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PubMed1999

Motor skills training enhances lesion-induced structural plasticity in the motor cortex of adult rats.

To assess behavioral experience effects on synaptic plasticity after brain damage, the present study examined the effects of complex motor skills training (the acrobatic task) on synaptic changes in layer V of the motor cortex opposite unilateral damage to the forelimb sensorimotor cortex (FLsmc). Adult male rats were given lesions or sham operations followed by 28 d of training on the acrobatic task [acrobat condition (AC)]. As a motor activity control [motor control (MC)], lesion and sham animals were given simple repetitive exercise. Previously, FLsmc lesions and acrobatic training have independently been found to result in increases in synapse to neuron ratios in the intact motor cortex relative to controls, and both of these effects were replicated in the present study. In addition, acrobat training after lesions significantly increased layer V synapses per neuron relative to sham-AC and lesion-MC rats. Thus, the combination of acrobatic training and lesions resulted in an enhanced synaptogenic response. Synapse subtypes were also differentially affected by the conditions. Lesion-MC and sham-AC primarily had increases in the number of synapses per neuron formed by multiple synaptic boutons in comparison to sham-MC. In contrast, lesion-AC had increases in both multiple and single synapses. Multiple synaptic spines and perforated synapses were also differentially affected by training versus lesions. On tests of coordinated forelimb use, lesion-AC rats performed better than lesion-MC rats. In addition to supporting a link between behavioral experience and structural plasticity after brain damage, these findings suggest that adaptive neural plasticity may be enhanced using behavioral manipulations as "therapy."

Animals↗
PubMed1982

[Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex].

The field potentials in response to stimulation of the cerebral sensorimotor cortex and of the limb nerves were recorded in the granular layer of the cerebellar paramedian lobule in nonanesthetized cats. The field potentials contained long-latency components, i.e. slow negative waves generated by granule cells. The long-latency component to nerve stimulation was recorded both inside and outside the projection area of the given limb, while the cerebral stimulation with a low intensity (1.8-2.5 thresholds) evoked this component in the given projection area only. The long latency component to cerebral stimulation followed higher rates and was less sensitive to the action of the barbital anaesthesia than the component following the nerve stimulation. Simultaneous cerebral and nerve stimulation evoked the long latency component equal to the sum of the separate components. It is suggested that slow conduction spinal and cerebral inputs form separate mossy fibres - granule cell pathways.

Animals↗
PubMed2000

Motor cortical potentials precede long-latency EMG activity evoked by imposed displacements of the human wrist.

Rapid angular displacements of the wrist evoke cerebral potentials that precede the onset of the long-latency electromyographic (EMG) activity generated in muscles stretched by the displacement. The initial segment of the long-latency EMG activity (termed the M2 response) is thought to be mediated by a transcortical reflex. We used dipole source analysis to examine the source generators of the early components of the cerebral potentials and their relationship to the timing and magnitude of the M2 response. Subjects (n=10) were presented with instructions to either actively flex or extend the wrist in response to a torque motor-imposed extensor displacement or allow the wrist to be passively extended. Electroencephalographic (EEG) recordings were obtained from 32 scalp-surface electrodes, and EMG was recorded from the wrist flexors and extensors. For all three tasks, the M2 response was preceded by cerebral potentials that could be explained by a three-dipole model. One source generator localised to deep within the cerebrum, and the other two localised to the region of the contralateral sensorimotor cortex. We used the P20-N20 dipole evoked by electrical stimulation of the median nerve at the wrist, corresponding to synaptic activity within cortical area 3b, as a local spatial reference to examine the contributions of the pre- and postcentral cortex. This analysis showed that one of the sensorimotor dipoles was consistently located anterior to the P20-N20 dipole at a displacement (average 11.5 mm) appropriate for a generator originating within the deep layers of area 4 on the anterior bank of the central sulcus. The orientation of this dipole was also consistent with a precentral generator and not a reversal of the potentials generated by input to area 3b. The time course of the area-4 dipole moment (onset =35 ms, peak =54 ms) was appropriate to reflect synaptic activity onto corticospinal neurons whose descending volleys mediate the M2 response. Comparisons across tasks showed that the magnitude of the M2 was modulated with task instruction, being largest with active and smallest with passive resistance. In contrast, the magnitude of the early evoked potentials (up to 75 ms) did not grade across tasks. We interpret these results as suggesting that instruction-dependent modulation of the M2 response occurs downstream from inputs to the primary motor cortex.

Adult↗
PubMed1988

Recovery of sensorimotor function after frontal cortex damage in rats: evidence that the serial lesion effect is due to serial recovery.

Multiple-staged brain lesions produce fewer and smaller behavioral effects than does damage produced in a single surgery. This is called the serial lesion effect. Two hypotheses were tested, the reduced deficit hypothesis and the serial recovery hypothesis, which attempt to explain the serial lesion effect. The effects of lesions of the medial frontal cortex on sensorimotor behavior were investigated in rats that received bilateral damage in a single surgery (n = 7), in two unilateral stages separated by 3 weeks (n = 16), or unilateral damage followed 3 weeks later by a sham surgery (n = 5). Unilateral damage produced deficits on the contralateral side in responsivity to visual, tactile, and olfactory stimuli and impairments in roll-over and paw withdrawal motor responses. All behavioral impairments except visual placement recovered over the next 3 weeks. A second unilateral lesion on the contralateral side produced the same symptoms but on the opposite side of the body. There was no reinstatement of the previously recovered deficits. Bilateral damage incurred in a single stage produced these same deficits on both sides. Because the effects of the second unilateral lesion in the two-stage group produced comparable contralateral effects to those produced in the single-stage group, but no reinstatement of ipsilateral deficits occurred, the reduced deficit hypothesis was rejected. It was concluded that at least for medial frontal cortex damage, the serial lesion effect occurred as a result of serial recovery of the deficits.

Animals↗
PubMed2003

Enactment effect in memory: evidence concerning the function of the supramarginal gyrus.

Experimental behavioral data show that written action descriptions are remembered better when encoded by enacting them compared with merely verbal encoding. To explore this facilitating effect of encoding by performing actions ('enactment effect'), a functional magnetic resonance imaging (fMRI) study was conducted with n=18 normal subjects. During a learning condition, subjects encoded action phrases like 'cut the bread' either by reading aloud or by enacting them. The same phrases plus additional distractors were presented during fMRI scanning, and the task was to decide (yes/no key press) whether a displayed phrase was previously learned or whether it was a new one. Retrieval--independent of encoding type--activated anterior cingulate, SMA, and visual cortex bilaterally. Activations of the inferior frontal and sensorimotor cortex, and the precentral sulcus, were only left sided. The right cerebellum was also activated. The subtraction of the brain activations in the verbal condition from the enactment condition resulted in significant clusters located in middle temporal and inferior parietal left cortical areas, and, on the right side, in superior temporal, postcentral and inferior parietal cortical areas. Most striking were the bilateral inferior parietal activations, covering the supramarginal gyrus (SMG). Therefore it is concluded that SMG may be a central structure in a neurofunctional explanation of the enactment effect.

Adult↗
PubMed1997

Differential psychopathology and patterns of cerebral glucose utilisation produced by (S)- and (R)-ketamine in healthy volunteers using positron emission tomography (PET).

Until recently, racemic ketamine (S-ketamine/R-ketamine = 50:50) has been used to study NMDA receptor hypofunction in relation to pathophysiological models of schizophrenia. Ketamine given to normal humans in subanesthetic doses produces a model psychosis including both positive and negative symptoms of schizophrenia. More recently it has been shown that at subanesthetic doses the pure (S)- and (R)-ketamine enantiomeres interact differently with the NMDA and sigma receptor sites in human brain. It was found that (S)-ketamine binds with a 3-4 time higher affinity to the PCP binding site of the NMDA receptor than (R)-ketamine, and that at these concentrations (R)-ketamine interacts also weakly with the sigma receptor sites, where (S)-ketamine binds only negligibly. To further investigate the role of NMDA-receptor mediated neurotransmission in schizophrenic psychosis, the effects of pure (S)- and (R)-ketamine enantiomeres on brain energy metabolism in normal humans using positron emission tomography and [18F]fluorodeoxyglucose (FDG) are reported here. Psychotomimetic doses of (S)-ketamine increased cerebral metabolic rates of glucose (CMRglu) markedly in the frontal cortex including the anterior cingulate, parietal and left sensorimotor cortex, and in the thalamus. The metabolic changes in the frontal and left temporal cortex correlated with ego-disintegration and hallucinatory phenomena. Equimolar doses of (R)-ketamine tended to decrease CMRglu across brain regions and significantly suppressed CMRglu in the temporomedial cortex and left insula. (R)-ketamine did not produce psychotic symptoms, but a state of relaxation. The (S)-ketamine-induced metabolic hyperfrontality appears to parallel similar metabolic findings in acute psychotic schizophrenic patients and encourages further investigations of glutamatergic disturbances in schizophrenia.

Adult↗
PubMed2001

Sensory disturbances after focal extirpations of the human "motor" cortex.

From the late 1800s until approximately the middle of the 20th century, neurosurgeons made discrete motor cortex lesions in humans in attempts to reduce or eliminate a variety of involuntary movements, resulting mainly from epilepsy. In some cases, the neurosurgeons tested and recorded their patients' ability to perform various movements and to perceive various types of sensory stimuli after the operation. Although these studies have been largely forgotten, they have an immense advantage over primate lesion studies for understanding the function of the motor cortex because the patients were able to attempt to perform complex movements upon request, and to describe their perceptions of cutaneous stimuli, including integrated sensations (e.g., recognition of objects by palpation alone). We provide here a table containing the results of these studies pertaining to sensory deficits. The most consistent and persistent sensory deficits reported relate to object recognition and position sense. This finding is in keeping with recent electrophysiological studies in primates. Our analysis suggests that the "motor" cortex serves important sensory functions; hence, the term sensorimotor cortex, remains appropriate for the primate precentral (and postcentral) cortex.

Epilepsies, Partial↗
PubMedDate not supplied

[Changes in the cholinosensitivity of sensomotor cortex neurons during conditioned reflex extinction].

Characteristics of neuronal responses of the sensorimotor cortex to ionophoretically administered neuromediators (acetylcholine, L-glutamate) were studied in rabbit in the course of extinction of conditioned defensive reflex. In the majority of neurones the extinction of the conditioned reflex is accompanied by a drop of cholinosensitivity. In a number of neurones the extinction of reflexes either does not change the reaction to acetylcholine, or enhances it. The analysis of these reactions permits to assume the existence of a group of neurones directly involved in the formation, fixation and storage of the temporary connection.

Acetylcholine↗
PubMedDate not supplied

[Correlation between the amplitude of action potentials and the rate of conduction along axons of the output cells of the sensomotor cortex].

Antidromic responses of neighbouring neurones in micro-areas of the sensorimotor cortex to the stimulation of fibers of the pyramidal tract as well as of the red nucleus and thalamic nuclei VPL and MGB, were studied in acute experiments on unanesthetized immobilized cats. Depending on the velocity of conduction along the axon, the neurones of all the categories were divided into fast and slow cells. When examining the two neuronal groups most differing in AP amplitude (N1 and N3), it was found that N1 neurones were mainly fast-conducting and N3 neurones-- slow-conducting. The conclusion is made that at multineuronal recording, each of the examined categories of the output neurones is characterized by positive correlation between AP amplitude and the axon conduction velocity and consequently, the size of the cell.

Animals↗
PubMed1996

[Effects of small fluxes of heavy charged particles on neurons of the rats' cerebral cortex in delayed periods following irradiation].

Dystrophic changes in neurons of the sensorimotor cortex of rat's brain in delayed periods following exposure to small fluxes, i.e. 104 and 105 particles/cm2, of accelerated carbon, fluorine, and oxygen ions with an energy of 300 MeV/nucleon and 137Cs gamma-rays at a dose of 1.0 Gy were quantitatively analyzed. Some structural changes of varying degree including death of a part of neurons were observed; however, most of the cells looked unaltered. Glial elements and small blood vessels also developed a reaction. Dynamics of the morphologic changes was studied. Higher effectiveness of small fluxes of heavy charged particles versus gamma-radiation at a dose of 1.0 Gy and dependence of the depth of structural disorders on linear energy transfer were demonstrated.

Animals↗
PubMed1989

An anterograde tracer study on the development of corticospinal projections from the medial prefrontal cortex in the rat.

The aim of the present study is to investigate, both qualitatively and quantitatively, the development of corticospinal (CS) projections from the medial prefrontal cortex of the rat. This study was carried out with the use of anterogradely transported wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) after iontophoretic injections in the medial prefrontal cortex. For comparison similar injections are made in the sensorimotor cortex. The CS axons of neurons situated in the medial prefrontal cortex have reached the first thoracic segment (T1) at postnatal day 3 (P3) and reach their most caudal extension in the spinal cord sixth thoracic segment (T6) at postnatal day 7 (P7) and then gradually disappear during the second postnatal week. Quantitative results revealed that after labelling of the medial prefrontal cortex no peaks in labelling density, neither at the cervical nor at the lumbar intumescence, were present. Furthermore, the CS axons of medial prefrontal neurons never showed any outgrowth into the spinal grey matter at any age studied. Concludingly, the extension and subsequent elimination of CS axons originating in the medial prefrontal cortex follow a similar time course as those from the occipital cortex (Dev. Brain Res., 36 (1987) 121-130).

Animals↗
PubMed2006

An animal model of capsular infarct: endothelin-1 injections in the rat.

In this study stereotaxic injections of the vasoconstrictive peptide endothelin-1 (ET-1) were used to create infarcts in the white matter of the internal capsule underlying sensorimotor cortex in rats. Resulting deficits were assessed using established sensorimotor tests conducted on each rat before and after the ET-1-induced infarct. After a 14-day survival period, histological examination revealed tissue necrosis and demyelination in the infarcted white matter of ET-1-injected rats, but not saline-injected control rats. Infarcts resulted in measurable sensorimotor deficits in rats that received ET-1 injections. The same sensorimotor tests showed no deficits in surgical-control rats. The present model of white matter infarct should be valuable in examining the underlying mechanisms of subcortical ischemic stroke and to evaluate potential therapeutic interventions.

Animals↗
PubMed2000

Tickling expectations: neural processing in anticipation of a sensory stimulus.

Predictions of the near future can optimize the accuracy and speed of sensory processing as well as of behavioral responses. Previous experience and contextual cues are essential elements in the generation of a subjective prediction. Using a blocked fMRI paradigm, we investigated the pattern of neural activation in anticipation of a sensory stimulus and during the processing of the somatosensory stimulus itself. Tickling was chosen as the somatosensory stimulus rather than simple touch in order to increase the probability to get a high degree of anticipation. The location and nature of the stimulus were well defined to the subject. The state of anticipation was initiated by attributing an uncertainty regarding the time of stimulus onset. The network of activation and deactivation during anticipation of the expected stimulus was similar to that engaged during the actual sensory stimulation. The areas that were activated during both states included the contralateral primary sensory cortex, bilateral areas in the inferior parietal lobules, the putative area SII, the right anterior cingulate cortex and areas in the right prefrontal cortex. Similarly, common decreases were observed in areas of sensorimotor cortex located outside the area representing the target of stimulus, i.e., areas that process information which is irrelevant to the attended process. The overlapping pattern of change, during the somatosensory stimulation and the anticipation, furthers the idea that predictions are subserved by a neuronal network similar to that which subserves the processing of actual sensory input. Moreover, this study indicates that activation of primary somatosensory cortex can be obtained without intra-modal sensory input. These findings suggest that anticipation may invoke a tonic top-down regulation of neural activity.

Adult↗
PubMed2002

MR changes after acute cyanide intoxication.

We describe MR changes that occurred 3 and 6 weeks after a suicide attempt with cyanide. The toxicity of cyanide causes damage, primarily to the basal ganglia, and those changes were visible as altered signal intensity on the first MR images. Extensive areas of hemorrhagic necrosis were seen 6 weeks later. Our case shows pseudolaminar necrosis along the central cerebral cortex 3 weeks after cyanide poisoning, showing that the sensorimotor cortex is also a site for toxic necrosis because of its high oxygen dependency.

Adult↗
PubMed1977

Stabilization of the thalamocortical motor system by cerebellar stimulation.

Epilepsy typifies instability in a complex control system. We have previously identified parameters of the thalamocortical motor system of the cat which correlate with epileptiform activity and are controlled by common anticonvulsants. This study is concerned with the control of such parameters by cerebellar stimulation, potencially promoting stability within the motor system. Under computer control, stimuli were delivered to both ventrolateral thalamus and cerebellar cortex, with multichannel recording of evoked responses obtained from sensorimotor cortex. Cortical evoked responses were plotted as an excitability curve (mean response amplitude as a function of pulse interval) or a family of threshold curves (mean response amplitude as a function of stimulus amplitude at various fixed intervals). The present study reveals that cerebellar epidural stimulation can reduce both the height and duration of the excitability curve, as well as increase the response threshold and reduce the saturation level of the threshold curve. The degree and direction of these parameter changes are dependent on the frequency, polarity, and amplitude of cerebellar stimulation, with the amount of parameter change exceeding that achieved by monotoxic doses of anticonvulsants. These data suggest that control of parameters related to excitability and threshold in the thalamocortical motor system may be the means by which cerebellar stimulation accomplishes control of clinical seizures.

Animals↗
PubMed1982

The premotor cortex of the monkey.

The relationship of single unit activity to limb movements guided by visuospatial cues supports the view that the premotor cortex is a distinct cortical field within the somatic sensorimotor cortex. The premotor cortex is similar to the precentral motor cortex (MI) in that most of its units are clearly related to voluntary movements but differs from MI by its higher threshold for microstimulation-evoked movements, its cytoarchitecture, and the presence of a larger population of neurons with activity related to the occurrence of visuospatial signals rather than, or in addition to, the movement cued by those signals.

Animals↗
PubMedDate not supplied

[The effect of acetylcholine and atropine on the temporal connection in the neuronal populations of the motor cortex].

On alert non-immobilized rabbits the activity of neurones in the sensorimotor cortex was studied at pair combination of brain structures stimulations. During omission of the reinforcing stimulus at the place of its expected presentation a complicated complex develops of neurones impulses reconstructions, consisting in reproduction of responses and activity changes which by their configuration differ from them and usually appear in later terms. Direct acetylcholine application on the cortex promotes manifestation of both types of neurones activity reconstructions. But atropine application depresses mainly the second type of reconstructions. Besides, acetylcholine increases the general duration of the given conditioned effects, but atropine decreases it.

Acetylcholine↗
PubMedDate not supplied

[Participation of neurons from symmetrical parts of the sensomotor cortex in conditioned reflex activity].

Spike activity of the symmetrical points of the sensorimotor cortex was studied in the course of formation and extinction of a defensive conditioned reflex in cats. In the process of pairings the impulse responses in the hemisphere contralateral to the paw stimulated with electric current (reinforcement) increased, and were inhibited in the ipsilateral hemisphere. Extinction of the reflex or functional switching off of the contralateral hemisphere restored the conditioned reactions of the ipsilateral hemisphere neurones. An assumption has been made that conditioned connections appear in both hemispheres, but under ordinary conditions the reactions are ensured by the dominating (in learning) hemisphere. If it is switched off, a duplicate conditioned connection appears in the other hemisphere, as one of the mechanisms providing for the reliability of manifestation of the conditioned relfex.

Animals↗