Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sensorimotor Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,711 records · Page 95Linked to original sources
PubMed1995

Effect of early cortical lesion on the acute model of epilepsy.

The experiments were performed in order to investigate the sparing of function following early postnatal cortical lesion in the acute rat model of epilepsy. Sensorimotor cortex was unilaterally removed at 9 and 10 days of postnatal age in lesioned animals, while control animals were only sham operated (at the same early stage of life) or non-operated (before implantation of the electrodes). Seizure activity was recorded by means of electroencephalograms at adult stage of life induced by parenteral administration of penicillin (1,000,000 I.U./kg, i.p.). Our results showed that when the cortical lesion was performed in infancy (on the contrary to the lesion performed in adulthood) there was no prolongation of seizure activity in an acute model of epilepsy.

Aging↗
PubMed1987

Delta-guanidinovaleric acid as an endogenous and specific GABA-receptor antagonist: electroencephalographic study.

Sporadic spike discharges recorded on EEGs from epidural electrodes appeared 5-10 min after topical application of 0.3 nmol delta-guanidinovaleric acid (DGVA) on the pia mater of the sensorimotor cortex, on the same side as the application. Spike discharges induced by DGVA were completely suppressed within 10 min of supplementary application of GABA (50 nmol), (3R)-(-)-4-amino-3-hydroxybutanoic acid (L-GABOB) (5 nmols) or muscimol (5 nmols) on the pia mater, but the discharges were not affected by supplementing with 500 nmol of alpha-amino-DGVA, i.e., arginine (Arg). Whereas spike discharges were not induced by DGVA together with L-GABOB or muscimol, DGVA applied together with Arg induced spike discharges. Neither phenobarbital (PB) (20 mg/kg, i.m.), diazepam (DZ) (10 mg/kg, i.p.), sodium valproate (200 mg/kg, i.p.) nor diphenylhydantoin (20 mg/kg, i.p.) showed any suppressive effects on spike discharges induced by DGVA. DGVA induced spike discharges 20 min after pre-injection of PB or DZ. These electroencephalographic findings suggest that DGVA, which has one more carbon in its chain than N-amidino-GABA, might act directly on the GABA-receptor to induce spike discharges and might be a specific GABA-receptor antagonist.

Animals↗
PubMedDate not supplied

R(-)-baclofen: focal epilepsy after intracortical administration in the rat.

R(-)- or S(+)-baclofen were injected into lamina IV-V of the sensorimotor cortex of the rat. Clinical observation and ECoG registration revealed that partial epilepsy with focal motor symptoms developed following injection of R(-)-baclofen, with an ED50 of 0.25 nmoles, a mean latency of 17 min independent of the dose, and a duration of more than 5 h at a dose of 5 nmoles. S(+)-Baclofen was ineffective at doses of up to 5 nmoles (2 x ED100 (-)-baclofen), indicating a stereoselective action of the (-)-isomer.

Animals↗
PubMedDate not supplied

A selective decrease in the number of GABAergic somata occurs in pre-seizing monkeys with alumina gel granuloma.

Previous studies have shown that a loss of GABAergic neuronal somata is associated with a loss of GABAergic terminals at chronic cortical epileptic foci in monkeys. The present study was undertaken to determine whether GABAergic neuronal loss occurs prior to the onset of clinical seizures in monkeys that were treated with alumina gel but did not display seizures. Seven adolescent (Macaca mulatta) monkeys received alumina gel implants into the left pre- and post-central gyri, specifically centered in hand-face regions of sensorimotor cortex. Three other monkeys were used as controls. Two of these were surgical controls and the third was a normal animal. Three monkeys (pre-seizing) were sacrificed 2-4 weeks after the alumina gel implant but prior to clinically active seizures. Three other monkeys with chronic seizure activity (chronically seizing) were sacrificed 3-6 months after the implant. Tissue sections were taken from an area adjacent to the alumina gel granuloma (focus), from a site distal to it (parafocus) and from the non-epileptic contralateral side. Sections from all monkeys were processed for glutamate decarboxylase (GAD) immunocytochemistry and then examined with a light microscope. In addition, adjacent sections were stained with a Nissl stain and the total number of neurons was counted in these sections. Statistical analysis showed a significant decrease in the number of GAD-positive cells in the pre-seizing and chronic animals. The pre-seizing monkeys showed a significant loss of 23-44% at the focus in contrast to the total number of neurons which did not change significantly. The loss of GAD-positive cells was greater in the chronic animals that showed significant losses at both the focus and parafocus, 42-61% and 15-26%, respectively. It is important to note that the chronic monkeys displayed an 11-61% significant loss of total neurons at the epileptic focus. The surgical control animals showed no seizure activity and no significant loss of total neurons or GAD-positive cells. The main finding of this study indicates that a selective loss of GAD-positive neuronal somata occurs in pre-seizing monkeys with alumina gel implants. This finding is consistent with the previously reported loss of GABAergic terminals in pre-seizing monkeys. Since virtually all monkeys treated with alumina gel develop seizures, the results of this study add further support to the hypothesis that GABA neuronal loss plays a causal role in focal epilepsy.

Aluminum↗
PubMedDate not supplied

Abnormalities in the levels of extracellular and tissue amino acids in the brain of the seizure-susceptible rat.

Basal and high potassium-stimulated release of endogenous amino acids was measured using brain dialysis in the hippocampus of urethane-anesthetized seizure-resistant (SR) and seizure-susceptible (SS) rats. Moreover, the tissue level of amino acids was determined in the hippocampus, sensorimotor cortex, cerebellum and corpus striatum. The basal extracellular concentration of amino acids did not differ between SR and SS rats. However, aspartate release was higher, and taurine and phosphoethanolamine release was lower in SS rats during stimulation with 100 mM K+. Several strain differences were observed with regard to regional tissue levels of amino acids. Aspartate was significantly elevated in the hippocampus, cortex and cerebellum of SS animals, and the catecholamine precursor tyrosine was diminished in all regions examined. Other disparities included a depressed gamma-aminobutyrate concentration in the hippocampus and cortex, slightly increased levels of phosphoethanolamine in the cerebellum and minor decreases in striatal and cortical taurine. Glutamate, glutamine, serine and alanine concentrations were not significantly altered in any brain area of the SS rat. The results confirm and extend previous findings on abnormalities in aspartate, taurine and phosphoethanolamine regulation in this model. In addition, decreased availability of tyrosine may provide a partial explanation for the well-documented deficiency in cerebral norepinephrine in the SS strain.

Amino Acids↗
PubMed1991

Amygdaloid kindling during wakefulness and paradoxical sleep in the cat. 1. Inhibitory influence of paradoxical sleep on kindling development.

The development of amygdaloid kindling during wakefulness (W) and paradoxical sleep (PS) was compared in chronically implanted adult male cats. The animals were divided into 2 groups. One group was kindled during W (W-K) and the second during a burst of pontogeniculo-occipital (PGO) potentials during PS (PS-K). The threshold of amygdaloid afterdischarge (AD) was determined during W in the W-K group and during PS in the PS-K group. For the development of kindling, amygdala stimulation was applied daily. Results demonstrate that kindling development was markedly retarded in the PS-K group. From the first kindling trials, mean AD duration in the PS-K group was significantly shorter than in the W-K group and this difference was sustained until generalized convulsive seizures (GCSs) were reached by the W-K animals. Also, mean AD frequency in the PS-K group was significantly lower than in the W-K group. AD propagation to the contralateral amygdala and sensorimotor cortex was significantly retarded in the PS-K animals. Time spent in behavioral stages I and II of kindling was significantly longer in the PS-K animals than in W-K animals and the number of daily electrical stimuli required to reach the first GCS was significantly higher in group PS-K than in group W-K. It is concluded that PS exhibits an inhibitory influence over amygdaloid kindling development and this influence is mainly exerted during the early stages of epileptogenesis.

Amygdala↗
PubMed1992

Kainic acid-induced thalamic seizure in cats--a possible model of petit mal seizure.

Bipolar depth electrodes were implanted stereotaxically in the thalamus, hippocampus and midbrain reticular formation of cats. Cortical screw electrodes were placed over the bilateral sensorimotor cortex. A guide cannula with an inner injection cannula was inserted unilaterally into the posterolateral ventral nuclei (VPL) of the thalamus. Eight days after the procedures, kainic acid (2.0 micrograms) was injected unilaterally into the VPL via the injection cannula in freely moving animals and electro-clinical observations were made. About 1 h after the kainic acid injection, multiple spikes were observed in the VPL (injection site), which propagated to the subcortical structures. These seizures finally propagated bilaterally to the cortex about 2 h after the injection. About 3-4 h after the injection, small spike and wave complexes repeatedly appeared for a short period of time in cortical leads and cats exhibited behavioral arrest with unresponsiveness during the seizures. About 24 h after the injection, generalized small spike and wave complexes were observed intermittently in cortical and subcortical structures. They persisted for 4-5 s and were associated with behavioral arrest and staring. The results demonstrate that a unilateral microinjection of kainic acid into VPL induced petit mal-like seizure, and suggest that VPL plays an important role in the generation or transfer of spike and wave complexes.

Animals↗
PubMed2004

Ipsilateral motor pathway confirmed by combined brain mapping of a patient with hemiparetic stroke: a case report.

This study investigated the motor control pathway using both functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulation (TMS) in a patient with left hemiparesis with an infarction on the posterior limb of the right internal capsule. fMRI was performed using the blood oxygen level-dependent technique at 1.5 T with a standard head coil. The motor activation task consisted of hand grasp-release movements in 1-Hz cycles. TMS was performed using a butterfly coil; the intersection of the wings (center of the coil) was applied tangentially to the scalp 1.0 cm apart. Stimulation was performed at 100% of maximal output. Motor evoked potentials (MEPs) from both abductor pollicis brevis (APB) muscles were obtained simultaneously. fMRI showed that the unaffected (left) primary sensorimotor cortex (SM1) was activated by movements of the unaffected (right) hand. Conversely, the bilateral SM1 were activated by movements of the affected (left) hand. Brain mapping using TMS showed that ipsilateral MEPs were obtained at the affected (left) APB muscle when the unaffected (left) motor cortex was stimulated. We concluded that the ipsilateral motor pathway from the unaffected motor cortex to the affected hand was present in this patient.

Activities of Daily Living↗
PubMed2004

The effects of intracortical endothelin-1 injections on skilled forelimb use: implications for modelling recovery of function after stroke.

Different methods of inducing experimental brain lesions can result in distinct neuropathological sequelae. This could be of consequence in attempts to establish animal models of recovery of function following stroke, as differences in the progression of experimental lesion pathology may have an impact on the magnitude and rate of recovery of function observable with any particular lesioning method. In the present study, a novel method of producing a focal ischaemic lesion by intracortical microinjection of endothelin-1 (ET-1) was compared with excitotoxic (microinjection of quinolinic acid) and mechanical (aspiration) lesioning procedures. Lesions were unilateral and were targeted at the forelimb representation zone in sensorimotor cortex. It was found that all three types of lesion had an essentially identical effect with regard to reaching accuracy in a paw-reaching task. All lesioned animals displayed a similar, significant long-term deficit in reaching accuracy and limited degree of recovery relative to sham animals. Off-line analysis of the performance of animals during post-lesion week 9 indicated that animals in each lesion group also displayed a similar deficit. The current results suggest that the spontaneous behavioural consequences of a unilateral lesion of FL in the rat appear to be independent of the nature of lesion production. However, the increased face validity of an ET-1-induced lesion, coupled with the ease of control of lesion placement and extent offered by this technique make for a potentially important animal model for research into drug effects on recovery of function following stroke.

Animals↗
PubMed2004

Attentional processes and cognitive performance during expectancy of painful galvanic stimulations: a high-resolution EEG study.

In the present high-resolution electroencephalographic (EEG) study, an omitted-stimulus paradigm induced a strong expectancy for a predictable painful stimulation (nonpainful in the control condition). During the expectancy of pain, concurrent cognitive demands were superimposed. The aim was to investigate the effects on primary sensorimotor and central midline areas of the competition among concurrent attentional processes related to cognition and pain expectancy, as indexed by behavioral performance and EEG data. A main issue was whether cognitive performance decreases, due to a re-allocation of attentional resources on primary sensorimotor and midline areas for the anticipation of pain. Behavioral results showed no differences in the cognitive (working memory) performance during the expectancy of nonpainful versus painful stimulations. In parallel, anticipatory event-related potentials (ERPs) were negligible in line with a low emotional reactivity/alertness as revealed by heart rate deceleration (HRD), skin conductance response (SCR), and low-band (6-10Hz) alpha EEG oscillations. In contrast, high-band alpha EEG oscillations (10-12Hz) over the contralateral primary sensorimotor cortex decreased more during the expectancy of painful compared to nonpainful stimuli, in line with an increased anticipatory preparation of the somatosensory channel. These findings provide further evidence on the fact that attentional processes at the basis of cognition can be defended by the anticipation of pain, at least when the incoming painful stimuli are repetitive and predictable. This happens even if the brain increases preparatory processes of the specific sensory channel to be targeted by the painful stimulus.

Adult↗
PubMed2005

Long-term effects of sequential cortical infarcts on scar size, brain volume and cognitive function.

Focal ischemia induces long-term pathophysiological consequences in widespread brain areas. Here we analyzed long-term effects of sequential cortical lesions on brain volume and cognitive function. Rats received either single photothrombotic lesions in the forelimb sensorimotor cortex (SL) or two lesions in sequence either immediately (DL0), 2 days (DL2), 7 days (DL7), or 10 days (DL10) after the first surgery in the homotopic contralateral area. Infarct and global brain volume were measured 7 days (SL and DL2 groups) and one month (all groups) after the last period of ischemia. In the weeks following a stroke, the single lesion shrank considerably. This shrinkage was accentuated by a further lesion received either earlier or later. Thirty-one days after obtaining the second lesion, the lesion scars on both sides had a mean volume of 5.8 +/- 2.3 mm3 in DL2 as compared to 8.5 +/- 3.5 mm3 in SL-animals. In addition, there was a super-additive loss of residual brain volume by 2.2-8.0% in each hemisphere in animals with sequential lesions. In the watermaze, this loss of brain volume corresponded to a slight but significant impairment in performance. The present study revealed a complex interaction of lesions in animals with sequential strokes associated with global reduction of brain volume and cognitive impairment indicating degenerative processes beyond the lesions itself.

Animals↗
PubMed2006

A choice reaction-time task in the rat: a new model using air-puff stimuli and lever-release responses.

We have developed a two-lever choice reaction-time (RT) task to investigate the behavioral and neural mechanisms of stimulus-response compatibility in rats. In the task, the rat pressed two levers with its forepaws during the preparation period of each trial, and then quickly responded to an air-puff stimulus on its left or right forepaw by releasing the lever on the same side (compatible condition) or the opposite side (incompatible condition) of the stimulus. Twenty rats successfully learned the task in both the compatible and incompatible conditions. Two stimulus-response compatibility effects were observed: the RT was shorter and the error rate was lower in the compatible condition than in the incompatible condition. The trial sequence also affected the results and a speed-accuracy tradeoff was observed. These results are consistent with those reported for human RT tasks. Furthermore, a lesion in the forepaw-sensorimotor cortex caused increases in the RTs for stimulus detection and/or response movement with the contralateral forepaw, suggesting that the task was mediated by this brain area. We conclude that this instrumental task for rats can be regarded as a model for human RT tasks and can be used to investigate the neural basis of the compatibility effects.

Air↗
PubMed2005

Fatigue induced by intermittent maximal voluntary contractions is associated with significant losses in muscle output but limited reductions in functional MRI-measured brain activation level.

The main purpose of this study was to characterize brain activation patterns during a fatigue task involving repetitive maximal voluntary contractions (MVC) of finger flexor muscles. Fourteen young, healthy human participants performed approximately 100 handgrip MVCs (each 2-s contraction was followed by a 1-s rest) while their brain was imaged by functional MRI (fMRI). The handgrip force and electromyograms (EMG) of the finger flexors declined progressively to about 40% of the initial values at the end of the fatigue task, suggesting that significant muscle fatigue had occurred. In contrast, the level of the fMRI signal in the primary (sensorimotor), secondary (supplementary motor), and association (prefrontal and cingulate) motor-function cortices did not change significantly throughout the fatigue task (although the signal of the primary sensorimotor cortex showed a clear trend of decline). The fMRI data from the task of intermittent handgrip MVCs differed dramatically from those obtained in a 2-min sustained handgrip MVC published in a recent report, in which the overall fMRI-measured brain activation level was substantially lower and followed an increase-then-decrease pattern compared to the linear decreases in force and EMG. These results support the notion that the motor cortical centers control the tasks of repetitive and continuous muscle contractions differently and that there is a decoupling in the signal changes of the brain and muscles during muscle fatigue processes induced by maximal voluntary contractions.

Electromyography↗
PubMed2005

Cellular proliferation and migration following a controlled cortical impact in the mouse.

Neurogenesis following neural degeneration has been demonstrated in many models of disease and injury. The present study further examines the early proliferative and migratory response of the brain to a controlled cortical impact (CCI) model of traumatic brain injury. The CCI was centered over the forelimb sensorimotor cortex, unilaterally, in the adult mouse. To examine proliferation, bromo-deoxyuridine (BrdU) was injected i.p. immediately post-injury and on post-injury days 1, 2, and 3. To assess migration, we labeled SVZ cells with inert latex microspheres immediately post-injury. By combining microsphere labeling with BrdU, we determined if migrating cells had gone through the S-phase of the cell cycle after the lesion. In addition, we used a marker of neurogenesis and migration, doublecortin, to further characterize the response of the SVZ to the injury. Lastly, we determined whether subregions of the SVZ respond differentially to injury. The current study demonstrates that 3 days following CCI cellular proliferation is seen around the cortex, in the SVZ, corpus callosum, and subcortical areas anatomically connected to, but not directly damaged by the impact. It delineates that an increase in proliferation occurs in the dorsal-most aspect of the ipsilateral SVZ following impact. Lastly, it demonstrates that proliferating cells migrate from the SVZ to cortical and subcortical structures affected by the injury and that some of these cells are migrating neuroblasts.

Animals↗
PubMed2006

Biphasic effect of chronic postnatal caffeine treatment on cortical epileptic afterdischarges during ontogeny in rats.

EEG and motor phenomena elicited by stimulation of sensorimotor cortex were used to study the effects of chronic postnatal administration of caffeine (10 and 20 mg/kg, s.c. from P7 to P11) in rats. Rhythmic electrical stimulation was applied to 12-, 18-, 25- and 67-day-old rats with implanted electrodes. Animals with the higher dose of caffeine exhibited increased thresholds for elicitation of stimulation-bound movements, spike-and-wave afterdischarges (ADs) and clonic seizures accompanying these ADs at the age of 12 days and decreased duration of spike-and-wave ADs at postnatal days (P) 18 and 25. In contrast, chronic administration of the lower dose of caffeine resulted in a proconvulsant effect expressed as a significant prolongation of spike-and-wave ADs in P12, P18 and P25 groups as well as of the second "limbic" type of ADs (significant only in P12 and P25). The biphasic action of chronic postnatal caffeine treatment was transient and was no longer present in 67-day-old rats. Our results demonstrate that early postnatal caffeine exposure results in either pro- or anticonvulsant effect during brain maturation in relation to the dose used. Caffeine is a mixed adenosine receptor antagonist, therefore its effects could be due to a different action on adenosine receptor subtypes; an additional mechanism of action cannot be excluded.

Age Factors↗
PubMed2006

Prolonged bihemispheric alterations in unfolded protein response related gene expression after experimental stroke.

After ischemia, endoplasmic reticulum (ER) stress pathways are activated that include unfolded protein response (UPR) and protein synthesis inhibition (PSI). Both of these mechanisms aim to restore ER functioning mainly by inhibition of translation and increased processing of excess proteins in ER. We were interested in the role of these pathways during spontaneous recovery after transient middle cerebral artery occlusion (MCAO) in rats. The spontaneous recovery of rats was assessed with a limb-placing test. The expression of ER-stress-related genes (IRE1, ATF6, GRP78, eif2alpha, ATF4, PERK) was studied by using in situ hybridization in different brain areas on post-operative days 2, 7, 14 and 28. Elevated signals were detected in striatum contralateral to the lesion on days 2 (PERK and IRE1) and 14 post-ischemia (IRE1). Gene expression was elevated on day 7 in the striatum ipsilateral to the lesion (ATF6 and GRP78) and on day 14 (GRP78) post-ischemia. Furthermore, elevated levels of GRP78 were detected on day 14 after ischemia in the ipsilateral sensorimotor cortex. These results suggest that altered gene expression related to unfolded protein response may be more long lasting than expected following focal cerebral ischemia. In addition, these results show that the response to ER stress differs ipsi- and contralaterally after MCAO in rats. Since these differences are detected in both hemispheres only in areas adjacent to the lesion, UPR may contribute to spontaneous recovery after MCAO in rats.

Animals↗
PubMed2006

Knowing when to respond and the efficiency of the cortical motor command: a Laplacian ERP study.

The objective was to test whether motor preparation can modulate the efficiency of the cortical motor command. The electroencephalogram (EEG) was recorded from electrodes located over the primary sensorimotor cortices during the performance of a between-hand choice reaction time task in which foreperiod duration (the interval between the warning and the imperative signals, 800 vs. 2800 ms) was varied across blocks of trials. In order to increase the spatial resolution of the EEG traces, surface Laplacian was estimated. The amplitude of the negative wave developing over the hemisphere contralateral to the response was smaller for the short foreperiod associated with the best performance level. These results indicate that the activation of the primary sensorimotor cortex involved in the response is less pronounced for the short foreperiod, suggesting that temporal advance information increases the efficiency of the cortical motor command.

Adult↗
PubMed2006

Subcortical motor plasticity in patients with sporadic ALS: An fMRI study.

OBJECTIVE: To address the potential contribution of subcortical brain regions in the functional reorganization of the motor system in patients with sporadic ALS (sALS) and to investigate whether functional changes in brain activity are different in sALS patients with predominant upper motor neuron (UMN) or lower motor neuron (LMN) dysfunction. METHODS: We studied 16 patients with sALS and 13 healthy controls, using BOLD-fMRI, while they performed a simple visually paced motor task. Seven patients had definite clinical UMN signs while nine patients had prevalent clinical and electrophysiological LMN involvement. fMRI data were analyzed with Brain Voyager QX. RESULTS: Task-related functional changes were identified in motor cortical regions in both patients and healthy controls. Direct group comparisons revealed relatively decreased BOLD fMRI responses in left sensorimotor cortex, lateral premotor area, supplementary motor area and right posterior parietal cortex (p < 0.05 corrected) and relatively increased responses in the left anterior putamen (p < 0.001 uncorrected) in sALS patients. Additional analyses between the two patients subgroups demonstrated significant BOLD fMRI response differences in the anterior cingulate cortex and right caudate nucleus (p < 0.001 uncorrected) with more robust activation of these areas in patients with greater UMN burden. Importantly, there were no significant differences in performance of the motor task between sALS patients and controls as well as between sALS patient subgroups. CONCLUSIONS: Our data demonstrate a different BOLD fMRI pattern between our sALS patients and healthy controls even during simple motor behavior. Furthermore, patients with sALS and greater UMN involvement show a different reorganization of the motor system compared to sALS patients with greater LMN dysfunction.

Adult↗