Cortical Taste Research Articles

Chemotopic Arrangement for Taste Quality Discrimination in the Cortical Taste Area

Signals from various sensory organs are delivered to the brain where sensory information is generated from the signals. The information is represented on the brain in the form of temporal and spatial codes, which enable us to create inner an representation of the outer world (Florey, 1990). In the neocortex, the information consisting of the spatial codes is principally arranged in the primary sensory area as a receptive field, by way of anatomical column formation. The information consisting of temporal codes, such as frequency and phase dynamics, also plays an important role for synchronization of neural activities or strengthening signal amplitudes. Interaction or integration of the information by way of intra-cortical or cortico-cortical connections enables the temporal and spatial codes to link (Singer and Gray, 1995; Gilbert et al., 1996; Salinas and Sejnowski, 2001). As for taste information processing, controversy still exists as to whether cortical taste neurons use temporal codes or spatial codes for discriminating taste information in the cortical taste area. However, it may be presumed that cortical taste neurons use spatial codes as well as frequency codes in order to discriminate taste information efficiently. Previous electrophysiological studies predict that there is a chemotopic arrangement for taste quality discrimination in the cortical taste area, but this hypothesis has not been confirmed because of lacking for the evidence with high resolution of spatial dimension. Optical imaging based on intrinsic signals has a high spatial resolution (Frostig et al., 1990) and is useful for studying the functional organization of the brain (Bonhoeffer and Grinvald, 1996). Here, we investigated the spatial aspects of optical intrinsic signal (OIS) responses in the gustatory insular cortex that were elicited by delivering a solution of tastants on the tongue.

P.6.065 Anti-stigma projects against the discrimination of psychiatric patients. A literature search and a world-wide survey

To investigate the neural encoding of glutamate taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex taste area, with a small number in adjacent taste areas. First, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. The correlation between the responses to these two tastants was higher than between any other pair of tastants, which included glucose (sweet), sodium chloride (salty), HCl (sour), and quinine HCl (bitter). Accordingly, the responsiveness to glutamic acid clustered with the response to monosodium glutamate in a cluster analysis with this set of stimuli, and glutamic acid was close to sodium glutamate in a space created by multidimensional scaling. Second, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Third, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fourth, neurons have not yet been found in this cortical region that showed synergism of monosodium glutamate and the nucleotide inosine 5′-monophosphate: it was shown that mixtures of 0.0001 M inosine 5′-monophosphate with different concentrations (0.001, 0.01, and 0.1 M) of monosodium glutamate did not have a greater effect than the monosodium glutamate alone. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety. In some cases this reduction was sensory-specific. These findings show that the taste neurons activated by monosodium glutamate can also be activated by other umami tastants, including glutamic acid and the nucleotide inosine 5′-monophosphate. The responses to these umami tastants were more similar to each other than to any of the other prototypical tastant, providing evidence that in this system umami is encoded differently from the other tastants. Moreover, the findings with these tastants provide additional evidence that the responses to monosodium glutamate are not due just to activation of a sodium taste channel.

Cortical spatial aspects of optical intrinsic signals in response to sucrose and NaCl stimuli.

To examine whether cortical taste neurons use spatial codes for discriminating taste information, we investigated the spatial aspects of optical intrinsic signal (OIS) responses in the gustatory insular cortex (GC) elicited by the administration of two essential tastants, sucrose and NaCl, on the tongue. OIS responses to sucrose appeared in the rostral part of the GC, whereas those to NaCl appeared in the central part of the GC. Local anesthetization of the tongue abolished OIS responses, and the administration of distilled water elicited no OIS response. Thus, taste information elicited by sucrose and NaCl from the peripheral sensory organs is segregated in the GC, suggesting that the information from two essential tastants is assembled as spatial codes in the primary cortical taste area through the process of taste quality perception.

Taste-related activity in the human dorsolateral prefrontal cortex

Taste remains one of the least-explored human senses. Cortical taste responses were investigated using neuroimaging in 40 subjects tasting a range of different taste stimuli compared to a neutral tasteless control. Activation was found in the anterior insula/frontal opercular taste cortex and caudal orbitofrontal cortex, both areas established as taste cortical areas by neuronal recordings in primates. A novel finding in this study was a highly significant response to taste in the dorsolateral prefrontal cortex. This may reflect an effect of taste on cognitive processing to help optimise or modify behavioural strategies involved in executive control; or it could reflect the engagement of this region in attentional processing by a taste input.

Responsiveness of the cortical taste area neurons to a mixture of the four basic tastants in rats.

The taste coding mechanism in the cortical taste area was investigated by analyzing the responses of 59 neurons in the cortical taste area of the anesthetized rat to a mixture of the four basic tastants in both absence and presence of bicuculline methiodide, a specific antagonist to the GABA(A) receptors. The mixture caused response suppression more frequently than response facilitation, both in the control state and during bicuculline application. Cluster analysis revealed that only a group of the neurons with the best response to both NaCl and HCl (group NH) showed the best response to the mixture in the control state, whereas during bicuculline application, in addition to group NH, two other groups of neurons responding to sucrose, or to HCl and quinine responded vigorously to the mixture. Multidimensional scaling located the mixture outside the space of the four basic tastants facing an NaCl-HCl line in both states. GABAergic inhibition caused the group NH to represent the taste of the mixture in the control state. Thus, the mixture probably tastes salty and sour to rats. No cortical neuron was found which specifically responded to the mixture.

Columnar organization of mechanoreceptive neurons in the cortical taste area in the rat.

Mechanoreceptive neurons with or without taste responsiveness were recorded in the cortical taste area (CTA) of rats every 50 or 100 micro m along an electrode track made as perpendicular to the surface as possible. Three groups of mechanoreceptive neurons were recognized based on the adequate stimulus, i.e., low-threshold mechanoreceptive ( n=16), nociceptive-specific ( n=48), and wide-dynamic range neurons ( n=392). Except for nine neurons, almost all had receptive fields (RFs) in the oral cavity ( n=447). They were categorized into three RF types: those with RFs only in the oral cavity (OC type; n=23), those with RFs both in the oral cavity and on the lip (OL type; n=44) and those with RFs in the oral cavity and on the external surface of the body (WB type; n=380), e.g., tail. Neurons with inhibitory RFs were often located in the infragranular layers. Several neurons with the same receptive features were sequentially recorded along the track, suggesting the presence of columnar organization. The diameter of the possible functional column was the largest (mean 113.85 micro m) for WB type neurons, but smaller in the other two types (mean 85 micro m for the OC type and 62.5 micro m for the OL type). Neurons were segregated according to the adequate stimulus within the column for WB type neurons. Taste-responsive mechanoreceptive neurons ( n=33) were recorded at 15 tracks, and two taste neurons were sequentially recorded in five cases, in three of which two successive neurons sharing the best stimulus were recorded. Taste neurons are possibly arranged in a column with a very small diameter within the large column of mechanoreceptive neurons.

Neurons in the cortical taste area receive nociceptive inputs from the whole body as well as the oral cavity in the rat

Almost all mechanoreceptive neurons in the cortical taste area (CTA) of the rat had receptive fields (RFs) in the oral cavity, except for a few neurons at the border with the primary somatosensory area that had RFs on the contralateral rhinarium or upper lip. About one-third of the mechanoreceptive neurons with RFs in the oral cavity had additional RFs on the tips of limbs, earflaps or tail, i.e. the glabrous skin or skin with sparse hairs of the external surface of the body (whole body type). Most of these neurons received both innocuous and noxious inputs (wide dynamic range type), but some had either type of input (low threshold mechanoreceptive or nociceptive specific type). Some nociceptive neurons were responsive to taste, as previously found. Nociceptive neurons with the whole body type of RFs were diffusely distributed across the CTA without clustering. The corticocortical afferents, probably originating from the visceral part of the insula, may code body condition to modulate the taste responsiveness of the cortical taste neurons.

Callosal connections of the cortical taste area in rats

The granular and dysgranular insular subregions of the cortical taste area in rats are shown to connect anatomically with the homotopical regions in the opposite hemisphere through the corpus callosum. Cells of callosal efferents and terminals of callosal fibers were found in almost all cortical layers. The findings clarify the current understanding of the morphological substrate of callosal interactions in the gustatory system.

The representation of umami taste in the human and macaque cortex

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate which is separate from the representation of the other prototypical tastants sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration-response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety, revealing a mechanism of satiety. In some cases this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g. monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex. Seventh, in neuroimaging experiments with functional magnetic resonance imaging (fMRI) in humans, it was shown that in humans umami taste produced by monosodium glutamate or by inosine monophosphate produced activation in a region of the anterior insula which is the putative human primary taste cortex and in a part of the orbitofrontal cortex which is the putative human secondary taste cortex.

Effects of reversible block of callosal afferent inputs on the response characteristics of single neurons in the cortical taste area in rats.

We examined the change in magnitude of the taste responses of single neurons in the cortical taste area (CTA) in one side by reversibly blocking the CTA in the other side with a local anesthetic, procaine-HCl, in urethane-anesthetized rats. Taste responses of 68 taste neurons were continuously recorded for up to 2 h until recovery from the treatment, and those in 50 of them were found to be affected significantly. No remarkable difference was noted in the spatial distribution of the affected and non-affected neurons in the CTA. Many of the affected neurons were located in layers IV and V of area GI and in layer V of area DI. In most cases, changes in the taste responses of single neurons were in one direction, i.e., either a decrease or an increase, but in a few cases they decreased or increased depending on the stimulus. The taste profile of callosal inputs was estimated by subtracting responses after treatment from the control responses before treatment. The results suggest that the CTAs on both sides are functionally connected by way of callosal fibers as anatomical studies indicate, and that the CTA in one side receives excitatory or inhibitory inputs from the other side.

Action of calcitonin gene-related peptide (CGRP) and substance P on neurons in the insular cortex and the modulation of taste responses in the rat.

Using multibarrel electrodes, recordings were made from single neurons in the insular cortex including the cortical taste area (CTA) of urethane-anesthetized rats. The effects of an iontophoretic application of calcitonin gene-related peptide (CGRP) and substance P (SP) on the spontaneous discharges and taste responses were tested. In a total sample of neurons (mostly non-taste), CGRP affected the spontaneous discharges in 35.6% of the 571 neurons studied and SP in 38.3% of the 775 neurons studied. The effects were mostly (approximately 85-87%) facilitatory. Peptide-sensitive neurons were found at a similar frequency in all three insular areas-granular, dysgranular and agranular (areas GI, DI and AI). This is in contrast to previous reports that CGRP receptors were rich in area DI and CGRP-immunoreactive afferents numerous in area AI, but consistent with previous reports that the distribution of SP receptors and SP fibers was dense in the insular cortex. In approximately 40% of the 76 taste neurons recorded from areas GI and DI, the peptides affected the spontaneous discharges (mostly facilitated). When the taste responses were examined during application of the peptides, significant (mainly depressant) effects were seen in 61% of 18 neurons for CGRP and in 70.5% of 17 for SP. Such effects were not recognized on responses to specific taste stimuli and were not correlated with the effects on the spontaneous discharges. The findings indicate that both peptides modify taste coding in CTA neurons presynaptically and/or postsynaptically, independently of the existence of receptors on the neurons.

Artificial neural networks estimate the contribution of taste neurons to coding

Taste qualities are believed to be coded in the activity of populations of taste neurons. However, it is not clear whether all neurons are equally responsible for coding. To clarify the point the relative contribution of each taste neuron to coding was assessed by constructing simple three-layer neural networks with input neurons that represent cortical taste neurons of the rat. The networks were trained by the back-propagation learning algorithm to classify the neural response patterns to the basic taste stimuli (sucrose, HCl, quinine–hydrochloride, and NaCl). The networks had four output neurons representing the basic taste qualities, the values of which provide a measure for similarity of test stimuli to the basic taste stimuli. We estimated relative contributions of input neurons to the taste discrimination of the network by examining their significance S j , which is defined as the sum of the absolute values of the connection weights from the jth input neuron to the hidden layer. When the input neurons with a smaller S j (e.g., 15 out of 39 input units) were “pruned” from the trained network, the ability of the network to discriminate the basic taste qualities was not greatly affected. On the other hand, the taste discrimination of the network progressively deteriorated much more rapidly with pruning of input neurons with a larger S j . These results suggest that cortical taste neurons differentially contribute to the coding of taste qualities. Input neurons with a larger S j tended to be with a larger variation of neural discharge rates to the basic taste stimuli. The variation of neural discharges may be important in the coding of taste qualities.

The Representation of Umami Taste in the Taste Cortex

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste-responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate that is separate from the representation of the other prototypical tastants, sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5'-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration-response curves showed that concentrations of monosodium glutamate as low as 0.001 mol/L were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioral satiety, revealing a mechanism of satiety. In some cases, this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g., monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex.

Chemcial aspects of information processing in gustatory cortex : Contribution of neurotransmitters and neurornodulators to the formation of taste profiles of cortical taste neurons

Chemcial aspects of information processing in gustatory cortex : Contribution of neurotransmitters and neurornodulators to the formation of taste profiles of cortical taste neurons

The neurophysiology of taste and olfaction in primates, and umami flavor.

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate which is separate from the representation of the other prototypical tastants sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5'-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioral satiety, revealing a mechanism of satiety. In some cases this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g., monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex.

GABAergic inhibition and modifications of taste responses in the cortical taste area in rats

Using multibarrel electrodes, recordings were made in the cortical taste area (CTA), specifically in the granular and dysgranular parts of the insular cortex (areas GI and DI), of urethane-anesthetized rats. The effects of an iontophoretic application of γ-aminobutylic acid (GABA) and bicuculline methiodide (BMI), a specific antagonist to the GABA A receptor, were tested. GABA decreased background discharges in ca. 69% of 509 neurons in both areas, and in ca. 58% of 64 taste neurons. BMI antagonized the inhibitory action of GABA in CTA neurons and facilitated background discharges in ca. 51% of the 390 neurons tested, including ca. 69% of the 52 taste neurons, which indicates that CTA neurons have GABA A receptors to receive inhibitory inputs from interneurons. In both areas, the effects of BMI (6–20 nA) on taste responses of the 85 CTA neurons (49 and 36 in areas GI and DI, respectively) to the four basic taste stimuli were examined: 65 neurons were recognized in the absence of BMI, whereas 20 only in the presence of the drug. BMI increased taste responses in 25 of the former group and changed the type of their response profiles in 25 including 12 neurons whose responses were increased. It also changed the best stimulus in 34 neurons. The drug affected the receptive fields in almost all cases examined ( n=23) and increased the size in 78.2% when the value for all four basic taste stimuli were totaled. New receptive fields were uncovered by BMI in varying regions of the oral cavity depending on the taste stimulus. But the drug decreased taste responses in several neurons ( n=8). These findings indicate that the GABAergic inhibitory system apparently contributes to modifying or selecting taste information in both areas of the CTA.

Plasticity of cortical taste responses in the Human: a joint psychophysical and fMRI study.

Plasticity of cortical taste responses in the Human: a joint psychophysical and fMRI study.

Cortical connections of the primary somatosensory cortex and cortical taste area in rats

The EU legislation requests post-market environmental monitoring (PMEM) of a genetically modified (GM) organism even if its pre-market risk assessment indicated negligible risks. It has been claimed that the monitoring of the only currently commercially cultivated GM plant in the EU, Bt MON810 maize, has not revealed any adverse effects. However, the implementation of its PMEM has been criticised repeatedly by the European Food Safety Authority (EFSA).Although EFSA agreed with the monitoring plan consisting of four tools, as proposed by the company which markets MON810, in practice PMEM has relied on famers’ questionnaires, a farmers’ complaint system, and a literature survey. The fourth approach, environmental surveillance networks, has not been utilised yet. Furthermore, PMEM requires that farmers plant a refuge of non-Bt maize in order to sustain the efficiency of the plant in combating the targeted pest.This paper aims to contribute to improved PMEM by means of a critical evaluation of its implementation in the Czech Republic based on interviews and a questionnaire survey of farmers who cultivated MON810. The results indicate that a quarter of the farmers who were surveyed did not comply with the refuge requirement. Moreover, farmers often lacked the knowledge, time, and motivation to observe and report the potential impacts of Bt maize on biodiversity, which is supposed to be monitored by the PMEM farmers’ questionnaire.The findings of this study compound the previous criticism and suggest that the current practice of PMEM limits its aim of detecting unanticipated adverse effects of MON810 maize cultivation on human and animal health and the environment. The PMEM plan should be revised before the approval process of the application for the renewal of the authorisation for MON810 cultivation in the EU continues.

Neural interaction between cortical taste neurons in rats: a cross-correlation analysis.

In the rat cortical taste area (CTA), we recorded 31 pairs of taste neurons and seven pairs of taste and non-taste neurons, with single or double electrodes. By using a cross-correlogram (CCG) in a stationary state, we examined the functional interaction between neurons of the pairs while activating them by taste stimulation. Though only 14.3% of the taste and non-taste neuron pairs were correlated, 54.8% of the taste neuron pairs showed correlated activities, 41.9% of them showing common inputs, including one with an additional excitatory connection. The remainder (12.9%) showed excitatory connections with a time lag of 1-3 ms. When pairs were recorded using single or double electrodes with an intertip distance of < 50 microns in a dorsoventral direction, a larger fraction had correlated activities than when the intertip distance was > 50 microns. Whereas pairs of neurons showed correlated activities in area DI whatever the vertical intertip distance was, most of the pairs having correlated activities in area GI were found within 50 microns of the vertical intertip distance. The taste profiles of common inputs to the pair were estimated on the basis of peak at time 0 in CCGs for various taste stimuli. The efficacy contribution of the source to target neurons tended to be larger when both had the same best stimulus. This tendency held true for pairs showing excitatory connections. Interlayer excitatory connections were also evident. It is concluded that a functional column with a diameter of 50 microns may present in the CTA in rats, and that information flow is larger between pairs of neurons with the same best stimulus.

Responses of neurons in the primate taste cortex to the glutamate ion and to inosine 5′-monophosphate

To investigate the neural encoding of glutamate taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex taste area, with a small number in adjacent taste areas. First, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. The correlation between the responses to these two tastants was higher than between any other pair of tastants, which included glucose (sweet), sodium chloride (salty), HCl (sour), and quinine HCl (bitter). Accordingly, the responsiveness to glutamic acid clustered with the response to monosodium glutamate in a cluster analysis with this set of stimuli, and glutamic acid was close to sodium glutamate in a space created by multidimensional scaling. Second, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Third, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fourth, neurons have not yet been found in this cortical region that showed synergism of monosodium glutamate and the nucleotide inosine 5′-monophosphate: it was shown that mixtures of 0.0001 M inosine 5′-monophosphate with different concentrations (0.001, 0.01, and 0.1 M) of monosodium glutamate did not have a greater effect than the monosodium glutamate alone. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety. In some cases this reduction was sensory-specific. These findings show that the taste neurons activated by monosodium glutamate can also be activated by other umami tastants, including glutamic acid and the nucleotide inosine 5′-monophosphate. The responses to these umami tastants were more similar to each other than to any of the other prototypical tastant, providing evidence that in this system umami is encoded differently from the other tastants. Moreover, the findings with these tastants provide additional evidence that the responses to monosodium glutamate are not due just to activation of a sodium taste channel.