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Results for “gustatory cortex”

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PubMed1996

The effect of satiety on responses of gustatory neurons in the amygdala of alert cynomolgus macaques.

An alert cynomolgus macaque was fed a sweet solution to satiety as the activity of a gustatory neuron in the amygdala was recorded to that solution and to four other taste stimuli. This experiment was conducted a total of 14 times in two monkeys. The responses of individual neurons to the satiety stimuli were suppressed by as little as 1%, and as much as 100% by the induction of satiety (mean suppression = 58%). Nine of the 14 cells responded to the satiety solution with excitation, and their responses were suppressed by a mean of 62% by satiety. Five neurons responded with inhibition, and their responses were suppressed by a mean of 50%. Responses to other taste stimuli, not associated with satiety, were affected to a lesser extent. 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. The data presented here indicate that the amygdala is a functional as well as anatomical intermediary between these two areas, and serves as a stage in the process through which sensory stimuli are imbued with motivational significance.

Amygdala↗

PubMed1998

The taste of sodium.

Sodium is crucial to physiological function. The responsibility for detecting it is assumed by the taste system, which devotes perhaps one quarter of its resources to the task. Sodium is transduced by passage into a subset of receptor cells, whose activity is relayed to the brain through a discrete gustatory channel. Responses in hindbrain, thalamus, and gustatory cortex identify the quality and concentration of sodium on the tongue. Coding of reinforcement may begin with the pons and ventral forebrain, particularly the lateral and medial hypothalamic nuclei. When body stores are sufficient, behavioral preference for sodium is mild, encompassing low concentrations and marked by weak avidity. This languid response disappears during sodium shortages. Avidity increases, and hypertonic concentrations are most preferred. This behavioral change may result from altered responsiveness in sodium-specific neurons that offer the sodium signal access to mechanisms of reinforcement. Thus, the taste system detects and recognizes sodium, and accords it a reward value commensurate with the needs of the animal.

Animals↗

PubMed2005

Preferring one taste over another without recognizing either.

Stimuli can be discriminated without being consciously perceived and can be preferred without being remembered. Here we report a subject with a previously unknown dissociation of abilities: a strong behavioral preference for the taste of sugar over saline, despite a complete failure of recognition. 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.

Aged↗

PubMed1997

Sensitivity of rat cortical neurons in distinguishing taste qualities by individual and correlative activities.

To examine the possibility that different taste qualities are represented by the correlative activity of cortical gustatory neurons, we made simultaneous recordings of neuron pairs during application of four basic tastes into the oral cavity of anesthetized rats and the following observations were made: (i) in 30 of 67 pairs of taste responsive neurons, peaks (troughs in a few cases) were produced in the cross-correlograms (CCs) during stimulation with some tastants; (ii) the correlative discharges occupied 6-8% of the total spikes discharged by individual neurons during taste stimulation and occurred, in a considerable number of cases, even during stimulation with tastants to which one or both of the component neurons of a pair were apparently non-responding (often sucrose and quinine); (iii) the number of tastants to which a neuron pair responded with a significant correlative activity was often greater than the number of tastants to which the component neurons of the same pair responded with significant changes in discharge rate; (iv) there was no significant difference between the correlative (formation of peaks or troughs in the CC) and individual (change in discharge rate of individual neurons) ways of coding in the sensitivity to distinguish between two taste qualities ranked to be adjacent on the basis of the number of spikes composing the response; and (v) the peaks or troughs appearing in two CCs during stimulations with two kinds of tastants were compared with regard to overlapping of their delay ranges and widths. The spikes in the non-overlapping portion of each peak (suppressed spike number in the case of troughs) are supposed to be able to contribute to two-taste discrimination: the correlated discharges occurring with a delay time that corresponds to the overlapping portion can in no way be judged differently, but the spikes falling in the non-overlapping portion may contribute to the differentiation. The ratio of the non-overlapping portion to the entire peak (or trough) was 0.35 on average. It is concluded that temporal coding of taste qualities seems to operate effectively in the gustatory cortex.

Animals↗

PubMedDate not supplied

Hippocampal inactivation enhances taste learning.

Learning tasks are typically thought to be either hippocampal-dependent (impaired by hippocampal lesions) or hippocampal-independent (indifferent to hippocampal lesions). Here, we show that conditioned taste aversion (CTA) learning fits into neither of these categories. Rats were trained to avoid two taste stimuli, one novel and one familiar. Muscimol infused through surgically implanted intracranial cannulae temporarily inactivated the dorsal hippocampus during familiarization, subsequent CTA training, or both. As shown previously, hippocampal inactivation during familiarization enhanced the effect of that familiarization on learning (i.e., hippocampal inactivation enhanced latent inhibition of CTA); more novel and surprising, however, was the finding that hippocampal inactivation during training sessions strongly enhanced CTA learning itself. 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. Thus, we suggest that hippocampal memory processes interfere with the specific learning mechanisms underlying CTA, and more generally that multiple memory systems do not operate independently.

Animals↗

PubMed2005

Protein synthesis underlies post-retrieval memory consolidation to a restricted degree only when updated information is obtained.

Consolidation theory proposes that through the synthesis of new proteins recently acquired memories are strengthened over time into a stable long-term memory trace. However, evidence has accumulated suggesting that retrieved memory is susceptible to disruption, seeming to consolidate again (reconsolidate) to be retained in long-term storage. 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. Our results suggest that retrieved memory can be modified as part of a mechanism for incorporating updated information into previously consolidated memory.

Analysis of Variance↗

PubMed1991

Gustatory neural coding in the monkey cortex: stimulus intensity.

1. We analyzed the activity of single neurons in gustatory cortex of alert cynomolgus monkeys in response to a range of stimulus intensities. Chemicals were deionized water, fruit juice, and several concentrations of the four prototypical taste stimuli: 10(-3)-1.0 M glucose, 10(-3)-1.0 M NaCl, 10(-4)-3 x 10(-2) M HCl, and 10(-5)-3 x 10(-3) M quinine HCl. 2. Taste-evoked responses could be recorded from a cortical gustatory area that measured 2.5 mm in its anteroposterior extent, 6.0 mm dorsoventrally, and 3.0 mm mediolaterally. Taste-responsive cells constituted 62 (3.7%) of the 1,661 neurons tested. Nongustatory cells gave responses associated with mouth movement (10.1%), somatosensory stimulation (2.2%), and approach or anticipation (0.9%). 3. Intensity-response functions were determined across 62 gustatory neurons. Neural thresholds for each stimulus quality conformed well to human psychophysical thresholds. Mean discharge rate was a direct function of stimulus concentration for glucose, NaCl, and quinine HCl. The most effective of the basic stimuli was glucose. 4. Power function exponents were calculated from the responses of neural subgroups most responsive to each basic stimulus. Those for glucose, NaCl, and quinine were within the range of psychophysically derived values. Thus the perceived intensity of each basic quality is presumably based on the activity of the appropriate neural subgroup rather than on the mean activity of all taste cells. 5. The mean breadth-of-tuning (entropy) coefficient for 62 gustatory neurons was 0.65 (range, 0.00-0.98). 6. There was no clear evidence of chemotopic organization in the gustatory cortex. 7. An analysis of taste quality indicated that sweet stimuli evoked patterns of activity that were clearly distinct from those of the nonsweet chemicals. Among the latter group, NaCl was differentiable from HCl and quinine HCl, whose patterns were closely related. 8. The response characteristics of cortical taste cells imply gustatory thresholds and intensity-response functions for the nonhuman primate that conform well to those reported in psychophysical studies of humans, reinforcing the value of this neural model for human taste intensity perception.

Action Potentials↗

PubMed1983

Cortical and thalamic afferent connections of the insular and adjacent cortex of the rat.

Thalamic and cortical afferents to the insular and perirhinal cortex of the rat were investigated. Unilateral injections of horseradish peroxidase (HRP) were made iontophoretically along the rhinal sulcus. HRP injections covered or invaded areas along the rhinal fissure from about the level of the middle cerebral artery to the posterior end of the fissure. The most anterior injection labeled a few cells in the mediodorsal nucleus. More posterior injections labeled neurons in the basal portion of the nucleus ventralis medialis, thus suggesting that this cortical region constitutes the rat's gustatory (insular) cortex. 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. It includes parts of the cortex termed perirhinal in other studies. The cortex dorsal and posterior to the insular cortex we consider auditory cortex, as it receives afferents from the principal part of the medial geniculate nucleus, and the cortex ventral to the insular cortex (below the fundus of the rhinal sulcus) we consider to constitute the prepiriform cortex, which is athalamic. The posterior part of the perirhinal cortex (area 35) receives afferents from nonspecific thalamic nuclei (midline nuclei). Cortical afferents to the injection loci arise from a number of regions, above all from regions of the medial and sulcal prefrontal cortex. Those injections confined to the projection cortex of the suprageniculate-magnocellular medial geniculate nuclear complex also led to labeling in contralateral prefrontal regions, particularly in area 25 (infralimbic region). A comparison of our results with those on the insular cortex of cats and monkeys suggests that on the basis of thalamocortical connections, topographical relations, and involvements of neurons in information processing and overt behavior, the insular cortex has to be regarded as a heterogeneous region which may be separated into prefrontal insular, gustatory (somatosensory) insular, and associative insular portions.

Afferent Pathways↗

PubMed1992

Gustatory neural coding in the monkey cortex: L-amino acids.

1. 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. Tastants included the four prototypical stimuli (glucose, NaCl, HCl, and quinine), fruit juice, and 12 amino acids selected for their chemical characteristics, nutritional significance, and biological importance, as well as for the availability of human psychophysical data on their perceived qualities. 2. Taste-evoked responses could be recorded from a cortical area that measured 3.5 mm in its anteroposterior extent, 2.0 mm mediolaterally, and 6.0 mm dorsoventrally. Gustatory cells constituted 4.8% of the 1,129 neurons tested. Nongustatory cells gave responses associated with mouth movements (11.1%), somatosensory stimulation (3.8%), approach or anticipation of the taste stimulus (2.2%), and tongue extension (0.4%). 3. The most effective taste stimuli were those with qualities that humans describe as salty or sweet: NaCl, monosodium glutamate, glucose, proline, glycine, and fruit juice. The least effective tastants were those rated bitter or insipid: tyrosine, tryptophan, phenylalanine, and leucine. Accordingly, 79% of the gustatory neurons responded best to glucose (46%) or NaCl (33%) among the basic stimuli; only 19% responded best to quinine (13%) or HCl (6%). One cell (2%) responded exclusively to fruit juice. 4. Cortical gustatory neurons showed a moderate breadth of sensitivity, with a mean breadth of tuning coefficient of 0.71 across 54 cells. There was no evidence of chemotopic organization in the taste cortex. 5. The taste quality of each stimulus was inferred from the relative similarity of the profiles they evoked. The clearest distinction among stimuli was between those that humans characterize as sweet versus those with other qualities. Several amino acids that have dominant sweet (glycine and proline), salty (arginine and monosodium glutamate), sour (tryptophan), or bitter (phenylalanine) components to humans evoked activity profiles that were associated with those of the appropriate prototypical stimuli. Others (cysteine and lysine) were not closely related to any single prototype. 6. Conclusions based on the responses of cortical cells in the monkey are in close agreement with those that derive from human psychophysical studies of L-amino acids, reinforcing the value of this neural model for human taste perception.

Amino Acids↗

PubMed1993

Gustatory neural coding in the monkey cortex: the quality of sweetness.

1. 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. 2. We recorded taste-evoked responses from a cortical area that measured 4.0 mm in its anteroposterior extent, 5.6 mm dorsoventrally and 2.2 mm mediolaterally. Taste-responsive neurons constituted 4.7% of the 3,066 neurons tested in the course of 66 recording tracks. Nongustatory cells included those responsive to mouth movement (34.1%), tongue touch (1.9%), stimulus approach (0.7%), and tongue extension (0.5%). The functions of 58.2% of the cells we isolated could not be determined. 3. The mean breadth of tuning of these cortical taste neurons was a moderate 0.59 (range 0.00-0.93). 4. There was no evidence that taste cells with similar functional attributes were clustered in the cortex, i.e., there was no apparent topographic organization of taste qualities. 5. A taste space was generated from the correlations among patterns of neural activity evoked by the stimulus array. Within the space, NaCl was most isolated from other stimuli; the profiles elicited by HCl, quinine HCl, and water were all moderately intercorrelated and were clearly distinct from the cluster of sweet stimuli. 6. The 19 sweet chemicals formed a coherent cluster centered on the simple carbohydrates (glucose, fructose, sucrose, maltose) and sorbitol. Nearest this core were calcium cyclamate, aspartame, and cran-raspberry juice. In the next concentric ring were acesulfame potassium, xylose, xylitol, sorbose, polycose, and myoinositol. Increasingly distant from the sugars were sodium saccharin, stevioside, neohesperidin DHC, L-tryptophan and monellin. 7. We compared these results with those of a human psychophysical study of sweet stimuli. Using the position of glucose as a reference, we measured the distances to all other stimuli that were common to the two studies (n = 15). The correlation between the human psychophysical data and those derived from evoked activity in the macaque cortex was +0.82. 8. The high correlation between human psychophysical and macaque electrophysiological data implies that the subtle distinctions among stimuli that are predominantly sweet are quite similar for these two species and reinforces the value of this neural model for human taste perception.

Action Potentials↗

PubMed1998

Neurons in the posterior insular cortex are responsive to gustatory stimulation of the pharyngolarynx, baroreceptor and chemoreceptor stimulation, and tail pinch in rats.

Extracellular unit responses to gustatory stimulation of the pharyngolaryngeal region, baroreceptor and chemoreceptor stimulation, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Of the 32 neurons identified, 28 responded to at least one of the nine stimuli used in the present study. Of the 32 neurons, 11 showed an excitatory response to tail pinch, 13 showed an inhibitory response, and the remaining eight had no response. Of the 32 neurons, eight responded to baroreceptor stimulation by an intravenous (i.v.) injection of methoxamine hydrochloride (Mex), four were excitatory and four were inhibitory. Thirteen neurons were excited and six neurons were inhibited by an arterial chemoreceptor stimulation by an i.v. injection of sodium cyanide (NaCN). Twenty-two neurons were responsive to at least one of the gustatory stimuli (deionized water, 1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose); five to 11 excitatory neurons and three to seven inhibitory neurons for each stimulus. A large number of the neurons (25/32) received converging inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (23/32) received converging inputs from different modalities (gustatory, visceral, and tail pinch). The neurons responded were located in the insular cortex between 2.0 mm anterior and 0.2 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.2 mm (n=28) anterior to the AC. This indicates that most of the neurons identified in the present study seem to be located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from gustatory, baroreceptor, chemoreceptor, and nociceptive organs.

Animals↗

PubMed1996

The primary gustatory area in human cerebral cortex studied by magnetoencephalography.

Magnetic fields (MFs) from gustatory stimulation with 1 M NaCl and 3 mM saccharin were recorded from the human brain by using a whole-cortex SQUID system. The averaged onset latency of MFs was 93 ms for NaCl and 172 ms for saccharin and no response was obtained for water. A high correlation coefficient was noted between the difference of onset MFs latencies in two tastants and that of behavioral reaction times, and responses to saccharin were delayed or abolished after treatment of a subject's tongue with a sweet-suppressing agent. This finding indicates that the MFs obtained were caused by gustatory stimulation. By plotting the estimated current dipole on the magnetic resonance image, we could locate the primary gustatory area at the transition area between the operculum and insula, as reported in macaque monkeys.

Adult↗

PubMed1978

An experimental study of the central gustatory pathways in the monkey, Macaca mulatta and Cercopithecus aethiops.

1. The cortex at the base of the central fissure, that is the fronto-parietal operculum, represents primary sensory receptive cortex for gustatory modalities. 2. This primary receptive cortex for taste is linked to the anterior Island of Reil by short inter- and intracortical association fibers. Thus the anterior island is a gustatory association area involved in the subjective recognition of gustatory modalities. 3. The nucleus ventralis posteromedialis pars parvocellularis of the dorsal thalamus is the thalamic receptive nucleus for gustatory impulses in the macaque. 4. Fibers which originate at rostral glossopharyngeal levels from the dorsal visceral gray terminate in the contralateral mucleus ventralis posteromedialis pars parvocellularis.

Animals↗

PubMed1999

Gustatory neural coding in the cortex of the alert cynomolgus macaque: the quality of bitterness.

We sought to define the gustatory neural representation in primates for stimuli that humans describe as predominantly bitter. Thus we analyzed the responses of single neurons from the insular cortex of two alert, male cynomolgus macaques in response to the oral application of four basic taste stimuli (glucose, NaCl, HCl, and quinine HCl) and fruit juice, and to a series of 15 other chemicals to which humans ascribe a bitter component. Gustatory neurons occupied a volume of 109 mm3 across an area of 4.0 mm in the anterposterior plane, 4.4 mm in the mediolateral, and 6.2 mm in the dorsoventral. Taste cells represented 161 (8.6%) of the 1881 neurons tested for chemical sensitivity. Fifty of these could be monitored throughout the delivery of the entire stimulus series, and their responses constitute the data of this study. The mean spontaneous discharge rate of the cortical gustatory cells was 3.2 +/- 3.3 spikes/s (range = 0.2-17.7 spikes/s). The mean breadth-of-tuning coefficient was a moderate 0.77 +/- 0.15 (range = 0.25-0.99). Forty-eight neurons responded to taste stimuli with excitation, and two responded with inhibition. Forty-one of the 50 neurons were able to be classified into one of four functional types based on their responses to the four basic stimuli used here. These were sugar (n = 22), salt (n = 7), acid (n = 7), and quinine (n = 5). A two-dimensional space was generated from correlations among the response profiles elicited by the stimuli array. The 16 bitter chemicals formed a coherent group that was most closely related to HCl, moderately to NaCl, and bore no relationship with glucose. Within the bitter stimuli, six formed a subgroup that was most separated from all nonbitter chemicals: quinine HCl, phenlythiocarbamide, propylthiouracil, caffeine, theophylline, and phenylalanine. Humans describe these stimuli as rather purely bitter. Of the remaining 10 bitter compounds, 4 were on the fringe of the bitter group leading to NaCl: MgCl2, CaCl2, NH4Cl, and arginine. Humans characterize these as bitter-salty. Three were on the fringe leading to HCl: urea, cysteine and vitamin B1. Humans call these bitter-sour. The remaining three (nicotine, histidine, and vitamin B2) occupied the center of the bitter group. Taste quality, inferred from the position of each stimulus in the space, correlated well with human descriptions of the same stimuli, reinforcing the value of the macaque as a neural model for human gustation.

Action Potentials↗

PubMed2003

Age-dependent appearance of an insulo-parietal cortical signal propagation that elicits a synchronized population oscillation in the parietal cortex in rats.

We investigated postnatal development of a functional connectivity from the gustatory insular cortex to the parietal cortex, which is known to contain many more neurons responding to oral somesthetic stimulation than the insular cortex, in slices obtained from 9-35-day-old rats. Field potentials were evoked by stimulation to the insular cortex. In the mature cortex, insular stimulation elicited a solitary field potential in both the insular and parietal cortices and, as the simulation continued, the initial solitary potential came to be followed by a population oscillation of field potential in the parietal cortex, but not in the insular cortex. In the immature cortex, by contrast, insular stimulation failed to evoke both the initial solitary potential and the subsequent population oscillation in the parietal cortex. In the mature cortex, application of neither thapsigargin nor AP5 prevented elicitation of the initial solitary potential in the parietal cortex, but either of them abolished the parietal oscillation. In immature cortex bathed with low Mg(2+) medium, insular stimulation elicited both the initial solitary potential and the subsequent parietal oscillation, which were both prevented by thapsigargin or AP5. Theses results suggest that the insular and parietal cortices are anatomically connected but functionally unlinked at an early postnatal stage, and that a functional linkage, dependent both on NMDA and ryanodine receptors, is formed during the first postnatal month.

2-Amino-5-phosphonovalerate↗

PubMed1995

Gustatory neural coding in the monkey cortex: acid stimuli.

1. We sought to define the gustatory neural code for acidic stimuli. Therefore we analyzed the responses of 44 single neurons in the insular cortex of four alert cynomolgus macaques in response to the oral application of four basic taste stimuli (glucose, NaCl, HCl, and quinine HCl) and fruit juice, and to a series of 20 additional acids. 2. Neurons responsive to gustatory stimulation were encountered within a volume of 38.2 mm3 (3.5 mm anteroposterior x 2.1 mm mediolateral x 5.2 mm dorsoventral). Taste cells constituted 81 (5.2%) of the 1,552 neurons whose sensitivities were tested. Of these, the activity of 44 was followed through at least one complete application of the stimulus series, and those responses compose the data of this study. Nongustatory cells included those responsive to mouth movements (36.3%), tactile stimulation within the mouth (2.1%), visual approach of the taste stimulus (1.4%), and extension of the tongue (0.1%). The functions of the remaining 54.8% were not determined. 3. The mean spontaneous discharge rate of these cortical taste cells was 3.0 spikes/s (range 0.0-14.4 spikes/s). The mean breadth of tuning coefficient was a moderate 0.72 (range 0.26-0.98). Most evoked activity was excitatory, although inhibition was a prominent response option for four (9%) taste cells. 4. There was no evidence that taste cells with similar functional characteristics were clustered within the cortex, i.e., there was no apparent topographic organization of taste quality. 5. Thirty-four of the 44 cells were divisible into three functional types on the basis of their response profiles to the four basic stimuli used here.(ABSTRACT TRUNCATED AT 250 WORDS)

Acids↗

PubMed2006

NMDA receptor antagonist MK-801 infused into the insular cortex prevents the attenuation of gustatory neophobia in rats.

Gustatory neophobia dissipates with repeated exposures to an initially novel taste solution. The aim of the present study was to determine whether NMDA receptors in the insular cortex are involved in this experience-dependent process. Results showed that acute microinfusion of MK-801 into the insular cortex prevented the attenuation of gustatory neophobia indicating that this process is an NMDA receptor-dependent phenomenon.

Animals↗

PubMed2004

Dual separate pathways for sensory and hedonic aspects of taste.

It is proposed that in the gustatory system there exist separate sensory and hedonic (reward-aversion) representations in each of the primary structures in which processing of gustatory stimuli occurs. Anatomical and physiological data are used to determine putative separate sensory and hedonic representations in the nucleus of the solitary tract, parabrachial complex, gustatory thalamus, and cortical gustatory areas. In the nucleus of the solitary tract, the sensory representation is located in the rostralmost part of the nucleus, and the hedonic representation most probably in the intermediate parts. In the parabrachial complex, the sensory representation is located in the central medial and ventral lateral subnuclei, and in the waist area, and the hedonic representation in the inner division of the external lateral subnucleus and in the external medial subnucleus. In the rodent gustatory thalamic relay, the sensory representation occurs in the dorsal lateral parts of the nucleus, and the hedonic representation in the ventromedial parts. In rodent gustatory insular cortex, the sensory representation is found in anterior parts of the gustatory area, and the hedonic representation caudal to the sensory representation. The function of the separate sensory and hedonic representations is discussed in relation to the conditioned taste aversion paradigm.

Animals↗