We and others have recently identified a series of molecular alterations in the gustatory cortex (GC) of the rat at different time intervals following novel taste learning. 
The MRI signal intensities at the gustatory cortex (GC), the core subregion of the nucleus accumbens (NAcC), the shell subregion of the nucleus accumbens (NAcSh), the ventral pallidum (VP), the central nucleus of amygdala (CeA), the lateral hypothalamus (LH), and the basolateral nucleus of amygdala (BLA) of the conditioned group were higher than those of the control group.
Using Hidden Markov modeling, a method of analysis that can make use of such trial-to-trial response variability, we have uncovered sequences of discrete states of neural activity in gustatory cortex during taste processing.
We tested this hypothesis by examining the role of neural ensembles in gustatory cortex (GC) during receipt of gustatory stimuli (sucrose and water) and cues associated with those stimuli using the immediate early genes (IEGs) Arc and Homer1a.
These animals also showed significantly larger percent decreases in BOLD in mammillary bodies, secondary motor cortex, gustatory cortex, prelimbic prefrontal cortex, orbital cortex, and the anterior olfactory nucleus.
To address this issue we simultaneously recorded activity from neuronal ensembles in primary [ gustatory cortex GC)] and secondary gustatory [ orbitofrontal cortex (OFC)] cortices while rats made a taste-guided decision between two response alternatives.
Dams treated with V1a antagonist showed significantly greater BOLD responses in the anterior olfactory nucleus, infralimbic prefrontal cortex, gustatory cortex, somatosensory cortex, and substantia innominata when presented with a novel male intruder.
We report here that novel taste learning induces two waves of mTOR activation in the gustatory cortex. Inhibition of mTOR, specifically in the gustatory cortex, has two effects.
Brain imaging studies suggest that obese relative to lean individuals show greater activation of the gustatory cortex (insula/frontal operculum) and oral somatosensory regions (parietal operculum and Rolandic operculum) in response to anticipated intake and consumption of palatable foods. Results imply that individuals who show greater activation in the gustatory cortex and somatosensory regions in response to anticipation and consumption of food, but who show weaker activation in the striatum during food intake, may be at risk for overeating, particularly those at genetic risk for lowered dopamine receptor signaling..
One neuron type produced long, protracted responses with dynamics that were strikingly similar to those previously observed in gustatory cortex.
Moreover, rat gustatory cortex (GC) neural ensemble activity could also discriminate between these two bitter tastants.
To test this, we recorded the activity of single neurons throughout PFC and gustatory cortex (GUS) from two subjects while they performed a gustatory delayed-match-to-sample task with intervening gustatory distraction.
Main effects of TDE valence were observed for the entire sample in the midbrain, left putamen, left cerebellum, and primary gustatory cortex, bilaterally.
Rostral forebrain structures like the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) send projections to the nucleus of solitary tract (NST) and the parabrachial nucleus (PBN) that modulate taste-elicited responses.
Obese relative to lean adolescent girls showed greater activation bilaterally in the gustatory cortex (anterior and mid insula, frontal operculum) and in somatosensory regions (parietal operculum and Rolandic operculum) in response to anticipated intake of chocolate milkshake (vs. Results suggest that individuals who show greater activation in the gustatory cortex and somatosensory regions in response to anticipation and consumption of food, but who show weaker activation in the striatum during food intake, may be at risk for overeating and consequent weight gain..
The gustatory cortex (GC) processes chemosensory and somatosensory information and is involved in learning and anticipation.
WGA was not detected in the parabrachial nucleus, or the gustatory cortex.
The present study used bilateral ibotenic acid lesions to examine the role of the gustatory cortex in the suppression of CS intake induced by cocaine, morphine, and LiCl. The results show that bilateral lesions of the insular gustatory cortex (1) fully prevent the suppressive effects of both a 15 and a 30 mg/kg dose of morphine, (2) attenuate the suppressive effect of a 10 mg/kg dose of cocaine, but (3) are overridden by a 20 mg/kg dose of the drug.
Using taste learning, we found learning-related induction of PSD-95 in the gustatory cortex, which was temporally restricted, coupled to the learning of a novel, but not familiar, taste and controlled by ERK.
In controls, compared with water, sham ingesting sucrose produced significantly more Fos-positive neurons in the nucleus of the solitary tract, PBN, TTA, and gustatory cortex (GC).
However, not only was a strong taste input unable to rescue an immediately subsequent strong taste input when the gustatory cortex was under the influence of the protein-synthesis inhibitor, anisomycin, but the effect of the interaction was to reduce the variation among individual taste memories.
The parvicellular portion of the ventroposteromedial nucleus of the thalamus (VPMpc) receives projections from the bilateral PbN and transmits taste information to the gustatory cortex.
The parvicellular part of the ventroposteromedial nucleus of the thalamus (VPMpc) is positioned at the key site between the gustatory parabrachial nuclei (PbN) and the gustatory cortex for relaying and processing gustatory information via the thalamocortical pathway.
Here, we studied the effect of a visceral malaise on taste representations in the gustatory cortex (GC).
Previous studies show that activation of the gustatory cortex (GC), bed nucleus of the stria terminalis (BNST), central nucleus of the amygdala (CeA), and lateral hypothalamus (LH) inhibits PBN taste responses, GABAergic neurons are present in these forebrain regions, and GABA reduces the input resistance of PBN neurons.
Thus, it is likely that, in addition to serving as higher-order gustatory cortex, the OFC integrates multiple sensory inputs and computes reward value to guide feeding behavior..
Devalue rats showed greater FOS expression than Maintain rats in several brain regions implicated in devaluation task performance and the display of aversive responses, including the basolateral amygdala, orbitofrontal cortex, gustatory cortex (GC), and the posterior accumbens shell (ACBs), whereas the opposite pattern was found in the anterior ACBs.
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.
A modest increase in labeled neurons occurred bilaterally within the gustatory cortex.
However, much less is known about the cortical processing of taste sensation and the organizing principles of the gustatory cortex (GC).
We evaluated their effect (i) on the level of noradrenaline in the gustatory cortex using microdialysis, (ii) on glycaemia that is an essential factor of taste learning and (iii) on the comparative SD versus IO conditioned taste aversion protocol mentioned above. Injecting RX821001 increased the level of noradrenaline in the gustatory cortex up to two-fold of the baseline. The noradrenaline level of the gustatory cortex decreased, but only down to 20% of the baseline.
Here, we first show that these characteristic features are also applicable in bursting spike sequences that are obtained from the rat gustatory cortex. Our study implies that (1) the characteristic features of CV and LV are the results of the endogenous bursting and (2) the bursting behavior in the gustatory cortex is caused mainly by the persistent sodium current..
Recently, cholinergic innervation of the gustatory cortex (GC) was reported to be involved in certain taste learning in rats.
INTRODUCTION: It is known that taste is centrally represented in the insula, frontal and parietal operculum, as well as in the orbitofrontal cortex (secondary gustatory cortex). Our aim was to localize taste in the human cortex at 3 T, specifically in the orbitofrontal cortex as well as in the primary gustatory cortex.
Using a multi-electrode recording technique, the present study aimed to elucidate the role of broadly-tuned taste-sensitive neurons in the rat gustatory cortex in discriminating between salt and acid.
In addition, we detected an increase of C/EBPbeta protein expression in the gustatory cortex 18 h after novel taste learning.
For this reason, we investigated whether neurons in the primary gustatory cortex (GC), a cortical area necessary for tastant identification and discrimination, contain sufficient information in a single lick cycle, or approximately 150 ms, to distinguish between tastants at different concentrations. In summary, these results suggest that the gustatory cortex is capable of processing multimodal information on a rapid timescale and provide the physiological basis by which animals may discriminate between tastants during a single lick cycle..
These phenomena were not caused by specific aspects of our infusion technique--muscimol infusions into the hippocampus during familiarization sessions did not cause CTAs, muscimol infusions into gustatory cortex caused the expected attenuation of CTA, and hippocampal inactivation caused the expected attenuation of spatial learning.
Here we show that intracortical blockade of protein synthesis in the gustatory cortex after retrieval of taste-recognition memory disrupts previously consolidated memory to a restricted degree only if the experience is updated.
We examined the laterality of the human gustatory neural pathway by measuring gustatory-evoked magnetic fields (GEMfs) and demonstrating the activation of the human primary gustatory cortex (PGC).
CONCLUSION: Changes in mu-OR binding in the insula may be important in the pathogenesis or maintenance of the self-perpetuating behavioral cycle of bulimic subjects because the insula is the primary gustatory cortex and has repeatedly been implicated in the processing of the reward value of food..
The pattern of brain damage responsible for the dissociation suggests that reliable behavioral choice among tastes can occur in the absence of the gustatory cortex necessary for taste recognition..
The precentral extension of area 3 as well as the transition between the frontal operculum and insula (area G) comprises the primary gustatory cortex in the subhuman primate, receiving projections from the thalamic taste relay.
Naive individuals activated the primary gustatory cortex and brain areas, including the amygdala, implicated in emotional processing..
Deep parietal cells discriminated behavioral context, whereas deep gustatory cortex neurons encoded the two conditions identically.
Sweet and salty tastes are readily distinguishable, but a bitter or painful stimulus leads to a deactivation of the primary gustatory cortex, which is in keeping with the need to focus on an avoidance response.
We conclude that obesity is associated with an abnormal brain response to the sensory aspects of a liquid meal after a prolonged fast especially in areas of the primary gustatory cortex.
We trained head-restrained, water-restricted rats to perform a simple variant of a timed fluid self-administration task, while recording local field potentials from gustatory cortex (GC).
Time-frequency wavelet analysis indicated that sensory input from the tongue simultaneously activated caudolateral sensorimotor and primary gustatory cortex, which appeared to prime the superior sensory and motor cortical areas, involved in the volitional phase of swallowing.
The insular gustatory cortex may be essential for the evaluation of saliency and representation of the incentive values of tastes. gustatory cortex lesions should interfere with conditioned taste avoidance according to these factors, which depend on the conditioned taste avoidance protocol used. The present study was aimed at investigating the effects of bilateral lesions of the gustatory cortex-focusing on electrolytic and excitotoxic lesions. Electrolytic gustatory cortex lesions impaired but did not suppress conditioned taste avoidance in both protocols.
Ample data indicate that the gustatory cortex (GC) subserves the processing, encoding, and storage of taste information.
Electrical stimulation of the gustatory cortex evoked a characteristic field potential in the endopiriform nucleus. Voltage-sensitive dye studies showed that stimulation of the piriform cortex induced signal propagation from the piriform cortex to endopiriform nucleus, whereas stimulation of the gustatory cortex did the same from the gustatory cortex to endopiriform nucleus via the agranular division of the insular cortex. After stimulation of the endopiriform nucleus, optical signals propagated not only to the piriform cortex but also to the gustatory cortex via the agranular division of the insular cortex.
In the stimulation studies, the effects of electrical stimulation of the gustatory cortex (GC) or the central nucleus of amygdala (CeA) were examined on firing of PBN taste units.
The present study investigates how activity in 2 other similarly interconnected forebrain sites, the lateral hypothalamus (LH) and gustatory cortex (GC), might influence PBN gustatory processing in rats.
Previous studies have shown a modulatory influence of forebrain gustatory areas, such as the gustatory cortex and lateral hypothalamus, on the activity of taste-responsive cells in the nucleus of the solitary tract (NST).
In gustatory cortex, single-neuron activity reflects the multimodal processing of taste stimuli.
Based on previous proposals, and on anatomical, physiological and lesion data, we propose that in addition to primary gustatory cortex, located in primate opercular cortex and rodent granular insular cortex, three association areas exist.
Studies on epileptic gustatory aura have demonstrated that the insula and the anteromedial temporal lobe are the primary and secondary gustatory cortex, respectively.
Activation in the superior insula, the presumed location of primary gustatory cortex, was predominantly, but not exclusively, in the right hemisphere, whereas central (more inferior) insular activations were more evenly bilateral.
Multiple trials of each tastant were delivered during recordings made in oral somatosensory (SI) and gustatory cortex (GC).
Two neurons recorded simultaneously in rat gustatory cortex often show, when the oral mucosa is stimulated with effective taste solutions, correlative activities (CAs), which can be quantified with a cross-correlation technique. The present experiment was undertaken (1) to determine the three-dimensional size of putative functional units in rat gustatory cortex on the basis of the interneuronal distance (IND) in individual CA pairs, and (2) to examine to what extent the CA is related to the intrapair similarity in taste responses.
Preliminary data show that GABAergic inhibition can be produced by stimulation of the gustatory cortex.
Significantly higher densities of NADPH-d neurons appeared in the areas of the gustatory cortex, the piriform cortex, the entorhinal cortex and in area 1 of the temporal cortex in DBA/2 mice.
Responses in hindbrain, thalamus, and gustatory cortex identify the quality and concentration of sodium on the tongue.
Moreover, the ketamine-induced blockade of latent inhibition was disrupted by tetrodotoxin injections (10 ng/microl)-induced reversible inactivation of gustatory cortex, applied after each preexposure. A specific gustatory cortex mediation of the ketamine effect is discussed..
It is concluded that temporal coding of taste qualities seems to operate effectively in the gustatory cortex..
We have studied the physiological involvement of protein kinase C (PKC) in the formation of conditioned taste aversion (CTA) by means of microinjections of PKC inhibitors into the gustatory cortex (GC), amygdala (AMY) and thalamic gustatory area at various time-windows of the CTA paradigm.
The amygdala is a taste relay between the primary gustatory cortex, where satiety has no influence on responses to taste stimuli, and the lateral hypothalamic area where the effect of satiety is total.
Our findings suggest that cholinergic neuromodulation participates in processing the CS in the gustatory cortex in CTA, either by encoding novelty at the cellular level, or by instructing the neural circuits to store the novel taste representation..
We have recently shown that in the gustatory cortex of the rat, taste learning enhances protein tyrosine phosphorylation and taste memory is blocked by muscarinic antagonists.
During application of tastants into the oral cavity correlated activities were observed in 27 of 64 neuron pairs recorded simultaneously in the gustatory cortex of anesthetized rats.
The dorsal part of VPMpc projected to the adjacent gustatory cortex.
The release of extracellular acetylcholine (ACh) in the insular gustatory cortex of conscious rats during taste stimulation was measured using the microdialysis technique. Although intraoral infusions of quinine or distilled water caused a significant increase in ACh in the parietal cortex, the magnitude of increased ACh was smaller than that in the gustatory cortex. These results suggest that ACh release in the insular gustatory cortex is related to behavioral expression to aversive taste stimuli..
Lesions of the gustatory cortex (GC) and hippocampus induced moderate effects, but lesions in the other subnuclei of the amygdala, such as the medial and central amygdaloid nuclei, entorhinal cortex, lateral hypothalamic area, and ventromedial hypothalamic nucleus induced slight or no effects.
Neuronal activity was recorded in the gustatory cortex of the golden Syrian hamster in response to application of taste stimuli to the anterior tongue.
Experiment 1 examined the effects of bilateral reversible inactivation of amygdala (Amy), hippocampus (Hipp), gustatory cortex (GC), bed nucleus of stria terminalis (BNST), lateral hypothalamic area (LHA), ventral thalamus (VT) or LHA+VT, induced by intracerebral injection of tetrodotoxin (TTX; 10 ng/microliters per site) applied before i.p.
The gustatory cortex (GC) may modify the strength of this association depending on the nature of the CS, viz., novel or familiar.
There were no changes in choline uptake in the gustatory cortex, the amygdala, or the striatum. There were no correlations between any of the behavioral measures and HAChT in the striatum, gustatory cortex, or the amygdala, or between serotonergic or noradrenergic parameters in the HPC.
To determine the relative contributions of taste and smell in the consumption of alcohol by rats, the present experiment tested normal rats (n = 14) and rats with either gustatory cortex ablations (n = 10), olfactory bulbectomies (n = 11), or combination gustatory cortex and olfactory bulb ablations (n = 12). Results showed that at strong alcohol concentrations (7% through 11%) rats with combined gustatory cortex and olfactory bulb ablations consumed significantly more alcohol than normal control rats. Rats lacking gustatory cortex displayed a similar increased level of consumption with strong alcohol concentrations.
We analyzed the activity of single neurons in gustatory cortex of alert cynomolgus monkeys in response to the four basic taste stimuli and to a range of chemicals, all of which are predominantly sweet to humans.
Application of the protein synthesis inhibitor anisomycin to the rat gustatory cortex before and during training impairs conditioned taste aversion (CTA) to saccharin. Injection of anisomycin to the gustatory cortex immediately prior to the preexposure period attenuates the latent inhibition. These results suggest that protein synthesis in the gustatory cortex is required for normal acquisition of the memory of taste..
Single-neuron activity in the primary gustatory cortex of the alert cynomolgus monkey (Macaca fascicularis) was analyzed in response to a range of taste stimuli.
The activity of single neurons in the gustatory cortex of alert cynomolgus monkeys was analyzed.
Rats that lacked gustatory cortex (GC) learned to avoid drinking sucrose and NaCl, albeit at a slower rate than control rats.
We analyzed the activity of single neurons in gustatory cortex of alert cynomolgus monkeys in response to a range of stimulus intensities. There was no clear evidence of chemotopic organization in the gustatory cortex.
Regional decreases in [ 3H]diprenorphine [ (3H]Dpr) binding, suggesting increased release of an endogenous opioid peptide, were observed in the medial prefrontal cortex, medial septum, gustatory cortex, zona incerta, mediodorsal thalamus, and hippocampus of rats receiving ESLH.
Cortical projections of the VPMM are organized topically; the anterior part of the gustatory cortex receives fibers from the anterodorsal and posteroventral portions of the anterior two-thirds of the VPMM, whereas the posterior gustatory cortex receives fibers from the anteroventral, posterodorsal and posterior portions of the posterior two-thirds of the VPMM.
In order to determine whether the responsiveness of neurones in the primary gustatory cortex is influenced by hunger, the activity of neurones in the gustatory cortex in the frontal operculum was recorded while macaque monkeys (Macaca fascicularis) were fed to satiety. The responses of single neurones in the gustatory cortex to the prototypical taste stimuli glucose, NaCl, HCl and quinine hydrochloride, and to fruit juice, were measured before, while, and after the monkey was fed to satiety with glucose or fruit juice. It is concluded that in the gustatory cortex in the frontal operculum, neuronal responses to gustatory stimuli are not influenced by the normal transition from hunger to satiety. Thus the neurones in the primary gustatory cortex are involved in a motivation-independent analysis of gustatory stimuli, whereas the hypothalamic neurones may be more closely related to the influence of motivational state on behavioural responsiveness to gustatory stimuli..
Retrogradely labelled neurones were found in laminae V and V1 of primary motor cortex, lamina V1 of primary somatosensory cortex, and deep laminae of gustatory cortex; in the reticular thalamic nucleus and zona incerta; and in the caudate-putamen, entopeduncular nucleus, mesencephalic reticular formation and pretectum.
(1) In order to determine whether the responsiveness of neurons in the insular gustatory cortex is influenced by hunger, neuronal activity was analysed in it while macaque monkeys (Macaca fascicularis) were fed to satiety. The responses of single neurons in the insular gustatory cortex to the protypical taste stimuli glucose, NaCl, HCl and quinine HCl, and to fruit juice, were measured before, while, and after the monkey was fed to satiety with glucose or fruit juice. (3) It is concluded that in the insular gustatory cortex, neuronal responses to gustatory stimuli are not influenced by the normal transition from hunger to satiety. Thus the neurons in the insular gustatory cortex are involved in a motivation-independent analysis of gustatory stimuli, whereas the hypothalamic neurons may be more closely related to the influence of motivational state on behavioral responsiveness to gustatory stimuli..
These results provide support for our previous experiments correlating neurophysiological localization of rat gustatory cortex and regional cytoarchitecture, and contrast with the traditional assignation of gustatory cortex to the granular insular area..
Finally the gustatory cortex, which lies just dorsal to the rhinal sulcus, receives a basolateral projection from neurons in the lateroventral one-half of the basolateral nucleus.
We consider the cortex situated posterior to the gustatory cortex in and above the rhinal sulcus as the core region of the rat's (associative) insular cortex, as this cortex receives afferents from the regions of and between the nuclei suprageniculatus and geniculatus medialis, pars magnocellularis.
Activity of 526 neurones from the nucleus of the solitary tract, gustatory thalamus, gustatory cortex, lateral and ventromedial thalamus, and amygdala was recorded in naive or CTA trained rats during the above gustatory discrimination. Presentation of the aversive fluid induced inhibition of unit activity in the gustatory cortex, ventromedial hypothalamus, and amygdala and excitation in the lateral hypothalamus. The results indicate that the gustatory cortex, amygdala and hypothalamus participate in CTA retrieval but a more specific identification of the electrical correlates of memory readout and of drinking control was not possible..
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