Thalamic control of cortical states

We investigated the impact of thalamus on ongoing cortical activity in the awake, behaving mouse. We demonstrate that the desynchronized cortical state during active behavior is driven by a centrally generated increase in thalamic action potential firing, which can also be mimicked by optogenetic stimulation of the thalamus. The thalamus therefore is key in controlling cortical states.     

Thalamic syndrome and cortical hypoperfusion on technetium-99m HM-PAO brain SPECT

The six patients included in this study had painful dysesthesia, resulting from vascular lesions in or near the thalamus, confirmed by computerized tomography(CT) brain scan. Using hexamethyl propyleneamine oxime(HM-PAO) single photon emission computed tomography(SPECT) brain scanning, regional cerebral perfusion(rCP) was demonstrated. In contrast to three patients with lesions near the thalamus who showed symmetrical cortical radioactivity, the other three patients with thalamic lesions revealed decreased rCP in the ipsilateral cerebral cortex on HM-PAO brain SPECT. We thought that the loss of afferent activating stimuli from the thalamus led to decreased cortical neuronal activity and the following hypoperfusion. In patients with thalamic syndrome resulting from thalamic lesions, the role of the remote effect of the thalamic damage and consequent cortical deregulation in the development of thalamic pain and/or neuropsychological symptoms cannot be excluded completely.     

Synaptic interactions between thalamic and cortical inputs onto cortical neurons in vivo

To study the interactions between thalamic and cortical inputs onto neocortical neurons, we used paired-pulse stimulation (PPS) of thalamic and cortical inputs as well as PPS of two cortical or two thalamic inputs that converged, at different time intervals, onto intracellularly recorded cortical and thalamocortical neurons in anesthetized cats. PPS of homosynaptic cortico-cortical pathways produced facilitation, depression, or no significant effects in cortical pathways, whereas cortical responses to thalamocortical inputs were mostly facilitated at both short and long intervals. By contrast, heterosynaptic interactions between either cortical and thalamic, or thalamic and cortical, inputs generally produced decreases in the peak amplitudes and depolarization area of evoked excitatory postsynaptic potentials (EPSPs), with maximal effect at approximately 10 ms and lasting from 60 to 100 ms. All neurons tested with thalamic followed by cortical stimuli showed a decrease in the apparent input resistance (R(in)), the time course of which paralleled that of decreased responses, suggesting that shunting is the factor accounting for EPSP's decrease. Only half of neurons tested with cortical followed by thalamic stimuli displayed changes in R(in). Spike shunting in the thalamus may account for those cases in which decreased synaptic responsiveness of cortical neurons was not associated with decreased R(in) because thalamocortical neurons showed decreased firing probability during cortical stimulation. These results suggest a short-lasting but strong shunting between thalamocortical and cortical inputs onto cortical neurons.     

A cortical motor nucleus drives the basal ganglia-recipient thalamus in singing birds

The pallido-recipient thalamus transmits information from the basal ganglia to the cortex and is critical for motor initiation and learning. Thalamic activity is strongly inhibited by pallidal inputs from the basal ganglia, but the role of nonpallidal inputs, such as excitatory inputs from cortex, remains unclear. We simultaneously recorded from presynaptic pallidal axon terminals and postsynaptic thalamocortical neurons in a basal ganglia-recipient thalamic nucleus that is necessary for vocal variability and learning in zebra finches. We found that song-locked rate modulations in the thalamus could not be explained by pallidal inputs alone and persisted following pallidal lesion. Instead, thalamic activity was likely driven by inputs from a motor cortical nucleus that is also necessary for singing. These findings suggest a role for cortical inputs to the pallido-recipient thalamus in driving premotor signals that are important for exploratory behavior and learning.     

An analysis of penicillin-induced generalized spike and wave discharges using simultaneous recordings of cortical and thalamic single neurons

To study the relationship between cortical and thalamic single-neuron activity during spike and wave (SW) discharge of feline generalized penicillin epilepsy (FGPE), extracellular single-unit and local electroencephalogram (EEG) activity were recorded simultaneously from pairs of neurons, one located in the cortex of the middle suprasylvian gyrus (MSS), the other in the dorsal thalamic nuclei (n. lateralis posterior or pulvinar). These two areas are anatomically and functionally closely interrelated. Computer-generated EEG averages and histograms of single-unit activity triggered by either peaks of cortical or thalamic EEG transients or by cortical or thalamic action potentials (aps) showed that cortical neurons in the MSS fired at the time of the spike of the SW complex, while at the time of the wave they became silent. Two populations of thalamic neurons also fired maximally during the spike of SW discharge, but they differed in the precise timing of their firing in relation to that of the simultaneously recorded cortical neuron. The first group of thalamic neurons tended to fire 5-45 ms before the cortical neuron. Of these 28 neurons, 9 were antidromically and 2 orthodromically activated by cortical stimulation. The neurons of the second group tended to fire 0-45 ms after the cortical neuron. Cortical stimulation activated 15 of these 19 neurons orthodromically and 2 antidromically. A third and smaller population of thalamic neurons (n = 8) increased its firing probability during the wave of the SW complex and decreased it during the spike. In 74% of the pairs of neurons the cyclic alternation of excitation and "inhibition" associated with SW activity appeared in the cortex by 1-3 cycles earlier than in the thalamus. This was most common when the thalamic neuron of the pair reached its peak firing probability before the simultaneously recorded cortical neuron. In 11 pairs of neurons the same rhythmic alternation of excitation and "inhibition" of neuronal firing was seen in both the cortex and thalamus during SW discharges evoked by single-shock stimulation of nucleus centralis medialis. These data demonstrate that both cortical and thalamic neurons participate in the SW firing pattern of FGPE by undergoing periods of mutually phase-locked cyclic alternations of excitation and "inhibition" at the frequency of the EEG SW rhythm. Although the initial steps leading to generalized SW discharge in FGPE take place in the cortex, the thalamus soon becomes entrained in the SW rhythm.(ABSTRACT TRUNCATED AT 400 WORDS)     

Thalamic and cortical contributions to neural plasticity after limb amputation

Little is known about the substrates for the large-scale shifts in the cortical representation produced by limb amputation. Subcortical changes likely contribute to the cortical remodeling, yet there is little data regarding the extent and pattern of reorganization in thalamus after such a massive deafferentation. Moreover, the relationship between changes in thalamus and in cortex after injuries of this nature is virtually unexplored. Multiunit microelectrode maps were made in the somatosensory thalamus and cortex of two monkeys that had long-standing, accidental forelimb amputations. In the deprived portion of the ventroposterior nucleus of the thalamus (VP), where stimulation to the hand would normally activate neurons, new receptive fields had emerged. At some recording sites within the deprived zone of VP, neurons responded to stimulation of the remaining stump of the arm and at other sites neurons responded to stimulation of both the stump and the face. This same overall pattern of reorganization was present in the deprived hand representation of cortical area 3b. Thus thalamic changes produced by limb amputation appear to be an important substrate of cortical reorganization. However, a decrease in the frequency of abnormal stump/face fields in area 3b compared with VP and a reduction in the size of the fields suggests that cortical mechanisms of plasticity may refine the information relayed from thalamus.     

Thalamic projections of somatosensory cortical areas

The results of morphological investigations of degenerated fibers show that the first somatosensory cortical area is connected by descending cortico-thalamic fibers with the posterior ventral nucleus of the thalamus. The second somatosensory area is connected simultaneously with the caudal part of the posterior ventral nucleus and with the posterior group of thalamic nuclei. These cortico-thalamic connections are distributed on a somatotopic principle.     

Distinct populations of NMDA receptors at subcortical and cortical inputs to principal cells of the lateral amygdala

Fear conditioning involves the transmission of sensory stimuli to the amygdala from the thalamus and cortex. These input synapses are prime candidates for sites of plasticity critical to the learning in fear conditioning. Because N-methyl-D-aspartate (NMDA)-dependent mechanisms have been implicated in fear learning, we investigated the contribution of NMDA receptors to synaptic transmission at putative cortical and thalamic inputs using visualized whole cell recording in amygdala brain slices. Whereas NMDA receptors are present at both of these pathways, differences were observed. First, the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated component of the synaptic response, relative to the NMDA component, is smaller at thalamic than cortical input synapses. Second, thalamic NMDA responses are more sensitive to Mg2+. These findings suggest that there are distinct populations of NMDA receptors at cortical and thalamic inputs to the lateral amygdala. Differences such as these might underlie unique contributions of the two pathways to fear conditioning.     

Modeling the effects of midazolam on cortical and thalamic neurons

Controversy exists regarding the site where anesthetics act in the brain to produce sedation and unconsciousness. Actions in the cerebral cortex and thalamus are likely, although the relative importance of each site is unclear. We used in computo modeling to investigate the sensitivity of cortical and thalamic neurons to midazolam (MDZ) at concentrations that produce unconsciousness. The GABA_A receptor conductance of the model was manipulated to simulate the effects of MDZ at free-drug plasma concentrations ranging from 8 nM to 100 nM; sleepiness to complete unconsciousness occurs in humans in the 10–40 nM range. Prolongation of phasic inhibition was simulated by increasing the decay time constant and tonic inhibition was simulated by introducing a tonic current; the extent of phasic and tonic inhibition was appropriate for each simulated MDZ concentration. Phasic and tonic inhibition was simulated in cortex, and phasic inhibition was simulated in thalamus. Simulation of MDZ effect decreased cortical neuronal firing rate. For example, the mean cortical neuronal firing rate decreased by 15% (P < 0.01) and 26% (P < 0.01) at MDZ concentrations of 10 nM and 40 nM, respectively. However, thalamic firing rate did not change. In computo modeling of the thalamocortical system indicates that MDZ-induced GABAergic inhibition of cortical neurons plays a significant role in the transition from waking to unconsciousness. Although MDZ produces phasic inhibition in the thalamus, computer simulation suggests it is not significant enough to decrease thalamic neuronal firing. Thus, based on in computo modeling, MDZ at sedative/hypnotic concentrations produces its effects by decreasing cortical neuronal firing.     

Thalamic retrograde degeneration following cortical injury: an excitotoxic process?

Traumatic or stroke-like injuries of the cerebral cortex result in the rapid retrograde degeneration of thalamic relay neurons that project to the damaged area. Although this phenomenon has been well documented, neither the basis for the relay neuron's extreme sensitivity to axotomy nor the mechanisms involved in the degenerative process have been clearly identified. Physiological and biochemical studies of the thalamic response to cortical ablation indicate that pathological overexcitation might contribute to the degenerative process. The responses of thalamic projection neurons, protoplasmic astrocytes, and inhibitory thalamic reticular neurons in adult mice were examined from one to 120 days following ablation of the somatosensory cortex as part of an investigation of the role of excitotoxicity in thalamic retrograde degeneration. The responses of thalamic neurons to cortical ablation were compared with those produced by intracortical injection of the convulsant excitotoxin kainic acid, since the degeneration of neurons in connected brain structures distant to the site of kainic acid injection is also thought to occur via an excitotoxic mechanism. Within two days after either type of cortical injury, protoplasmic astrocytes in affected regions of the thalamic ventrobasal complex and the medial division of the posterior thalamic nuclei became reactive and expressed increased levels of immunohistochemically detectable glial fibrillary acidic protein. Within the affected regions of the ventrobasal complex an increased intensity of puncta positive for glutamate decarboxylase immunoreactivity, presumably due to an increase in its content within the terminals of the reciprocally interconnected thalamic reticular neurons, was also evident. These immunohistochemically detectable alterations in the milieu of the damaged thalamic neurons preceded the disappearance of the affected relay neurons by at least two days following cortical ablation and by seven to 10 days following intracortical kainic acid injection. Regions of the thalamus containing reactive astrocytes corresponded very closely to the regions undergoing retrograde degeneration. Protoplasmic astrocytes in these areas remained intensely reactive up to 60 days after cortical injury. Levels of glutamate decarboxylase were only transiently elevated in the degenerating regions of the ventrobasal complex following cortical ablation and returned to normal by 14 days. Increased glutamate decarboxylase immunoreactivity was transiently seen through the entire ventrobasal complex following intracortical kainic acid injection but was markedly more intense in degenerating regions. These patterns of labeling did not return to normal until 50 days after intracortical kainic acid injection, well after the death of the relay neurons. Cortical ablation and intracortical kainic acid injection produce similar alterations in thalamic neuronal and glial populations.(ABSTRACT TRUNCATED AT 400 WORDS)     

Role of cortical feedback in the receptive field structure and nonlinear response properties of somatosensory thalamic neurons

Previous studies have suggested that the descending pathway from the primary somatosensory (SI) cortex to the ventral posterior nucleus of the thalamus has only a mild facilitative influence over thalamic neurons. Given the large numbers of corticothalamic terminations within the rat somatosensory thalamus and their complex topography, we sought to examine the role of corticothalamic feedback in the genesis of spatiotemporal receptive fields and the integration of complex tactile stimuli in the thalamus. By combining focal cortical inactivation (produced by microinjection of the GABA(A) agonist muscimol), with chronic multielectrode recordings, we observed that feedback from the rat SI cortex has multiple influences on its primary thalamic relay, the ventral posterior medial (VPM) nucleus. Our data demonstrate that, when single-whisker stimuli were used, the elimination of cortical feedback caused significant changes in the spatiotemporal structure of the receptive fields of VPM neurons. Cortical feedback also accounted for the nonlinear summation of VPM neural responses to simultaneously stimulated whiskers, in effect "linearizing" the responses. These results argue that the integration and transmission of tactile information through VPM are strongly influenced by the state of SI cortex.     

Corticofugal axons from adjacent 'barrel' columns of rat somatosensory cortex: cortical and thalamic terminal patterns

The cortical representations of the vibrissae of the rat form a matrix in which each whisker has its own area of cortex, called a 'barrel'. The afferent pathways from the periphery travel first to the trigeminal nuclei and thence via the ventroposteromedial thalamus (VPM) to the cortical barrels have been described in detail. We have studied the output from barrels by filling adjacent areas of the primary somatosensory cortex (SI) with either Phaseolus vulgaris leucoagglutinin (PHA-L) or biotinylated dextran amine (BDA) and demonstrating the course and terminations of the axons that arise within the barrel fields. The method not only dramatically illustrates the previously described corticothalamic pathway to VPM but also demonstrates a strict topography in the cortical afferents to the thalamic reticular nucleus (RT). Cells supplying the RT projection are found below the barrels in layer IV. Connections to the posterior thalamus, on the other hand, have no discernible topography and are derived from cortical areas surrounding the barrels. Thus the outputs of these 'septal' areas return to the region from which they receive thalamic input. The corticocortical connections are also visible in the same material. Contralateral cortical connections arise from the cells of the septa between barrels. The projections to secondary somatosensory area (SII) are mirror images of the barrel pattern in SI with rather more overlap but nonetheless a recognisable topography.     

Effects of thalamic high-frequency electrical stimulation on whisker-evoked cortical adaptation

Activity in thalamocortical circuits depends strongly on immediate past experience. When the successive activity is attenuated on short timescales, this phenomenon is known as adaptation. Adaptive processes may be effectively initiated by ongoing exposure to sensory stimuli and/or direct electrical stimulation of neural tissue. Ongoing high-frequency electrical stimulation is increasingly employed as a treatment for a variety of neurological disorders. Neural stimulation with similar parameters to therapeutic electrical stimulation may modulate the way in which cortical neurons respond and adapt to sensory stimuli. Here, we studied the effects of high-frequency stimulation of the somatosensory thalamus on the transmission of sensory signals in thalamocortical circuits. We examined how whisker-evoked sensory inputs in layer IV cortical barrels are affected by concurrent 100 Hz thalamic electrical stimulation and how the latter modulates sensory-evoked adaptation. Even in the presence of ongoing thalamic stimulation, sensory transmission in thalamocortical circuits is maintained. However, cortical responses to whisker deflections are reduced in an intensity-dependent fashion and can be nearly abolished with high intensity currents. The electrical stimulation-induced reduction in cortical responsiveness likely reflects engagement of circuit mechanisms that normally produce sensory adaptation.     

Convergence of cortical and thalamic input to direct and indirect pathway medium spiny neurons in the striatum

The major afferent innervation of the basal ganglia is derived from the cortex and the thalamus. These excitatory inputs mainly target the striatum where they innervate the principal type of striatal neuron, the medium-sized spiny neurons (MSNs), and are critical in the expression of basal ganglia function. The aim of this work was to test directly whether corticostriatal and thalamostriatal terminals make convergent synaptic contact with individual direct and indirect pathway MSNs. Individual MSNs were recorded in vivo and labelled by the juxtacellular method in the striatum of BAC transgenic mice in which green fluorescent protein reports the expression of dopamine D1 or D2 receptors. After recovery of the neurons, the tissue was immunolabelled for vesicular glutamate transporters type 1 and 2, as markers of cortical and thalamic terminals, respectively. Three of each class of MSNs were reconstructed in 3D and second-order dendrites selected for electron microscopic analysis. Our findings show that direct and indirect pathway MSNs, located in the matrix compartment of the striatum, receive convergent input from cortex and thalamus preferentially on their spines. There were no differences in the pattern of innervation of direct and indirect pathway MSNs, but the cortical input is more prominent in both and synaptic density is greater for direct pathway neurons. The 3D reconstructions revealed no morphological differences between direct and indirect MSNs. Overall, our findings demonstrate that direct and indirect pathway MSNs located in the matrix receive convergent cortical and thalamic input and suggest that both cortical and thalamic inputs are involved in the activation of MSNs.     

Whisker maps in marsupials: nerve lesions and critical periods

In the wallaby, whisker-related patterns develop over a protracted period of postnatal maturation in the pouch. Afferents arrive simultaneously in the thalamus and cortex from postnatal day (P) 15. Whisker-related patterns are first seen in the thalamus at P50 and are well formed by P73, before cortical patterns first appear (P75) or are well developed (P85). This study used the slow developmental sequence and accessibility of the pouch young to investigate the effect of nerve lesions before afferent arrival, or at times when thalamic patterns are obvious but cortical patterns not yet formed. The left infraorbital nerve supplying the whiskers was cut at P0-93 and animals were perfused at P112-123. Sections through the thalamus (horizontal plane) and cortex (tangential) were reacted for cytochrome oxidase to visualize whisker-related patterns. Lesions of the nerve at P2-5, before innervation of the thalamus or cortex, resulted in an absence of patterns at both levels. Lesions from P66-77 also disrupted thalamic and cortical patterns, despite the fact that thalamic patterns are normally well established by P73. Lesions from P82-93 resulted in normal thalamic and cortical patterns. Thus, despite the wallaby having clearly separated times for the development of patterns at different levels of the pathway, these results suggest a single critical period for the thalamus and cortex, coincident with the maturation of the cortical pattern. Possible mechanisms underpinning this critical period could include dependence of the thalamic pattern on corticothalamic activity or peripheral signals to allow consolidation of thalamic barreloids.     

Some factors involved in the thalamic control of spontaneous barbiturate spindles

1. The origin of thalamic and cortical spontaneous spindles was studied in cats anaesthetized with sodium pentobarbital.2. Complete removal of all cortical grey matter left the thalamic rhythmic spindle activity unchanged.3. Removal of the entire thalamus or pronounced oedema in the thalamus abolished completely the spindle activity in the corresponding hemisphere.4. In a neuronally isolated cortical area, a fast, low voltage background activity appeared, interrupted by occasional irregular rapid potential changes (sharp waves) of high voltage. Regular spindle rhythms were seldom observed unless excited by a depolarizing drug. Spontaneous spindles did not invade the isolated cortex via a bridge of intact cortical tissue.5. With increasingly larger destruction of the thalamus in a rostro-caudal direction, the activity in the post-cruciate cortex did not change until the anterior third of the thalamus was encroached upon. A transverse section in front of the thalamus nearly eliminated the cortical spindles.6. Complete removal of the mid line and intralaminar nuclei left the spontaneous rhythmic activity of the lateral thalamic nuclei and of the frontal cortex principally unchanged.7. Removal of the laterally located thalamic nuclei, including the n. ventralis posterolateralis (VPL), abolished virtually all spontaneous spindle activity of the frontal cortex, including the post-cruciate area.8. Local cortical cooling reduced the amplitude but not the frequency of the cortical spindles.9. Cooling of the whole brain reduced both the amplitude and the frequency of the spindles. At low temperatures, all spindle activity in the cortex disappeared, and occasional sharp waves occurred, as with de-afferentation.10. It is concluded that the rhythm of the cortical spontaneous barbiturate spindles is generated exclusively by thalamic neurones. The electromotive force of the corticographic waves, however, has a cortical origin.     

Thalamic synchrony and the adaptive gating of information flow to cortex

Although it has long been posited that sensory adaptation serves to enhance information flow in sensory pathways, the neural basis remains elusive. Simultaneous single-unit recordings in the thalamus and cortex in anesthetized rats showed that adaptation differentially influenced thalamus and cortex in a manner that fundamentally changed the nature of information conveyed about vibrissa motion. Using an ideal observer of cortical activity, we found that performance in detecting vibrissal deflections degraded with adaptation while performance in discriminating among vibrissal deflections of different velocities was enhanced, a trend not observed in thalamus. Analysis of simultaneously recorded thalamic neurons did reveal, however, an analogous adaptive change in thalamic synchrony that mirrored the cortical response. An integrate-and-fire model using experimentally measured thalamic input reproduced the observed transformations. The results here suggest a shift in coding strategy with adaptation that directly controls information relayed to cortex, which could have implications for encoding velocity signatures of textures.     

The pathways connecting the hippocampal formation, the thalamic reuniens nucleus and the thalamic reticular nucleus in the rat

Most dorsal thalamic nuclei send axons to specific areas of the neocortex and to specific sectors of the thalamic reticular nucleus; the neocortex then sends reciprocal connections back to the same thalamic nucleus, directly as well indirectly through a relay in the thalamic reticular nucleus. This can be regarded as a 'canonical' circuit of the sensory thalamus. For the pathways that link the thalamus and the hippocampal formation, only a few comparable connections have been described. The reuniens nucleus of the thalamus sends some of its major cortical efferents to the hippocampal formation. The present study shows that cells of the hippocampal formation as well as cells in the reuniens nucleus are retrogradely labelled following injections of horseradish peroxidase or fluoro-gold into the rostral part of the thalamic reticular nucleus in the rat. Within the hippocampal formation, labelled neurons were localized in the subiculum, predominantly on the ipsilateral side, with fewer neurons labelled contralaterally. Labelled neurons were seen in the hippocampal formation and nucleus reuniens only after injections made in the rostral thalamic reticular nucleus (1.6-1.8 mm caudal to bregma). In addition, the present study confirmed the presence of afferent connections to the rostral thalamic reticular nucleus from cortical (cingulate, orbital and infralimbic, retrosplenial and frontal), midline thalamic (paraventricular, anteromedial, centromedial and mediodorsal thalamic nuclei) and brainstem structures (substantia nigra pars reticularis, ventral tegmental area, periaqueductal grey, superior vestibular and pontine reticular nuclei). These results demonstrate a potential for the thalamo-hippocampal circuitry to influence the functional roles of the thalamic reticular nucleus, and show that thalamo-hippocampal connections resemble the circuitry that links the sensory thalamus and neocortex.     

Taste responses of cortical neurons

Branches of the facial, glossopharyngeal and vagus nerves which synapse with the receptor cells in the taste buds convey taste messages to the rostral part of the nucleus of the solitary tract. The second relay nucleus for ascending taste input is the parabrachial nucleus of the pons. The third relay nucleus is the medial parvocellular component of the ventrobasal complex of the thalamus. This thalamic nucleus projects to the cortical taste area. Another ascending projection site of the parabrachial nucleus is to the lateral hypothalamus, amygdala and bed nucleus of the stria terminalis. In monkeys, neurons from the gustatory area of the solitary nucleus directly reach the thalamic taste area, bypassing the parabrachial nucleus. Taste-elicited reflex activities are based on a hedonic (acceptable or rejective) aspect of taste, and are basically determined in the brain stem without activation of cortical neurons. The cerebral cortical taste area is located dorsal to the rhinal sulcus in or near the insular cortex in different species of animals. Besides this taste area, taste inputs also project to the tongue tactile area of the SI in monkeys, cats and rats. Taste-responsive neurons in SI area are also responsive to light tactile stimulation of the tongue. Human clinical case reports suggest that discrimination or recognition of taste quality are processed in the cortical taste area. In animal experiments, it is difficult to determine the functional significance of this area. However, recent behavioral studies using the conditioned taste aversion technique in rats suggest that the cortical taste area plays an important role in cognitive (learning, memorial, associative and discriminative) processes of taste sensation. Summated cortical evoked potentials have been recorded in human and rats to electrical and taste stimulations applied to the tongue surface. Recording of gustatory primary evoked potentials is unsuccessful in human subjects. The responses to taste stimulation are composed of an early component, which is induced by mechanical stimulation of a test solution poured on the tongue surface and a slow component, which is assumed to be the gustatory response. Essentially similar results are obtained for cortical summated responses to taste stimuli in rats. Besides these averaged evoked potentials, arousal changes of EEG occur in response to taste stimulation. There is a possibility that the arousal response can be used an objective indicator for intensity and hedonics of perceived taste sensation.(ABSTRACT TRUNCATED AT 400 WORDS)