Age-dependent sparing of visual function after bilateral lesions of primary visual cortex.

Bilateral lesions of primary visual cortex (PVC) sustained early in life induce the visual system to undergo structural and functional reorganization and produce modified neuronal networks capable of mediating visual abilities that would be impaired if the lesions occurred in adulthood. Reorganization after early lesion is also accompanied by degeneration of the lateral geniculate nucleus of the thalamus, and 90% of beta retinal ganglion cells die via retrograde degeneration. It is unclear whether the high potential of the system to reorganize after early lesion could overcome the effects of beta retinal ganglion cell death. Visual acuity, which depends on an intact beta-cell array, was impaired in cats that underwent PVC lesions on postnatal day 1 and indicated that neuroplastic potential was insufficient to overcome early lesion-induced maladaptive plasticity. Animals with lesions made at 1 month of age, a stage accompanied by high levels of neuroplastic potential but no death of beta cells, achieved acuity measures equivalent to intact animals. The authors conclude that visual signals are rerouted to subserve functionality when the lesion is made at 1 month of age, but not at 1 day of age.

Opposite impact on 14C-2-deoxyglucose brain metabolism following patterns of high and low frequency repetitive transcranial magnetic stimulation in the posterior parietal cortex.

Repetitive transcranial magnetic stimulation (rTMS) appears capable of modulating human cortical excitability beyond the duration of the stimulation train. However, the basis and extent of this "off-line" modulation remains unknown. In a group of anesthetized cats, we applied patterns of real or sham focal rTMS to the visuo-parietal cortex (VP) at high (HF) or low (LF) frequency and recorded brain glucose uptake during (on-line), immediately after (off-line), or 1 h after (late) stimulation. During the on-line period LF and HF rTMS induced a significant relative reduction of (14)C-2DG uptake in the stimulated VP cortex and tightly linked cortical and subcortical structures (e.g. the superficial superior colliculus, the pulvinar, and the LPl nucleus) with respect to homologue areas in the unstimulated hemisphere. During the off-line period HF rTMS induced a significant relative increase in (14)C-2DG uptake in the targeted VP cortex, whereas LF rTMS generated the opposite effect, with only mild network impact. Moderate distributed effects were only recorded after LF rTMS in the posterior thalamic structures. No long lasting cortical or subcortical effects were detected during the late period. Our findings demonstrate opposite modulation of rTMS on local and distant effects along a specific network, depending on the pattern of stimulation. Such effects are demonstrated in the anesthetized animal, ruling out behavioral and non-specific reasons for the differential impact of the stimulation. The findings are consistent with previous differential electrophysiological and behavioral effects of low and high frequency rTMS patterns and provide support to uses of rTMS in neuromodulation.

Pattern motion selectivity in population responses of area 18.

It is commonly believed that the complexity of visual stimuli represented by individual neurons increases towards higher cortical areas. However, even in early visual areas an individual neuron's response is influenced by stimuli presented outside its classical receptive field. Thus, it has been proven difficult to characterize the coding of complex stimuli at the level of single neurons. We therefore investigated population responses using optical imaging in cat area 18 to complex stimuli, plaids. Plaid stimuli are composed of two superimposed gratings moving in different directions. They may be perceived as either two separate surfaces or as a global pattern moving in intermediate direction to the components' direction of motion. We found that in addition to activity maps representing the individual components' motion, plaid stimuli produced activity distributions matching the predictions from a pattern-motion model in central area 18. Thereby, relative component- and pattern-like modulations followed the degree of psychophysical pattern bias in the stimulus. Thus, our results strongly indicate that area 18 exhibits a substantial response to pattern-motion signals at the population level suggesting the presence of intrinsic or extrinsic mechanisms that allow for integration of motion responses from far outside the classical receptive field.

Functional circuitry underlying visual neglect.

Visuospatial neglect is a common neurological syndrome caused by unilateral brain damage to the posterior and inferior parietal cerebral cortex, and is characterized by an inability to respond or orient to stimuli presented in the contralesional hemifield. Neglect has been elicited in experimental models of the rat, cat and monkey, and is thought to result in part from a pathological state of inhibition exerted on the damaged hemisphere by the hyperexcited intact hemisphere. We sought to test this theory by assessing neural activity levels in multiple brain structures during neglect using 2-deoxyglucose (2DG) as a metabolic marker of neural activity. Neglect was induced in two ways: (i) by cooling deactivation of posterior parietal cortex or (ii) in conjunction with broader cortical blindness produced by unilateral lesion of all contiguous visual cortical areas spanning occipital, parietal and temporal regions. The direction and magnitude of changes in 2DG uptake were measured in cerebral cortex and midbrain structures. Finally, the 2DG uptake was assessed in a group of cats in which the lesion-induced neglect component of blindness was cancelled by cooling of either the contralateral posterior parietal cortex or the contralateral superior colliculus (SC). Overall, we found that (i) both lesion- and cooling-induced neglect are associated with decreases in 2DG uptake in specific ipsilateral cortical and midbrain regions; (ii) levels of 2DG uptake in the intermediate and deep layers of the SC contralateral to both cooling and lesion deactivations are increased; (iii) changes in 2DG uptake were not identified in the contralateral cortex; and (iv) reversal of the lesion-induced neglect component of blindness is associated with a reduction of contralesional 2DG uptake to normal or subnormal levels. These data are in accord with theories of neglect that include mutually suppressive mechanisms between the two hemispheres, and we show that these mechanisms operate at the level of the SC, but are not apparent at the level of cortex. These results suggest that the most effective therapies for visual neglect will be those that act to decrease neural activity in the intermediate layers of the SC contralateral to the brain damage.

Functional impact of primary visual cortex deactivation on subcortical target structures in the thalamus and midbrain.

The functional relationships between the primary visual cortex and its major subcortical target structures have long been a subject of interest. We studied these relationships by using localized cooling deactivation to silence portions of primary visual cortex and measuring 2-deoxyglucose (2DG) uptake to assess neural activity in subcortical and midbrain targets. We focused analysis on the largest subcortical targets of primary visual cortex: the superior colliculus (SC), the dorsal lateral geniculate nucleus of the thalamus (dLGN), and the lateral division of the lateral posterior nucleus of the thalamus (LPL). We found that localized cooling of different regions of primary visual cortex caused specific decreases in 2DG uptake in target structures such that the location of 2DG decrease varied according to joint retinotopy, and the magnitude of the decreases in target structures was associated with the amount of cooled cortex. In addition, we found that the impact of cortical cooling was more profound on the SC than on the dLGN. The functional impact of cortical deactivations on the LPL was weak for small deactivations but approximated the impact on the SC when deactivations were large. We discuss these findings in terms of neural circuits and in terms of drivers and modulators.

Impact of repetitive transcranial magnetic stimulation of the parietal cortex on metabolic brain activity: a 14C-2DG tracing study in the cat.

Transcranial magnetic stimulation (TMS) is increasingly utilized in clinical neurology and neuroscience. However, detailed knowledge of the impact and specificity of the effects of TMS on brain activity remains unresolved. We have used 14C-labeled deoxyglucose (14C-2DG) mapping during repetitive TMS (rTMS) of the posterior and inferior parietal cortex in anesthetized cats to study, with exquisite spatial resolution, the local and distant effects of rTMS on brain activity. High-frequency rTMS decreases metabolic activity at the primary site of stimulation with respect to homologue areas in the unstimulated hemisphere. In addition, rTMS induces specific distant effects on cortical and subcortical regions known to receive substantial efferent projections from the stimulated cortex. The magnitude of this distal impact is correlated with the strength of the anatomical projections. Thus, in the anesthetized animal, the impact of rTMS is upon a distributed network of structures connected to the primary site of application.

Neuroplasticity after unilateral visual cortex damage in the newborn cat.

Anatomical, electrophysiological, and behavioral studies implicate extrastriate cortex as a major contributor to the sparing of visually guided behaviors following lesions of primary visual cortex incurred early in life. Here we report considerable sparing of the ability to detect and localize stimuli in the hemifield contralateral to unilateral early lesions of all contiguous visually-responsive primary and extrastriate cortical regions (occipital, visuoparietal, and visuotemporal cortices). In the adult cat this same lesion induces a dense blindness and cats are unable to orient to any visual stimulus introduced into the contralesional hemifield. In the absence of cortical circuits, the neural sparing identified following the neonatal lesion is based on the superior colliculus and it occurs despite massive retrograde transynaptic degeneration of large numbers of retinal ganglion cells.

Cerebral areas mediating visual redirection of gaze: cooling deactivation of 15 loci in the cat.

In humans, damage to posterior parietal or frontal cortices often induces a severe impairment of the ability to redirect gaze to visual targets introduced into the contralateral field. In cats, unilateral deactivation of the posterior middle suprasylvian (pMS) sulcus in the posterior inferior parietal region also results in an equally severe impairment of visually mediated redirection of gaze. In this study we tested the contributions of the pMS cortex and 14 other cortical regions in mediating redirection of gaze to visual targets in 31 adult cats. Unilateral cooling deactivation of three adjacent regions along the posterior bend of the suprasylvian sulcus (posterior middle suprasylvian sulcus, posterior suprasylvian sulcus, and dorsal posterior ectosylvian gyrus at the confluence of the occipital, parietal, and temporal cortices) eliminated visually mediated redirection of gaze towards stimuli introduced into the contralateral hemifield, while the redirection of gaze toward the ipsilateral hemifield remained highly proficient. Additional cortical loci critical for visually mediated redirection of gaze include the anterior suprasylvian gyrus (lateral area 5, anterior inferior parietal cortex) and medial area 6 in the frontal region. Cooling deactivation of: 1) dorsal or 2) ventral posterior suprasylvian gyrus; 3) ventral posterior ectosylvian gyrus, 4) middle ectosylvian gyrus; 5) anterior or 6) posterior middle suprasylvian gyrus (area 7); 7) anterior middle suprasylvian sulcus; 8) medial area 5; 9) the visual portion of the anterior ectosylvian sulcus (AES); 10) or lateral area 6 were all without impact on the ability to redirect gaze. In summary, we identified a prominent field of cortex at the junction of the temporo-occipito-parietal cortices (regions pMS, dPE, PS), an anterior inferior parietal field (region 5L), and a frontal field (region 6M) that all contribute critically to the ability to redirect gaze to novel stimuli introduced into the visual field during fixation. These loci have several features in common with cortical fields in monkey and human brains that contribute to the visually guided redirection of the head and eyes.

Neuroplasticity in the cat's visual system: test of the role of the expanded retino-geniculo-parietal pathway in behavioral sparing following early lesions of visual cortex.

Sparing of the ability to redirect head and eyes to new stimuli and expansion of the retino-geniculo-parietal pathway are both robust aspects of the repercussions of early lesions of occipital visual areas in cats. The purpose of the present work was to test the proposition that the pathway expansions and spared behaviors are causally linked. The proposition was tested by deactivating either the dorsal lateral geniculate nucleus (dLGN) and thereby uncoupling the primary and secondary limbs of the retino-geniculo-parietal pathway, or silencing the terminus of the pathway, and then testing the ability of cats to detect and orient head and eyes to visual targets. Six cats sustained experimental unilateral lesions of occipital areas 17 and 18 and variable amounts of area 19 on postnatal days 1-2 or 26-30 to induce rewiring and expansion of visual pathways from retina through the dLGN onto a critical region of visuoparietal (VP) cortex. Unilateral lesions ensured that we could use the orienting performance of the intact hemisphere as a fiduciary marker of performance against which performance of the experimental hemisphere could be gauged. When the cats were adult, a secondary test lesion was made on the damaged side by injecting, under electrophysiological guidance, ibotenic acid into either dLGN of four cats or into VP cortex of two cats. Prior to injection of ibotenic acid, all cats oriented head and eyes with high proficiency throughout the contralesional field, and performance was indistinguishable from orienting to stimuli presented in the ipsilesional field; sparing of the orienting behavior was complete. Ibotenic acid lesions of both dLGN and VP cortex induced a profound neglect of stimuli introduced into the contralesional hemifield. Orienting into the ipsilesional field remained high throughout. Subsequently, there was restoration of orienting behavior over the next 4-6 (dLGN deactivation) and 9-12 (VP deactivation) days. The test results demonstrate the essential contribution made by the retino-geniculo-parietal pathway to the ability to detect and redirect head and eyes to look at visual stimuli following early lesions of occipital visual cortices. The subsequent post-test lesion restoration of high orienting proficiency shows that in the absence of dLGN, or the critical region of VP cortex, other regions of cerebral cortex, or other structures such as the superior colliculus, can emerge and make important contributions to orienting behavior. These results reveal a maintained residual, beneficial adaptive plasticity of mature neural circuits even in brains compromised by early lesions of occipital visual areas.

Greater sparing of visually guided orienting behavior after early unilateral occipital lesions: insights from a comparison with the impact of bilateral lesions.

We know that cats with bilateral lesions of occipital visual cortical areas 17, 18 and 19 sustained during the first postnatal week exhibit a modest level of sparing of the ability to re-orient head and eyes to new stimuli relative to cats that incurred equivalent lesions in adulthood. We now report that cats with equivalent unilateral lesions sustained during the first postnatal week (P1-4), or at the end of the first postnatal month (P27-30), orient to stimuli presented in the contralesional field as proficiently as to stimuli introduced into the ipsilesional field. Moreover, levels of proficiency are indistinguishable from those exhibited by intact cats. Thus, the sparing is greater following unilateral lesions than following bilateral lesions, and the level of sparing approaches completeness. The difference between the bilateral and unilateral lesion results suggests types of pathway reorganizations that may emerge as a result of unilateral occipital lesions. We postulate that the greater sparing is based on modifications in both excitatory and inhibitory circuitry linked to the intact hemisphere, and we provide a framework for future investigations that should be relevant to the comprehension of the repercussions of early unilateral and bilateral lesions sustained by monkeys and humans, which also show more robust residual vision following early relative to later damage of occipital cortex.

Functional circuitry underlying natural and interventional cancellation of visual neglect.

A large body of work demonstrates that lesions at multiple levels of the visual system induce neglect of stimuli in the contralesional visual field and that the neglect dissipates as neural compensations naturally emerge. Other studies show that interventional manipulations of cerebral cortex, superior colliculus or deep-lying midbrain structures have the power to attenuate, or cancel, the neglect and reinstate orienting into a neglected hemifield, and even into a profound cortically blind field. These results, and those derived from experiments on the behavioral impacts of unilateral and bilateral lesions, lead us to evaluate the repercussions of unilateral and bilateral deactivations, neural compensations and cancellations of attentional deficits in terms of an overarching hypothesis of neglect. The cancellations can be both striking and enduring, and they suggest that therapeutic strategies can be developed to reverse or ameliorate neglect in human patients. Animal studies show that in many instances of neglect adequate representations and the accompanying motor mechanisms are present despite the lesion and they simply need to be unmasked and brought into use to effect a remedy.

Non-invasive induction and cancellation of visuo-spatial deficits by repetitive Transcranial Magnetic Stimulation (rTMS): Lessons on “surgery-less” manipulation of complex visuo-spatial brain networks

Repetitive Magnetic Stimulation (rTMS) has shown to modify the excitability of targeted cortical regions in animals and humans, thus transiently altering the efficiency of neural projections within extended brain networks. Adequate processing and behavioral output depend on a given ‘state’ of functional interactions between cortical and subcortical nodes within this network. We applied rTMS trains targeted at the visuoparietal (VP) cortex, which is a crucial cortical node of an extended visuo-spatial neural network, in both, intact (n=2) and injured cats (n=2) with unilateral ablation of the VP region. All four intact cats were intensively trained in a set of visuo-spatial tasks consisting in the detection and localization of moving or static targets. In two of these cats, a 50 mm circular coil was centered on the left VP cortex and Sham or real rTMS was delivered during 20 minutes at 1 Hz. Real but not Sham rTMS significantly increased the number of errors in orienting responses towards static but not moving targets, presented at the contralateral visual hemifield (38±4%; and 48±3% p<0.05 vs. pre rTMS), whereas no increase respect to baseline was observed for ipsilateral targets (5±2%; 2±1%; n.s). Performance went back to baseline error levels 45 minutes after the end of the stimulation (4±2; 6±1%). In 2 other animals, the right or left parietal and primary visual cortex was surgically removed, generating a Daily stimulation with 1 Hz rTMS on the intact VP region resulted in a progressive reduction of detection¬orienting mistakes to moving but not static stimuli (down to 34±5% and 28±4% errors; p<0.05). We conclude that rTMS is able to interact with brain networks in both ways, transiently disrupting visuo-spatial processing in normal animals, and also canceling spatial neglect generated by lesions of the same areas. It constitutes, thus, a non-invasive ‘surgery-less’ method to manipulate brain activity and promote recovery after injuries.

Animal models of cerebral neglect and its cancellation.

The purpose of this perspective is twofold: 1) to alert and inform the neurospychology and neurology communities on how animal models can improve our understanding of spatial neglect in humans, and 2) to serve as a guide to rehabilitation strategies. Spatial neglect is a neurological syndrome that is inextricably linked to the ability to overtly or covertly reorient attention to new loci. Literature describing variants of neglect leads to the perception of lesion-induced neglect as a uniquely human syndrome for which there are limited treatment options. To the contrary, neglect has been reversed in laboratory animals, and results show that adequate neural representations and motor mechanisms for reversal are present despite damaged or deactivated cerebral cortex. These results and conclusions provoke thought on strategies that can be employed on humans to cancel neglect, and they suggest that long-term amelioration of neglect can be induced by training of specific bypass circuits.

Quantitative analyses of principal and secondary compound parieto-occipital feedback pathways in cat.

The purpose of our study was to quantify the magnitude of principal and secondary pathways emanating from the middle suprasylvian (MS) region of visuoparietal cortex and terminating in area 18 of primary visual cortex. These pathways transmit feedback signals from visuoparietal cortex to primary visual cortex. (1) WGA-HRP was injected into area 18 to identify inputs from visual structures. In terms of numbers of neurons, feedback projections to area 18 from MS sulcal cortex (areas PMLS, AMLS and PLLS) comprise 26% of inputs from all visual structures. Of these neurons, between 21% and 34.9% are located in upper layers 2-4 and the dominant numbers are located in deep layers 5 and 6. Areas 17 (11.8%) and 19 (11.2%) provide more modest cortical inputs, and another eight areas provide a combined total of 4.3% of inputs. The sum of neurons in all subcompartments of the lateral geniculate nucleus (LGN) accounts for another 34.8% of the input to area 18, whereas inputs from the lateral division of the lateral-posterior nucleus (LPl) account for the final 11.9%. (2) Injection of tritiated-((3)H)-amino acids into MS sulcal cortex revealed substantial direct projections from MS cortex that terminated in all layers of area 18, but with a markedly lower density in layer 4. Projections from MS cortex to both areas 17 and 19 are of similar density and characteristics, whereas those to other cortical targets have very low densities. Quantification also revealed minor-to-modest axon projections to all components of LGN and a massive projection throughout the LP-Pul complex. (3) Superposition of the labeled terminal and cell fields identified secondary, compound feedback pathways from MS cortex to area 18. The largest secondary pathway is massive and it includes the LPl nucleus. Much more modest secondary pathways include areas 17 and 19, and LGN. The relative magnitudes of the secondary pathways suggest that the one through LPl exerts a major influence on area 18, whereas the others exert more modest or minor influences. MS cortex in the contralateral hemisphere also innervates area 18 directly. These data are important for interpreting the impact of deactivating feedback projections from visuoparietal cortex on occipital cortex.

Bilateral impact of unilateral visual cortex lesions on the superior colliculus.

We examined the functional impact of a long-standing, unilateral primary visual cortex lesion on the superior colliculus (SC) using radiolabeled 2-deoxyglucose (2DG) as a marker of neural activity. In accord with known corticotectal connectivity and functional influence, 2DG uptake in the superficial layers of the ipsilesional SC was decreased. We also found a decrease in the superficial layers of the contralesional SC. These data suggest that modifications in activity in one SC can have a substantial influence on activity in its contralateral partner, and that processing in one visual hemifield does not occur independently of processing of signals in the opposite hemifield. The effects are not mediated by the contralateral hemisphere but are probably mediated by intercollicular circuitry.

Limit of spared pattern vision following lesions of the immature visual cortex.

Lesions of primary visual cortex sustained early in life spare certain aspects of visual processing that can be linked to expansions of bypass pathways to extrastriate cortex. They also trigger, in an age-dependent way, partial or complete transneuronal retrograde degeneration of beta (X) retinal ganglion cells, which are implicated in visual processing under conditions of low contrast. We used two-dimensional geometric patterns whose saliency was reduced by gradually increasing levels of superimposed masking lines, and by reductions in spatial contrast. Normative data were collected from intact cats, and baseline lesion data were collected from cats with lesions sustained as young adults (postnatal day 180, P180). Experimental data were collected from cats that sustained lesions on P1-3 or P26-30. For high contrast patterns, the adult group was impaired at both acquisition (sequential progressive levels of masking) and concurrent (parallel high and low levels of masking) performance, whereas the early-lesioned groups were impaired only at concurrent performance. All lesion groups were equally impaired when contrast was reduced to modest or lower levels. These results show that sparing of masked-pattern learning is limited to the high end of the spatial contrast domain.

Cancellation of visuoparietal lesion-induced spatial neglect.

In humans lesions of right visuoparietal cortex induce a neglect of the contralesional visual field that is characterized in its mild form by inattentiveness to objects and events and, in its more severe form, by a condition that has many features that are indistinguishable from blindness. Here we show that spatial neglect can be induced in cats by lesions of posterior and inferior visuoparietal cortex, and that the lesion-induced neglect can be cancelled by cooling deactivation of the same region in the opposite hemisphere.

The role of feedback in shaping neural representations in cat visual cortex.

In the primary visual cortex, neurons with similar response preferences are grouped into domains forming continuous maps of stimulus orientation and direction of movement. These properties are widely believed to result from the combination of ascending and lateral interactions in the visual system. We have tested this view by examining the influence of deactivating feedback signals descending from the visuoparietal cortex on the emergence of these response properties and representations in cat area 18. We thermally deactivated the dominant motion-processing region of the visuoparietal cortex and used optical and electrophysiological methods to assay neural activity evoked in area 18 by stimulation with moving gratings and fields of coherently moving randomly distributed dots. Feedback deactivation decreased signal strength in both orientation and direction maps and virtually abolished the global layout of direction maps, whereas the basic structure of the orientation maps was preserved. These findings could be accounted for by a selective silencing of highly direction-selective neurons and by the redirection of preferences of less selective neurons. Our data suggest that signals fed back from the visuoparietal cortex strongly contribute to the emergence of direction selectivity in early visual areas. Thus we propose that higher cortical areas have significant influence over fundamental neuronal properties as they emerge in lower areas.

Plasticity of the visual cortex after injury: what's different about the young brain?

The repercussions of localized injury of the cerebral cortex in young brains differ from the repercussions triggered by equivalent damage of the mature brain. In the young brain, some distant neurons are more vulnerable to the lesion, whereas others survive and expand their projections to bypass damaged and degenerated structures. The net result is sparing of neural processing and behaviors. This article summarizes both the modifications in visual pathways resulting from visual cortex lesions sustained early in life and the neural and behavioral processes that are spared or permanently impaired. Experiments using reversible deactivation show that at least two highly localizable functions of normal cerebral cortex are remapped across the cortical surface as a result of an early lesion of the primary visual cortex. Moreover, the redistributions have spread the essential neural operations underlying orienting behavior from the visual parietal cortex to a normally functionally distinct type of cortex in the visual temporal system, and in the opposite direction for complex-pattern recognition. Similar functional reorganizations may underlie sparing of neural processes and behavior following early lesions in other cerebral systems, and these other systems may respond well to emerging therapeutic strategies designed to enhance the sparing of functions.

Restoration of visual orienting into a cortically blind hemifield by reversible deactivation of posterior parietal cortex or the superior colliculus.

A contralateral hemineglect of the visual field can be induced by unilateral cooling deactivation of posterior middle suprasylvian (pMS) sulcal cortex of the posterior parietal region, and this neglect can be reversed by additional cooling deactivation of pMS cortex in the opposite hemisphere. The purpose of the present study was to test whether an enduring hemianopia induced by removal of all contiguous visual cortical areas of one hemisphere could be reversed by local cooling of pMS cortex in the opposite hemisphere. Two cats sustained large unilateral ablations of the contiguous visual areas, and cooling loops were placed in the pMS sulcus, and in contact with adjacent area 7 or posterior ectosylvian (PE) cortex of the opposite hemisphere. In both instances cooling of pMS cortex, but neither area 7 nor PE, restored a virtually normal level of orienting performance to stimuli presented anywhere in the previously hemianopic field. The reversal was highly sensitive to the extent of cooling deactivation. In a third cat, cooling deactivation of the superficial layers of the contralateral superior colliculus also restored orienting performance to a cortical ablation-induced hemianopia. This reversal was graded from center-to-periphery in a temperature-dependent manner. Neither the cortical ablation nor any of the cooling deactivations had any impact on an auditory detection and orienting task. The deactivations were localized and confirmed by reduced uptake of radiolabeled 2-deoxyglucose to be limited to the immediate vicinity of each cooling loop. The results are discussed in terms of excitation and disinhibition of visual circuits.