Sensory inattention in rats with 6-hydroxydopamine-induced degeneration of ascending dopaminergic neurons: apomorphine-induced reversal of deficits

Rats given intracerebral injections of 6-hydroxydopamine (6-OH-DA) that damaged the ascending dopamine-containing projection showed a syndrome of sensory inattention characterized by a failure to orient toward or otherwise investigate somatosensory, visual, or olfactory stimuli. Animals that were inattentive to those stimuli on both body sides were given apomorphine (0.05, 0.10, or 0.20 mg/kg or its vehicle, i.p.) 2, 3, 5, and 8 days after bilateral intranigral 6-OH-DA injections. At the lower two doses, apomorphine resulted in a significant restoration of orientation to all modalities of stimuli. The highest dose did not improve orientation, but only induced stereotyped sniffing behavior. The restorative effects of apomorphine administration were completely abolished by pretreatment with spiroperidol (0.05 mg/kg, i.p.). These results indicate that (i) the sensory inattention syndrome seen after intracerebral 6-OH-DA injections is a consequence of damaging dopamine-containing neurons, and (ii) the occurrence of normal-appearing sensorimotor integration requires optimal brain dopamine receptor activity.     

Responses of striatal neurons to peripheral sensory stimulation in symptomatic MPTP-exposed cats

Extracellular single unit activity was recorded in the dorsal lateral caudate nucleus of awake cats and the responses of these neurons to somatosensory, visual and auditory stimuli were assessed. Recordings were obtained when animals were normal and when they were symptomatic for a Parkinson-like syndrome as a result of exposure to the dopaminergic toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In normal animals, 22% of recorded neurons responded to tactile stimulation of the face, 7% had auditory responses, 6% had visual responses, and 6% were multimodal. The post-MPTP period was divided into an 'early' period, in which cats had received several MPTP injections but still remained asymptomatic, and a 'late' period, in which cats had severe motor and sensorimotor impairments. Unit responsiveness was essentially normal in the 'early' period but grossly abnormal in the 'late' period. When animals were symptomatic, only 6% of sampled neurons had responses to somatosensory stimulation, 0.8% had auditory responses and no cells were found with visual responses. Those cells that did respond to somatosensory stimulation did so in a non-specific fashion. Symptomatic animals had 93-96% depletion of dorsal striatal dopamine and extensive loss of substantia nigra pars compacta neurons. The results suggest that sensorimotor and motor abnormalities that accompany severe loss of striatal dopamine are at least in part due to a dopamine-dependent loss of sensory processing abilities of striatal neurons.     

Burst activity of ventral tegmental dopamine neurons is elicited by sensory stimuli in the awake cat

In light of evidence implicating dopamine in the pathophysiology of attention deficit disorder and schizophrenia, diseases involving attentional or sensory processing abnormalities, it was of interest to determine whether and how dopamine neurons in the ventral tegmental area respond to sensory stimuli. The single-unit responses of ventral tegmental dopamine neurons were recorded in freely-moving cats during the presentation of brief, non-conditioned auditory and visual stimuli. Both auditory and visual stimuli produced neuronal excitation, involving a greater than 5-fold increase in the probability of burst firing followed by a period of burst inhibition. The burst nature of the single-unit response suggests that sensory-induced dopamine release at target sites was disproportionally large relative to the discharge frequency. While characteristics of the dopaminergic sensory response were similar for auditory and visual stimuli, the response latency was longer for visual stimuli. The results demonstrate that dopamine neurons in the ventral tegmental area, the site of origin for mesolimbocortical dopamine neurons, are reliably activated by non-conditioned auditory and visual stimuli.     

Activity of dopamine-containing substantia nigra neurons in freely moving cats

The present series of studies examined the activity of presumed dopamine-containing neurons in the substantia nigra of freely moving cats. These neurons were found to have a slow (1-9 spikes/sec) discharge rate, unusually long duration action potentials (2-4 msec) and frequently fired in bursts with progressive decreases in the amplitude of the action potential within the burst. These neurons showed no significant change in their activity across the sleep-waking cycle, and showed no changes in activity with phasic movement. Most units were unresponsive to olfactory, noxious, tactile, auditory and visual stimulation, when unit activity was integrated over several seconds following stimulus presentation. However, phasic auditory and visual stimuli produced a period of excitation lasting approximately 120 msec after a delay of about 80 msec. The period of excitation was followed by a period of inhibition lasting approximately 60 msec. Presumed dopamine-containing substantia nigra units showed no significant circadian changes in activity. The firing rates of these units were inhibited by dopamine agonists, including the direct-acting agonist, apomorphine, the dopamine precursor, L-dihydroxyphenylalanine, a dopamine releasing agent, d-amphetamine, and a dopamine reuptake blocker, bupropion, and were excited by a dopamine receptor blocker, haloperidol. Thus, these neurons show many similarities to dopamine units recorded in anesthetized rats; however, they showed several notable differences as well. Recording the activity of these units in behaving animals allows one to examine behavioral correlates of unit activity. Furthermore, the data (sensory stimulation, pharmacological, etc.) obtained in the unanesthetized preparation are far more relevant to the physiological and pharmacological effects that may occur in humans.     

Insular cortex and neuropsychiatric disorders: a review of recent literature.

The insular cortex is located in the centre of the cerebral hemisphere, having connections with the primary and secondary somatosensory areas, anterior cingulate cortex, amygdaloid body, prefrontal cortex, superior temporal gyrus, temporal pole, orbitofrontal cortex, frontal and parietal opercula, primary and association auditory cortices, visual association cortex, olfactory bulb, hippocampus, entorhinal cortex, and motor cortex. Accordingly, dense connections exist among insular cortex neurons. The insular cortex is involved in the processing of visceral sensory, visceral motor, vestibular, attention, pain, emotion, verbal, motor information, inputs related to music and eating, in addition to gustatory, olfactory, visual, auditory, and tactile data. In this article, the literature on the relationship between the insular cortex and neuropsychiatric disorders was summarized following a computer search of the Pub-Med database. Recent neuroimaging data, including voxel based morphometry, PET and fMRI, revealed that the insular cortex was involved in various neuropsychiatric diseases such as mood disorders, panic disorders, PTSD, obsessive-compulsive disorders, eating disorders, and schizophrenia. Investigations of functions and connections of the insular cortex suggest that sensory information including gustatory, olfactory, visual, auditory, and tactile inputs converge on the insular cortex, and that these multimodal sensory information may be integrated there.     

Changes in sensory inattention, directional motor neglect and "release" of the fixation reflex following a unilateral frontal lesion: a case report

We recorded eye movements to and away from visual stimuli from a patient with left-sided neglect following a right frontal infarct in order to determine (a) whether and to what extent his neglect was due to sensory inattention and directional motor neglect and (b) whether he had difficulty suppressing inappropriate eye movements to visual stimuli ("release" of visual grasp) as his sensory inattention declined. In the first testing session, conducted 5 days following his stroke, he often failed to move his eyes when a stimulus on the left required a rightward eye movement, but he consistently moved his eyes to a stimulus on the right. Thus, he showed contralateral but not ipsilateral sensory inattention. Initially, he also was impaired in making leftward eye movements when right stimuli were presented. Thus, he also showed a directional motor neglect. In subsequent tests, his left-sided sensory inattention as defined above decreased, and was no longer present three weeks following his stroke, nor in a follow-up test conducted almost 6 months following this stroke. In contrast, his directional motor neglect, as defined above, was still present in the follow-up test. As his left-sided sensory inattention declined, his tendency to move his eyes incorrectly to stimuli on the left side (the side contralateral to his lesion) when these stimuli required eye movements to the right became stronger ("release" of visual grasp); he continued to show this strong tendency in the test conducted almost 6 months following his stroke.     

Pineal lesion produces bilateral visual and auditory inattention in the rat

Unilateral lesions in such brain regions as medial frontal cortex and superior colliculus produce polysensory neglect contralateral to the lesion. Since the pineal gland is an unpaired brain structure, both electrophysiologically and hormonally responsive to visual and auditory stimulation, it may modulate bilateral sensory attention mechanisms. Long-Evans male rats were given pineal or sham lesions and were tested behaviourally. Sensory assessment revealed that in comparison to sham animals rats with pineal lesion exhibited unilateral visual and auditory neglect to stimuli presented on either side of the body. Animals with pineal lesions were more likely than sham-lesioned animals to demonstrate visual allesthesis and, compared to sham-lesioned rats, showed extinction on the left side to bilateral simultaneous visual stimulation. This is the first report that midline neuroendocrine damage can produce bilateral sensory inattention.     

Normal tactile threshold in monkeys with neglect

To learn whether animals with parietotemporal lesions have sensory inattention or defective intention, we trained monkeys to respond with the contralateral limb to a threshold tactile stimulus. After parietotemporal lesions that induced neglect, the monkeys continued to respond normally to threshold stimuli on the side opposite the lesion (the neglected side), but made errors when stimulated on the normal side (ipsilateral to the lesion), often failing to use the contralateral extremity. On this learned task, there was no abnormality of sensory input or sensory attention. The problem was attributed to an impaired preparation to respond (intention).     

Orienting Behaviour and Superior Colliculus Sensory Representations in Mice with the Vibrissae Bent into the Contralateral Hemispace

When a tactile stimulus touches the body on one side, animals show an orienting response toward that side with the eyes, the head or the entire body. This movement requires the transformation of sensory information into motor commands. The superior colliculus is supposed to be a fundamental part of the brain where this sensorimotor transformation occurs and where one of the possible mechanisms could be the alignment among sensory and motor topographies. We changed the body shape of mice in order to analyse the development of new orienting responses following tactile stimulation. To do this, we bent the left vibrissae from left to right such that they were located in the right portion of the visual hemifield. If left-right inversion was performed in adults, tactile stimulation of the left vibrissae performed from the right produced wrong orienting movements to the left. Conversely, if left—right inversion was performed in newborns, mice learned to respond correctly to the right. By recording from superior colliculus multisensory neurons of mice whose vibrissae were displaced at birth, we found a shift of visual and auditory receptive fields from left to right in those multisensory neurons receiving tactile input from the displaced vibrissae. These results show the strict relation existing between the neuronal modifications in the superior colliculus and the changes in orienting behaviour. These findings also suggest two important conclusions. First, sensory mapping in the superior colliculus depends on sensory inputs coming from the same portion of space. Second, since the neuronal modifications we found involved sensory representations, the observed motor learning seems to be due, at least in part, to sensory changes, and the superior colliculus appears therefore to be an important brain region where the internal schema of the body is specified.     

Somatosensory cell response to an auditory cue in a haptic memory task

Neurons in the monkey's anterior parietal cortex (Brodmann's areas 3a, 3b, 1, and 2) have been reported to retain information from a visual cue that has been associated with a tactile stimulus in a haptic memory task. This cross-modal transfer indicates that neurons in somatosensory cortex can respond to non-tactile stimuli if they are associated with tactile information needed for performance of the task. We hypothesized that neurons in somatosensory cortex would be activated by other non-tactile stimuli signaling the haptic movements--of arm and hand--that the task required. We found such cells in anterior parietal areas. They reacted with short-latency activity changes to an auditory signal (a click) that prompted those movements. Further, some of those cells changed their discharge in temporal correlation with the movements themselves, with the touch of the test objects, and with the short-term memory of those objects for subsequent tactile discrimination. These findings suggest that cells in the somatosensory cortex participate in the behavioral integration of auditory stimuli with other sensory stimuli and with motor acts that are associated with those stimuli.     

Dopamine Axons in Dorsal Striatum Encode Contralateral Visual Stimuli and Choices

The striatum plays critical roles in visually-guided decision-making and receives dense axonal projections from midbrain dopamine neurons. However, the roles of striatal dopamine in visual decision-making are poorly understood. We trained male and female mice to perform a visual decision task with asymmetric reward payoff, and we recorded the activity of dopamine axons innervating striatum. Dopamine axons in the dorsomedial striatum (DMS) responded to contralateral visual stimuli and contralateral rewarded actions. Neural responses to contralateral stimuli could not be explained by orienting behavior such as eye movements. Moreover, these contralateral stimulus responses persisted in sessions where the animals were instructed to not move to obtain reward, further indicating that these signals are stimulus-related. Lastly, we show that DMS dopamine signals were qualitatively different from dopamine signals in the ventral striatum (VS), which responded to both ipsilateral and contralateral stimuli, conforming to canonical prediction error signaling under sensory uncertainty. Thus, during visual decisions, DMS dopamine encodes visual stimuli and rewarded actions in a lateralized fashion, and could facilitate associations between specific visual stimuli and actions.SIGNIFICANCE STATEMENT While the striatum is central to goal-directed behavior, the precise roles of its rich dopaminergic innervation in perceptual decision-making are poorly understood. We found that in a visual decision task, dopamine axons in the dorsomedial striatum (DMS) signaled stimuli presented contralaterally to the recorded hemisphere, as well as the onset of rewarded actions. Stimulus-evoked signals persisted in a no-movement task variant. We distinguish the patterns of these signals from those in the ventral striatum (VS). Our results contribute to the characterization of region-specific dopaminergic signaling in the striatum and highlight a role in stimulus-action association learning.     

Nucleus basalis of Meynert cell responses in awake monkeys

Extracellular cell activity was recorded in the intermediate and posterior subdivisions of the nucleus basalis of Meynert (NBM) of awake monkeys to determine cell characteristics and the motor and sensory participation. Animals were trained to move a lever by elbow flexion-extensions to receive a reward. Cell activity was recorded when the animal was at rest and executing the task. The electromyogram of the upper limb, contralateral to the recording site, was recorded simultaneously with NBM neuron activity. The effect of visual, auditory, and tactile stimuli were also studied after performance of the learned task. A moderate number of cells responded to the reward (16%), while a higher percentage of them was associated with unexpected, unspecific stimuli (22%). Firing rates correlated positively with limb movement (30%). Visual (34%) and auditory (15%) responses were also found. No NBM cell responded to tactile stimulation. Considering these findings and the anatomical projections over the cortex, the NBM role in complex integrative processes is discussed.     

Neglect: the phenomena of unilateral neglect following brain damage

The term "neglect" designates various kinds of failure to orient or respond to or to report stimuli appearing at the side contralateral to a cerebral lesion. This failure cannot be explained by primary sensory or motor disorders. Essentially the following symptoms of neglect have been reported: inattention to visual (or) acoustical stimuli in one hemifield under unilateral and simultaneous bilateral presentation reduction in orienting responses (eye and head movements) to the neglected hemispace and deviation of head and gaze axes towards the intact hemispace omission or incomplete reproduction of one side of a figure of a text when copying or drawing from memory omission of one half of a well-known scene or picture when reporting from memory deviation of the egocentre as tested by visual, acoustic and somatesthetic stimuli towards the intact hemispace reduction of motor activities, especially for the extremities of one half of the body, which cannot be attributed to a sensory motor deficit inattention to somatesthetic stimuli presented on one side of the body displacement of somatesthetic stimuli, presented on the affected body side, to the intact body side lack of "awareness" of the existence of one half of the body, resulting in, e.g., ignoring this body half when washing or dressing "reference" of the neglected body half to another person unawareness or denial of severe sensorimotor deficits (e.g. hemiparesis) in the affected body half. The syndrome of neglect should be carefully differentiated from inattention phenomena resulting from primary sensory (e.g. hemianopia, restriction of field of search) and motor deficits (hemiparesis, hemiakinesis). In some cases this differentiation is rather difficult, because both types of inattention may be combined. Thus, detailed testing of sensory and motor disorders is needed in order to avoid any precipitate diagnosis of "neglect". The neuropathology of the neglect syndrome is not yet known precisely. Damage to the parietal lobe (presumably of the nondominant hemisphere) is the most common cause for neglect. Lesions at the bank of the sulcus intraparietalis seem especially crucial. Lesions in the dorsolateral frontal lobe causing neglect are mainly situated in Brodmann's premotor areas 8, 9 and 46. Furthermore, lesions of the anterior cingular cortex (area 24), of the thalamus (intralaminar nuclei, nucleus ventralis lateralis, pulvinar) and of the basal ganglia seem to induce neglect.     

Recovery of function after mesotelencephalic dopaminergic injury in senescence

After intracerebral 6-hydroxydopamine injections that extensively damage the ascending mesotelencephalic dopaminergic projection, young adult rats develop severe sensorimotor deficits, including an inability to orient toward somatosensory stimuli. Many rats with such damage recover their localization of touch, and this recovery depends on the survival of a small proportion of the neostriatal dopaminergic terminals. Behavioral recovery appears to be mediated by an increased dopamine synthesis and release within surviving terminals and an increased responsiveness to dopamine of neostriatal neurons. The ability of aged rodents to increase activity at neostriatal dopaminergic synapses following partial injury to these neurons is remarkably intact, despite the reduced basal level of transmission at these synapses in senescence. First, 27-28-month-old rats recovered somatosensory localization after injury as readily as did 4-5-month-old animals that had equivalent neostriatal dopamine depletions. Second, old and young rats developed a similar degree of behavioral supersensitivity to apomorphine (0.25 mg/kg, i.p.) after unilateral 6-hydroxydopamine injections, as measured by contralateral turning. Third, injury to these neurons produced an equivalent increase in [3H]spiroperidol binding in the neostriatum of old and young rats at 5-7 weeks. Old rats suffered more extensive neostriatal dopamine depletions after intracerebral 6-hydroxydopamine injections than did young adult animals, particularly when small quantities (2 micrograms) of the neurotoxin were injected. This enhanced susceptibility to 6-hydroxydopamine of dopaminergic neurons in old rats could not be attributed to age differences in the placement of the injection cannula or the extent of the non-specific damage at the injection site. The implications of this enhanced susceptibility to the neurotoxin are discussed.     

Superior Colliculus Controls the Activity of the Rostromedial Tegmental Nuclei in an Asymmetrical Manner

Dopaminergic (DA) neurons of the midbrain are involved in controlling orienting and approach of animals toward relevant external stimuli. The firing of DA neurons is regulated by many brain structures; however, the sensory input is provided predominantly by the ipsilateral superior colliculus (SC). It is suggested that SC also innervates the contralateral rostromedial tegmental nucleus (RMTg)—the main inhibitory input to DA neurons. Therefore, this study aimed to describe the physiology and anatomy of the SC–RMTg pathway. To investigate the anatomic connections within the circuit of interest, anterograde, retrograde, and transsynaptic tract-tracing studies were performed on male Sprague Dawley rats. We have observed that RMTg is monosynaptically innervated predominantly by the lateral parts of the intermediate layer of the contralateral SC. To study the physiology of this neuronal pathway, we conducted in vivo electrophysiological experiments combined with optogenetics; the activity of RMTg neurons was recorded using silicon probes, while either contralateral or ipsilateral SC was optogenetically stimulated. Obtained results revealed that activation of the contralateral SC excites the majority of RMTg neurons, while stimulation of the ipsilateral SC evokes similar proportions of excitatory or inhibitory responses. Consequently, single-unit recordings showed that the activation of RMTg neurons innervated by the contralateral SC, or stimulation of contralateral SC-originating axon terminals within the RMTg, inhibits midbrain DA neurons. Together, the anatomy and physiology of the discovered brain circuit suggest its involvement in the orienting and motivation-driven locomotion of animals based on the direction of external sensory stimuli.SIGNIFICANCE STATEMENT Dopaminergic neurons are the target of predominantly ipsilateral, excitatory innervation originating from the superior colliculus. However, we demonstrate in our study that SC inhibits the activity of dopaminergic neurons on the contralateral side of the brain via the rostromedial tegmental nucleus. In this way, sensory information received by the animal from one hemifield could induce opposite effects on both sides of the dopaminergic system. It was shown that the side to which an animal directs its behavior is a manifestation of asymmetry in dopamine release between left and right striatum. Animals tend to move oppositely to the hemisphere with higher striatal dopamine concentration. This explains how the above-described circuit might guide the behavior of animals according to the direction of incoming sensory stimuli.     

Neonatal ventral hippocampal lesions modify pain perception and evoked potentials in rats

This work concerns the debate surrounding the modified pain reactivity of patients with schizophrenia and other possible perceptive distortions. Rats with a neonatal ventral hippocampal lesion (NVHL) were used to model the neuro-developmental aspect of schizophrenia, and their reactivity to various stimuli was evaluated. The results could also help understand sensory deficits in other neuro-developmental disorders. Behavioural reactions to graduated painful thermal and mechanical stimuli were observed, and evoked potential responsiveness to tactile, visual and acoustic non-painful stimuli was recorded and compared to non-operated and sham lesioned controls. A higher threshold was observed with painful mechanical stimuli and shorter paw withdrawal latency with thermal stimuli. This was particularly relevant as there was no change in the evoked potentials triggered by non-nociceptive tactile stimulation of the same part of the body. There was a 10dB(A) increase in the auditory threshold and a suppression of auditory sensory motor gating. Visually evoked potentials did not appear to be affected. Taken together, the results showed that NVHL-evoked alteration of brain development induces mechanical hypoalgesia, thermal hyperalgesia and auditory sensory changes. The data also contribute towards elucidating mechanisms underlying sensory deficits in neurodevelopmental diseases, including schizophrenia.     

Changes in sensory responsivity in deep layer neurons of the superior colliculus of behaving rats.

Neurons in the deep layers of the superior colliculus in behaving hooded rats were tested for responsivity to visual, auditory, or somesthetic stimuli. Some sensory cells, particularly those responsive to tactile stimuli, showed a change in responsivity (and sometimes an abolishment in firing rate or change in receptive field size) when the animal was gently restrained or placed onto an elevated platform. Thus, sensory neurons in the superior colliculus of the behaving rat have response properties that vary according to the conditions of testing.     

Parietal and frontal eye field neglect in the rat

Rats were given unilateral aspiration lesions of parietal, medial frontal, or dorsolateral frontal (motor) cortex and then tested for visual, auditory and tactile neglect, and for circling. All medial frontal lesion animals showed contralateral neglect in each modality and circled ipsiversively. The parietal lesion rats initially displayed contralateral visual and auditory neglect as severe as that in the medial frontal group. Three weeks after the lesions, the parietal group had a smaller residual deficit on the visual test than the medial frontal group. In the first week, parietal animals responded less than the medial frontals to stroking the vibrissae but were more responsive to mild pinching of a toe contralateral to the lesion side. In striking contrast to the medial frontal animals, the parietal group circled strongly to the contralateral side. No rat with a motor cortex lesion neglected or circled preferentially. Like medial frontal cortex, unilateral parietal lesions also produce neglect and circling, but there are important features distinguishing unilateral lesion effects in these two regions.     

Bilateral and multimodal sensory interactions of single cells in the pigeon's midbrain

Standard microelectrode recording techniques were employed to monitor single unit activity in the pigeon's nucleus intercollicularis and medial substantia grisea et fibrosa periventricularis in response to visual, tactile and auditory stimuli. Approximately 40% of the units were driven exclusively by visual stimuli, 8% by tactile stimuli, 47% by both visual and tactile stimuli and a very small percentage by auditory stimuli. Visual receptive fields were generally excitatory in the contralateral eye and suppressive in the ipsilateral eye. Most units were movement selective and some demonstrated direction sensitivity, summation and habituation. Units were generally insensitive to stimulus shape or contrast reversal. Somatosensory receptive fields were located on both sides of the body and were either excitatory or suppressive or both. Ipsilateral visual and somatosensory bimodal inputs were most often of the same sign while ipsilateral visual and contralateral somatosensory bimodal inputs tended to be of opposite sign. Visual and somatosensory receptive field locations of bimodal units tended to be in register.     

Cholinergic modulation of sensory interference in rat primary somatosensory cortical neurons

Sensory interaction was studied using extracellular recordings from 275 neurons in the primary somatosensory (SI) cortex of pentobarbital-anesthetized rats. Tactile stimulation was applied to the receptive field using a 1 mm diameter probe that indented the skin for 20 ms, at 0.5 Hz, (test stimulus). Tactile test responses of SI neurons decreased during simultaneous application of a gentle tickling (distracter stimuli) continuously for 60 s on a separate receptive field located in the same or the contralateral hindlimb (ipsi- or contralateral distraction). This decrease in neural response produced by distracter stimuli was interpreted as "sensory interference". Sensory interference was observed in 66% and 61% of recorded SI neurons when ipsi- or contralateral distracters were applied, respectively and was blocked by a novel stimulus obtained by increasing the stimulation frequency of the test tactile stimuli from 0.5 to 2 Hz. The number of neurons showing sensory interference in response to a contralateral distracter was not modified after corpus callosum transection, suggesting that interhemispheric connections are not crucial for sensory interference. In contrast, the number of neurons showing sensory interference decreased in animals with 192 IgG-saporin basal forebrain lesions that decreased the number of cortical cholinergic fibers. This finding indicates that cholinergic afferents from the basal forebrain are fundamental to sensory interference and suggests that the associative cortices - basal forebrain - sensory cortices network may be implicated in sensory interference.