demonstrated in behaving rats where GC neurons respond broadly to intraoral chemosensory stimuli, including both gustatory and olfactory components.^[59] Recent human studies using functional near-infrared spectroscopy (fNIRS) have shown that expectation-driven processing of bitter tastes activates the visual cortex, illustrating how GC-mediated gustatory signals can cross-modally influence visual areas via top-down mechanisms.^[60] In decision-making, GC neurons encode key attributes that guide choices, such as the subjective value and quantity of options in economic tasks involving juice selections in nonhuman primates.^[61] Specifically, single-neuron recordings reveal that GC activity represents the flavor identity, volume, and integrated subjective value of chosen juices, supporting consummatory behaviors during reward-directed decisions. Aversive signaling in this pathway involves thalamic neurons that transmit threat-related information to drive avoidance responses. For instance, activation of parabrachial CGRP neurons, which relay to thalamic gustatory regions, sustains conditioned taste aversions and modulates immediate rejection of unpalatable stimuli.^[62] Population-level activity in the GC further contributes to economic choice by representing flavor utility, which influences foraging-like behaviors in primates where animals weigh taste rewards against effort or alternatives.^[61] This encoding allows dynamic adjustments in decision thresholds, optimizing resource allocation in naturalistic settings. Recent advances highlight the GC's involvement in dynamic representations during multisensory and decision processes. A 2025 study in Nature Communications demonstrated that neurons in the ventral posteromedial nucleus parvocellularis (VPMpc), the thalamic relay to GC, drive avoidance behaviors by transmitting aversive gustatory signals to the insular cortex and amygdala.^[63] Post-2023 research, including two-photon imaging in mice, has revealed that learning enhances GC population codes for taste-guided decisions, shifting from sensory identity to behavioral relevance in discrimination tasks.^[50] These findings underscore evolving views of GC plasticity in integrating multisensory inputs for adaptive choice.

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https://doi.org/10.1016/j.neubiorev.2006.07.005
[43]
https://doi.org/10.1523/JNEUROSCI.0092-06.2006
[44]
https://doi.org/10.1152/jn.00917.2012
[45]
https://www.cell.com/current-biology/fulltext/S0960-9822(22)01553-6
[46]
Spatiotemporal dynamics of long-term potentiation in rat insular ...
The rat insular cortex (IC) plays a critical role in conditioned taste aversion (CTA) learning, a classical conditioning in which a single pairing of a novel ...
[47]
Photostimulation of Ventral Tegmental Area-Insular Cortex ...
Our results showed that VTA photostimulation improves the salience to consolidate a conditioned taste aversion memory through the D1-like receptor into the IC.
[48]
Neural Signature of Taste Familiarity in the Gustatory Cortex of the Freely Behaving Rat | Journal of Neurophysiology | American Physiological Society
### Summary of Findings on Neural Signature of Taste Familiarity in Gustatory Cortex
[49]
Gustatory insular cortex, aversive taste memory and taste neophobia
Mar 1, 2016 · Prior research indicates a role for the gustatory insular cortex (GC) in taste neophobia. Rats with lesions of the GC show much weaker avoidance ...
[50]
https://www.cell.com/current-biology/fulltext/S0960-9822(24)00374-9
[51]
The Insula and Taste Learning - Frontiers
Taste information is transferred from the oral cavity to the cortex by the main excitatory neurotransmitter of the mammalian brain, glutamate (Rosenblum, 2008; ...
[52]
Bilateral Ageusia and Tongue Anesthesia Following Unilateral ... - NIH
Loss of taste (ageusia) is a rare consequence of stroke and can present as its sole clinical finding. Ageusia may be considered at first a clinical deficit of ...
[53]
Taste Disorders in Acute Stroke - American Heart Association Journals
Jul 7, 2005 · Taste disorders after stroke are frequent. A significant association was found for male gender, high NIHSS score, swallowing disorder, and PACS, particularly ...
[54]
The Association Between Neurocognitive Disorders and Gustatory ...
Olfactory and gustatory dysfunction have been reported in mild and major neurocognitive disorders (NCDs), with variable results.
[55]
Characterization of cortical volume and whole-brain functional ...
Aug 28, 2024 · This study employed multiple MRI features to comprehensively evaluate the abnormalities in morphology, and functionality associated with Parkinson's disease ( ...
[56]
How to Manage Taste Disorders - PMC - PubMed Central - NIH
Sep 21, 2022 · The recovery rates are high, but the time range for full recovery is ... Transient hemiageusia in cerebrovascular lateral pontine lesions.
[57]
The Insula: A Stimulating Island of the Brain - MDPI
Nov 19, 2021 · Direct cortical stimulation (DCS) in epilepsy surgery patients has a long history of functional brain mapping and seizure triggering.
[58]
Multisensory Flavor Perception - ScienceDirect.com
Mar 26, 2015 · From there, the inputs from both senses project to the orbitofrontal cortex (OFC). Gustatory stimuli are thought to project to caudolateral OFC, ...
[59]
Multisensory Integration Underlies the Distinct Representation of ...
May 15, 2024 · ... 2024, 44 (20) ... Specifically, optogenetic or pharmacological perturbation of the gustatory cortex eliminates posterior piriform cortical ...
[60]
Gustatory-Visual Interaction in Human Brain Cortex: fNIRS Study
Jan 19, 2025 · The presented work aims to investigate, using fNIRS, whether a taste stimulus, in this case, the taste of bitter, also causes stimulation of the ...
[61]
Neuronal Activity in the Gustatory Cortex during Economic Choice
Aug 14, 2024 · Neurons in GC represented the flavor, the quantity, and the subjective value of the juice chosen by the animal.
[62]
Thalamic CGRP neurons define a spinothalamic pathway for ... - PNAS
Jul 9, 2025 · These neurons act as a central alarm system, integrating multisensory innate threat signals and processing aversive information, which is then ...Missing: gustatory | Show results with:gustatory
[63]
Parabrachial CGRP Neurons Establish and Sustain Aversive Taste ...
Nov 21, 2018 · Our results indicate that CGRP PBN neurons not only play a key role for learning food aversions but also contribute to the maintenance and expression of those ...
[64]
Gustatory thalamic neurons mediate aversive behaviors - Nature
Sep 26, 2025 · The projection from the VPMpc to the IC is a major component of the gustatory pathway from the taste buds in the tongue to the gustatory cortex ...