Ablation Of Cortex Research Articles

Individual corticorubral neurons project bilaterally during postnatal development and following early contralateral cortical lesions.

The corticorubral projections in adult cats are primarily uncrossed. However, early in development and after early unilateral lesions of the sensorimotor cortex, crossed corticorubral projections are also observed. The present study was performed to disclose (1) whether the crossed projections originate from neuronal subpopulations different from those producing uncrossed ones and (2) how the neurons that give rise to the crossed projections in the lesioned animals are related to those occurring in normal development. We injected fluorescent latex microspheres into the red nucleus of two groups of animals: (1) intact kittens at postnatal week 3 and (2) kittens that had received unilateral ablation of the cerebral cortex at this stage and were then allowed to survive for at least 4 weeks. Red fluorescing microspheres were injected on one side and green ones on the other. In both normal and lesioned kittens, a number of cells in the cortex were labeled as a result of the contralateral as well as the ipsilateral injections, and no difference in size or distribution was found between the cells labeled from contralateral and ipsilateral injections. More than half of the cells labeled from contralateral injections were double-labeled in both groups of animals. These results indicate that individual corticorubral cells project bilaterally in normal development as well as following unilateral lesions of the cortex. With respect to the cells producing crossed projections, they were similar in both laminar and regional distributions between the intact and lesioned animal, suggesting that the crossed projections arise from the same neuronal subpopulation before and after cortical lesions. This view was supported by sequential injections of the tracers, which indicated that cells normally projecting contralaterally maintained the crossed projection after the lesions. Taking into account our previous observations that growth and proliferation of crossed corticorubral axons took place in the red nucleus (Murakami et al. 1991a), it is likely that growth and proliferation of the axons in denervated targets play a major role in lesion-induced establishment of aberrant projections.

Differences in the recovery rate of a learned forelimb movement after ablation of the motor cortex in right and left hemisphere in white rats

After ablation of the motor cortex contralateral to the preferred limb, rats were forced to use this limb in grasping food out of a horizontal tube by restraining the non-preferred foreleg with a bracelet. In a right-handed rat the motor behaviour is less impaired and the recovery is better after a left hemisphere lesion in comparison with a left-handed rat after a right hemisphere lesion. This difference is primarily the time needed to use the limb in reaching for seed (testperiod 3) and the total time needed for 10 successive seizings of seed (testperiod 5). Surprisingly, the differences in the course of recovery do not correlate with the degree of preoperative limb preference: the initially ambidextrous rate also show the same differences in results of the motor cortex ablation in left and right hemisphere. However, in the group of initially consistent ambidextrous rats, after 10 weeks of tests with a restrained forelimb, the testing under unrestrained free conditions shows a gradual decrease in the induced limb preference and a shift to the use of the foreleg contralateral to the intact hemisphere, while in contrast the initially consistent left- or right-handed rats preserve the limb preference under the unrestrained testing conditions. Therefore the degree of initial preference still influences the choice of limb after motor cortex ablation and intensive training to use the ‘damaged’ limb.

Effect of unilateral motor cortex ablation on activity of choline acetyltransferase and levels of amino acid transmitter candidates in the spinal cord of adult monkeys

Evidence that L-glutamate is a neurotransmitter of corticofugal fibers was sought by measuring changes in several biochemical markers of neurotransmitter function in discrete regions of spinal cord after ablation of sensorimotor cortex in monkeys. One and five weeks after unilateral cortical ablation, samples from six areas of spinal cord (ventral, lateral and dorsal regions of the left and right sides) were analysed for choline acetyltransferase (ChAT) activity and contents of amino acid transmitter candidates-glutamic acid (Glu), aspartic acid (Asp), glycine (Gly), taurine (Tau) and gamma-aminobutyric acid (GABA). During one to five weeks after unilateral cortical ablation of the monkey, prolonged hemiplegia in the contralateral side was observed. Histological examination of the spinal cord 5 weeks after unilateral (left) cortical ablation showed no apparent change in either control (ipsilateral, left) or affected (contralateral, right) sides of the cord as examined by the Klüver-Barrera method. The ChAT activity as a cholinergic marker was scarcely changed in any region of either left (control) or right (affected) side of the spinal cord at one and five weeks after unilateral (left side) ablation of the motor cortex. Amino acid levels in each region of the spinal cord were not significantly changed one week after unilateral ablation of the motor cortex. However, a significant decrease of Glu content was observed in the lateral column of the affected (right) side compared to the control (left) side of cervical and lumbar cord five weeks after cortical ablation of the left motor area. No concomitant alterations of other amino acids were detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of bilateral and unilateral ablation of auditory cortex in cats on the unconditioned head orienting response to acoustic stimuli.

1. Reflexive head orienting responses (ORs) elicited by bursts of wide-band noise were investigated in cats after bilateral or unilateral ablation of the auditory cortex, and the cats' performance was compared with that of control cats. The OR was used as an indication of ability to orient toward the azimuthal direction of a source of sound. 2. To adequately test this ability, a unique combination of stimulus duration and position of the sound source was selected on each trial. Stimulus durations (0.1, 0.3, and 1.5 s) were selected so that the offset of a burst of noise occurred before, during, or after an OR. The stimuli were produced from speakers positioned approximately at the interaural horizontal plane within each quadrant of a cat's auditory field. The ORs were recorded on moving film and analyzed quantitatively. 3. In the control cats, the trajectory of the OR was characterized by a saccadic profile (rapid steplike movement, monophasic velocity, and biphasic acceleration). The accuracy of the OR varied directly with stimulus duration, suggesting that the response was modified by auditory feedback produced by a head movement during the stimulus. Corrective responses executed during long-duration (1.5 s) stimuli reduced residual mean error to < 7 degrees in each of the control animals. The mean error in orientation was smaller for sources located in the frontal sound field than for sources located behind the coronal plane the head (> 90 degrees). When brief (0.1 s) stimuli were presented behind the head, the cats confused back with front directions on most of the trials. 4. Compared with performance in the control cats, bilateral destruction of the auditory geniculocortical system severely impaired a cat's ability to orient consistently and accurately toward a source of sound. Latencies to the onset of ORs were increased, the magnitudes of ORs were reduced, average error in orienting to a sound source was larger under every stimulus duration-source position combination, relatively few corrective responses were executed, and residual mean error was significantly elevated (bilateral = 28.1 degrees; control = 3.1 degrees). Several animals with bilateral lesions also made vertical errors in orienting to azimuthal sources of sound. 5. However, in the bilateral lesion group, ORs were initiated in the correct right or left direction; and, rather than eliminating accurate responses altogether, the lesions reduced the probability of their occurrence. Furthermore, the saccadic profile of the response was preserved, providing evidence that the motor control system for the OR was not perturbed by the bilateral lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Gustatory and olfactory contributions to alcohol consumption in rats

To determine the relative contributions of taste and smell in the consumption of alcohol by rats, the present experiment tested normal rats ( n = 14) and rats with either gustatory cortex ablations ( n = 10), olfactory bulbectomies ( n = 11), or combination gustatory cortex and olfactory bulb ablations ( n = 12). Rats were tested under mild fluid deprivation using a two-bottle testing procedure. Thirteen concentrations of alcohol (0.5%, 1%, 2%, 3%, 4%, 5%, 6%, 7%, 8%, 9%, 10%, 11%, and 12%, v/v) were tested in ascending order. Results showed that at strong alcohol concentrations (7% through 11%) rats with combined gustatory cortex and olfactory bulb ablations consumed significantly more alcohol than normal control rats. Rats lacking gustatory cortex displayed a similar increased level of consumption with strong alcohol concentrations. It is suggested that the high level of consumption of strong alcohol concentrations by rats with central nervous system damage reflects an associative deficit rather than an alteration in taste or odor perception.

Transforming growth factor β1 and fibronectin messenger RNA in rat brain: Responses to injury and cell-type localization

Transforming growth factor-β1 rapidly increases in adult rat brain in response to experimental lesions. This study characterized the schedule of changes, regional distribution, and cellular localization of striatal transforming growth factor-β1 messenger RNA and fibronectin messenger RNA following partial striatal deafferentation by frontal cortex ablation. Frontal cortex ablation induced striatal transforming growth factor-β1 messenger RNA elevations that coincided temporally and overlapped anatomically with the course of degeneration of cortico-striatal afferent fibers. Within three days post-lesioning, transforming growth factor-β1 messenger RNA was localized at the cortical wound. By 10 days, the anatomical site of transforming growth factor-β1 messenger RNA expression shifted to the dorsal half of the deafferented striatum and co-localized with OX-42 + immunostained microgliamacrophage at the site of degenerating afferent terminals. Similarly, fibronectin messenger RNA also shifted from the cortical wound to the deafferented striatum by 10 days post-lesioning. Fibronectin messenger RNA was localized to glial fibrillary acidic protein + immunostained astrocytes surrounding degenerating corticostriatal afferents. Infusion of transforming growth factor-β1 peptide elevated striatal and cortical fibronectin messenger RNA. These findings suggest that microglia-macrophage associated with degenerating afferent fibres can upregulate transforming growth factor-β1 messenger RNA and may influence fibronectin messenger RNA synthesis in reactive astrocytes. This study suggests that transforming growth factor-β1 has a role in controlling extracellular matrix synthesis following brain injury, which is analogous to that in peripheral wound healing.

Effect of the somatosensory cortex on the development of the deafferentation pain syndrome

Effects of somatosensory cortex ablation and electrical stimulation on development of deafferentation pain syndrome in rats with sciatic nerve section have been studied. It has been demonstrated that both ablation and stimulation of somatosensory cortex delay the development of pain syndrome. The possible mechanisms of cortical effect on development of deafferentation pain are discussed.

Astrocytic messenger RNA responses to striatal deafferentation in male rat

This investigation describes the schedule and regional distribution of astrocytic responses in striatum following deafferentation by unilateral frontal cortex ablation. In the ipsilateral deafferented striatum, glial fibrillary acidic protein and clusterin (sulfated glycoprotein-2) messengerRNA showed peak elevations by 10 days postlesioning (Northern blots). Vimentin messengerRNA responded faster, with a transient elevation by three days postlesioning. The messengerRNA for glial fibrillary acidic protein, clusterin and vimentin returned toward control levels by 27 days postlesioning. However, the neuronal marker growth-associated protein messengerRNA, was decreased at all postlesion times. By in situ hybridization, the increased glial fibrillary acidic protein messengerRNA and clusterin messengerRNA signals were localized mainly to the dorsal half of the ipsilateral deafferented striatum and followed the same schedule as found by Northern blots. Glial fibrillary acidic protein messengerRNA was widely diffused in the dorsal striatum and was excluded from fascicles of the internal capsule; a similar distribution was found for glial fibrillary acidic protein-immunopositive astrocytes. While clusterin messengerRNA signal showed a distinct clustering, its immunoreactivity appeared as deposits in the deafferented striatal neuropil; Western blots confirmed the immunocytochemical results. By in situ hybridization, vimentin messengerRNA was mostly localized to the cortical wound cavity dorsal to the deafferented striatum and overlapped the distribution of vimentin-immunopositive cells. These findings suggest a coordination of striatal astrocytic messengerRNA responses with the degeneration of corticostriatal afferents. We also compared these same parameters with those from published reports on the hippocampus after deafferenting lesions. Certain astrocyte molecular responses to deafferentation are detected about five days earlier in the hippocampus than in the striatum. This different schedule in response to decortication may pertain to differences in synaptic remodeling in the hippocampus vs striatum.

Multiple brain systems generating the rat auditory evoked potential. II. Dissociation of auditory cortex and non-lemniscal generator systems

This study addressed the issue of multiple parallel auditory processing systems and their relationship to the skull-recorded auditory evoked potentials (AEPs) in the unanesthetized, unrestrained rat. In the preceding paper ( Brain Res., 602 (1993) 240–250) it has been shown that auditory cortex activity does not contribute significantly to the vertex maximal AEPs recorded from the dorsal skull of the rat. In the present study, mapping of the AEP skull distribution revealed two sets of components: one set maximal at the dorsal skull vertex, and another set maximal at the lateral skull over auditory cortex. Barbiturate anesthesia eliminated the dorsal skull maximal components (and later components at the lateral skull), but not the early (P7–P11, N15) lateral skull components generated in auditory cortex. Bilateral auditory cortex ablation eliminated the lateral skull maximal AEP components, but not the dorsal skull maximal components. These findings support extensive parallel processing of auditory inputs (reflected by the dorsal AEPs) in the absence of primary auditorycortex. Ablation of primary auditory cortex did result in a modulation of the dorsal skull AEPs, indicative of an interaction between the geniculocortical system and the parallel system which generates the dorsal AEPs.

Tritiated Uridine Uptake in the Retinal Ganglion Cell Layer of the Cat during Normal Development and after Visual Cortex Ablation

The short-term metabolic response of immature retinal ganglion cells to destruction of their target cells in the dorsal lateral geniculate nucleus (dLGN) was assessed in newborn cats. Retrograde degeneration of virtually all dLGN cells was induced by ablation of the 13 contiguous areas of visual cortex on the day of birth. The metabolic response of retinal ganglion cells to this loss of target cells in dLGN was determined by exposing the ganglion cell layer to tritiated uridine, a precursor of RNA. Control measurements were made from unoperated littermates. Following sectioning and processing of the retinae from both groups of kittens for autoradiography, silver grain densities overlying the cellular profiles in the ganglion cell layer were calculated. These calculations revealed levels of uridine incorporation at Postnatal Day 4 in both groups of kittens significantly higher than at either Postnatal Day 2 or 7, but no significant differences between the two groups on any day examined. These results show that the level of RNA synthesis in retinal ganglion cells increases temporarily during the first postnatal week and that this synthesis is unaffected by the death of target cells in the dLGN. The temporary increase may be related to the establishment of synaptic connections on retinal ganglion cells by their afferent bipolar and amacrine neurons in the inner nuclear layer.

Neurocognitive potentials, cortico-cortical homohemispheric two-way connections and prefrontal cortex ablation or degeneration

Neurocognitive potentials, cortico-cortical homohemispheric two-way connections and prefrontal cortex ablation or degeneration

The pyramidal tract of the hedgehog (Erinaceus europaeus) and its relationship with the olfactory bulb.

The pyramidal tract of the hedgehog has been investigated. The motor cerebral cortex was first located electrophysiologically and subsequently ablated. Ablation of the motor cortex did not apparently cause motor deficits. The cerebral hemisphere of the operated side, brain stem and spinal cord were removed for histological examination. The Nauta-Gygax and the horseradish peroxidase methods were employed to study the course and origin of the above mentioned tract. The pyramidal tract runs ipsilaterally in the cerebral peduncle, and does not go beyond the first cervical segments of the spinal cord (C3-C4); moreover, their fibers do not cross at spinal level. The close relation between this anatomical pathway and the olfactory bulb of the same side is also reported.

Noradrenergic pharmacotherapy, intracerebral infusion and adrenal transplantation promote functional recovery after cortical damage.

The research described in this review briefly summarizes evidence that short term pharmacological enhancement of noradrenergic (NA) synaptic activity, combined with symptom relevant experience (SRE), promotes functional recovery of some symptoms of cortical damage in rat, cat and human beings even when treatment is initiated from days to weeks after injury. A summary is provided of the numerous drugs tested in rodent cortical injury models which have been proven useful for predicting beneficial or harmful effects on behavioral outcome in human stroke. The pattern of drug effects indicates a central role for NA in functional recovery. Additionally, studies of the effects of direct intraventricular infusion of monoamine neurotransmitters are reviewed and further support the hypothesized role of NA in recovery from some symptoms of cortical injury. The site of NA/SRE interaction to promote recovery from hemiplegia apparently involves the cerebellar hemisphere contralateral to the cortical injury. Microinfusions of NA into the contra- but not ipsilaterai cerebellar hemisphere dramatically enhance recovery. Furthermore, like its systemic action, microinfusion of the α1- NA receptor antagonist, phenoxybenzamine, reinstates hemiplegia. A “permanent” symptom of motor cortex injury in the cat is the complete loss of tactile placing contralateral to the injury which does not spontaneously recover for as long as seven years after ablation. This posturai reflex is temporarily restored for 8-12 hours following amphetamine administration. However, this permanently lost reflex can be enduringly restored by transplanting catecholamine secreting adrenal tissue into the wound cavity. The experiment is reviewed in detail and involves chromaffin cell autografts into the frontal cortex ablation wound cavity producing a restoration of tactile placing for the 7-10 month duration of the study. This enduring restoration of tactile placing is considered a result of the release of catecholamines into the CNS from the grafted chromaffin cells found, by histochemical methods, surviving 7-10 months after transplant. Lastly, we attribute these delayed treatment effects to an attenuation of a diaschisis, or remote functional depression, in morphologically intact areas anatomically connected to the area of injury. The widespread reduction of glycolytic and oxidative metabolism, produced by focal cortical injury, is normalized by the same treatment which alleviates symptoms and is worsened by drugs which exacerbate deficits. These data support the hypothesis that providing SRE during a period of enhanced NA synaptic activity produces an enduring functional recovery after cortical injury by attenuating remote functional depression. This treatment for enhancing recovery is especially attractive since it is effective even when begun weeks after cortical damage.

Acute unilateral sensorimotor cortex injury in the rat blocks d-amphetamine induced norepinephrine release in cerebellum

Pharmacologic studies have implicated norepinephrine in amphetamine-facilitated motor recovery following sensorimotor cortex injury in rats. We studied the acute effects of unilateral sensorimotor cortex ablation on the release of norepinephrine in cerebellum with in vivo dialysis. In rats without a cortex lesion, the administration of a single dose of d-amphetamine (2.6 mg/kg base weight, i.p.) resulted in a substantial increase in dialyzable norepinephrine in cerebellum reaching its peak 30-40 min later (∼ 14 pg/μl, not corrected for recovery). The administration of the same dose of d-amphetamine to rats 60 min following a suction-ablation lesion of the right sensorimotor cortex did not result in norepinephrine release into the cerebellar dialysates. These data provide evidence for an acute remote effect of sensorimotor cortex injury on amphetamine-induced norepinephrine release in the cerebellum (diaschisis).

Atrophy and Degeneration of Ganglion Cells in Central Retina Following Loss of Postsynaptic Target Neurons in the Dorsal Lateral Geniculate Nucleus of the Adult Cat

Selective degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN) of the adult cat was produced by in situ injection of kainic acid. This rapid degeneration mimics the loss of lateral geniculate neurons seen after neonatal visual cortex ablation. Following survivals of 2, 4, or 6 months, the geniculate was injected with horseradish peroxidase (HRP) and the retinas were examined for the presence of retrogradely labeled, as well as unlabeled, cells. Total ganglion cell density in central nasal retina was not different from that of controls at 2 or 4 months, but by 6 months had decreased to 68% of control values. The proportion of cells labeled with HRP did not change at 2 months, but decreased from 84% in controls to less than 1% by 4 months, and none were labeled at 6 months. Surviving ganglion cells in central retina showed atrophy of the cell body, a finding not apparent in data from the retinal periphery. Shrinkage occurred in the few cells labeled with HRP surviving at 4 months, as well as among the unlabeled cells surviving at 4 and 6 months. These results show that the survival of central retinal ganglion cells in the cat continues to depend on intact target neurons beyond the period of development. Mature ganglion cells in central retina respond to loss of appropriate targets first by axon terminal retraction and then by atrophy and cell death. However, when compared to the response of cells located in far peripheral retina following dLGN neuron loss, central ganglion cells take longer to undergo axonal retraction and a greater proportion of the central ganglion cells, although atrophied, survive after 6 months.

Defensive responses to looming visual stimuli in monkeys with unilateral striate cortex ablation

A number of residual visual functions including detection, localization and discrimination of visual stimuli, have been demonstrated in the “blind” fields of monkeys and human patients following damage to striate cortex. We report here that avoidance movements of the head can also be elicited from monkeys with unilateral striate cortex ablations when a “looming” stimulus is presented within the hemianopic and presumably “blind” field. The possible role of the retinofugal projection to superior colliculus in the mediation of these defensive head movements is discussed.

Facilitation and recovery of shuttle box avoidance behavior after frontal cortex lesions in induced by a contingent electrical stimulation in the ventral tegmental nucleus

A bilateral ablation of the frontal cortex was performed in rats before and after training in an active avoidance task in a shuttle box. Animals with this lesion showed an impairment in learning and in the reversal of the avoidance task. If the animals with the lesion were implanted with an electrode in the ventral tegmental nucleus and received an electrical stimulation in this area contingent to a correct response (avoidance or escape response) in the behavioral task, they did not show any impairment in the performance of the task. Furthermore, the effect of the stimulation persisted after it was retrieved. The present findings indicate that the motivational and cue properties of the electrical stimulation of the ventral tegmental nucleus may serve to facilitate learning and reversal in an avoidance task and to induce at the long term a recovery process in animals in which the frontal cortex has been ablated. Therefore, this method may be useful to study the adaptative changes which take place in the nervous system after recovery from brain damage occurs.

Parallel processing in rabbit first (SI) and second (SII) somatosensory cortical areas: effects of reversible inactivation by cooling of SI on responses in SII.

1. Previous observations on the effect of ablation or inactivation of the primary somatosensory cortex (SI) on the responses of neurons within the second somatosensory area (SII) to tactile stimuli point to profound differences between monkeys and certain other mammals in the organization of thalamocortical systems. In the cat, for example, tactile information appears to be conveyed in parallel from the thalamus to both SI and SII, whereas, in macaque and marmoset monkeys, it is conveyed in a serial (or hierarchical) scheme from the thalamus to SI and thence to SII. The present study examined the responses of individual SII neurons during reversible, cooling-induced inactivation of SI in another nonprimate placental mammal, the rabbit, to obtain further evidence on whether the above differences might reflect a fundamental distinction between simian primates and other mammalian species. 2. When the temperature at the face of a silver cooling block over the forepaw and hindpaw regions of SI was lowered to 5-13 degrees C, the SI surface potentials evoked by brief tactile stimuli were abolished (indicative of SI inactivation), whereas SII potentials remained intact. 3. The responses of 25 SII neurons to controlled tactile stimuli (consisting of 1- to 1.5-s trains of vibration or rectangular mechanical pulses) were studied before, during, and after inactivation of SI. The effects on the spontaneous activity of a further three SII neurons that lacked identified receptive fields were also studied. 4. The response or activity levels of 26 of the 28 SII neurons examined (93%) were unaffected by SI inactivation.(ABSTRACT TRUNCATED AT 250 WORDS)

Origins and conducting pathways of motor evoked potentials elicited by transcranial magnetic stimulation in cats.

Spinal cord motor evoked potentials (MEPs-S) were elicited in cats by transcranial magnetic stimulation. The MEPs-S recorded from the epidural electrode at the first lumbar (L1) level consisted of four negative peaks (N1, 2.56; N2, 3.19; N3, 4.06; N4, 4.99 ms) followed by small, multiphasic waves. The mean conduction velocities of N1-N3 of the MEPs-S were calculated to be 90 to 115 m/s, which is consistent with extrapyramidal tract activation. A direct brain stem electrical stimulation and sequential transection of the spinal cord studies showed that N1-N3 of the MEPs-S originated primarily from the brain stem and conducted in the ventral funiculus of the spinal cord, which corresponded to the extrapyramidal tracts (e.g., the reticulospinal and vestibulospinal tracts). We also showed that N1 and N2 of the MEPs-S originated mainly from the lower medulla or upper cervical and that N3 originated from the lower pons or upper medulla (vestibular nucleus). On the other hand, N4 of the MEPs-S had a conduction velocity of 70 m/s, which disappeared by ablation of the sensorimotor cortex and pyramidotomy. A dorsal hemisection of the spinal cord, resulting in the disappearance of N4 of the MEPs-S, indicated that it conducted in the dorsolateral funiculus of the spinal cord. These results suggest that N4 of the MEPs-S originates from the sensorimotor cortex and conducts in the lateral corticospinal tract. MEPs-S by transcranial magnetic stimulation in cats constituted complex responses in both the pyramidal and extrapyramidal tracts.

Spontaneous and evoked activity of the caudate neurons to central and peripheral stimuli after brain lesions

The involvement of the cerebral cortex, commissural fibers and thalamus on caudate-caudate relations was studied in locally anesthetized, paralysed and artificially ventilated cats. This type of experimental preparation was necessary since a complete suppression of spontaneous and evoked activity is produced by subanesthetic doses of general anesthesia. Two types of caudate action potentials were encountered on the basis of their waveform characteristics: biphasic and triphasic spikes, the former being the largest population (80%). These waveforms were independent of the microelectrode resistance and the distance to recorded neurons. However, their responses were very similar to both central and peripheral stimuli. Caudate stimulation depressed the spontaneous discharges of the majority of the responsive units recorded within the opposite nucleus, while striatal neurons were activated by stimulation of the contralateral cortex. Decortication, thalamic lesion (motor nuclei and massa intermedia) and section of the corpus callosum decrease the firing rates of caudate neurons with biphasic spikes, while the discharges of the neurons with triphasic action potentials remained unchanged. Bilateral ablation of the cerebral cortex decreased the responsiveness of striatal neurons to contralateral nucleus and sciatic nerve and reduced the number of spontaneously active cells per recording tract. Section of the commissural fibers also depressed the caudate responses to the contralateral nucleus and to the opposite precruciate cortex, although thalamic lesion did not affect the responsiveness of caudate cells to both central and peripheral stimuli. Taking into account the present data and those from a previous paper [O'Donnell P. et al. (1989) Neuroscience 33, 543–548], we concluded that there is a functional relationship between both caudate nuclei, which is partially mediated by the corpus callosum.