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PubMed2006

Interruption of functional recovery by the NMDA glutamate antagonist MK801 after compression of the sensorimotor cortex: implications for treatment of tumors or other mass-related brain injuries.

Glutamate antagonists have recently been shown to limit tumor growth, providing potential new therapeutic targets and strategies against brain tumors. Here, we demonstrate that the glutamate NMDA receptor antagonist MK801, after a delay, adversely reverses functional recovery in rats with compressive mass lesions of the sensorimotor cortex. Our data suggest that the controlled focal cortical compression model may be a valuable pre-clinical tool to screen compounds for the treatment of brain tumors. It may be possible to use this model to develop interventions that maintain anti-cancer effects but with diminished harm to bystander tissue and brain plasticity.

Animals↗

PubMed1988

Neurons of layer Vb of rat sensorimotor cortex atrophy but do not die after thoracic cord transection.

Albino rats six weeks (wk) of age underwent transection of the spinal cord at the level of the seventh thoracic vertebra. They were killed ten wk later by several schedules of formaldehyde-glutaraldehyde, formaldehyde and formaldehyde-ethanol-acetic acid perfusion-fixation. Layer Vb of the sensorimotor cortex, the site of origin of corticospinal axons severed by the operation, was searched by light and electron microscopic methods for evidence of neuronal necrosis. Cord-transected rats were compared with control, unoperated animals of identical age. Nerve cell death was not evident to qualitative study, although shrunken, deeply-staining neurons of artefactitious origin occurred capriciously in paraffin sections when fixation was initiated with a dilute formaldehyde-glutaraldehyde solution. Quantitative light and electron microscopic studies were also negative for indications of neuronal death. However, mild somal atrophy could be substantiated for layer Vb neurons of cord-transected rats by light microscopic, morphometric methods. Neuronal atrophy was unaccompanied by qualitative or quantitative ultrastructural alterations. Subcellular organelles and the per cent of neuronal plasma membrane apposed by axosomatic boutons were unchanged. Neuroglia and neuronal processes always had a normal electron microscopic appearance.

Animals↗

PubMed2006

Sensorimotor cortex ablation prevents H-reflex up-conditioning and causes a paradoxical response to down-conditioning in rats.

Operant conditioning of the H-reflex, a simple model for skill acquisition, requires the corticospinal tract (CST) and does not require other major descending pathways. To further explore its mechanisms, we assessed the effects of ablating contralateral sensorimotor cortex (cSMC). In 22 Sprague-Dawley rats, the hindlimb area of left cSMC was ablated. EMG electrodes were implanted in the right soleus muscle and a stimulating cuff was placed around the right posterior tibial nerve. When EMG remained in a specified range, nerve stimulation just above the M response threshold elicited the H-reflex. In control mode, no reward occurred. In conditioning mode, reward occurred if H-reflex size was above (HRup mode) or below (HRdown mode) a criterion value. After exposure to the control mode for > or = 10 days, each rat was exposed for another 50 days to the control mode, the HRup mode, or the HRdown mode. In control and HRup rats, final H-reflex size was not significantly different from initial H-reflex size. In contrast, in HRdown rats, final H-reflex size was significantly increased to an average of 136% of initial size. Thus like recent CST transection, cSMC ablation greatly impaired up-conditioning. However, unlike recent CST transection, cSMC produced a paradoxical response to down-conditioning: the H-reflex actually increased. These results confirm the critical role of cSMC in H-reflex conditioning and suggest that this role extends beyond producing essential CST activity. Its interactions with ipsilateral SMC or other areas contribute to the complex pattern of spinal and supraspinal plasticity that underlies H-reflex conditioning.

Animals↗

PubMed2000

Peculiarities of ischemic cardiac arrhythmias in cats against the background of stimulation of sensorimotor cortex and administration of selective opiate receptor agonists.

In acute experiments on Nembutal-anesthetized cats, the effect of opiate receptor agonists DAGO, DSLET, and dinorphin A(1-13) on the incidence of idioventricular rhythm disturbances, including ventricular tachycardia and fibrillation, was studied under conditions of occlusion of circumflex branch of the left coronary artery and stimulation of the sensorimotor cortex. The most pronounced effects were observed with DSLET and dinorphin A(1-13). These preparations completely prevented ventricular fibrillation. DAGO produced a less pronounced protective effect probably because of parallel increase in plasma catecholamine concentration.

Analgesics, Opioid↗

PubMed2001

Age-related decline of presumptive inhibitory synapses in the sensorimotor cortex as revealed by the physical disector.

The synapse, as the site of functional neural interaction, has been suggested as a possible substrate for age-related impairment of cognitive ability. Using the physical disector probe with tissue prepared for ultrastructural analysis, we find an age-related decline in the numerical density of presumptive inhibitory synapses in layer 2 of the sensorimotor cortex of the Brown Norway x Fisher 344 rat. This age-related decline in presumptive inhibitory synapses is maintained when the density of synapses is combined with the numerical density of neurons quantified from the same anatomical space to arrive at a ratio of synapses per neuron. The numerical density of these synapses declines between middle-aged (18 months) and old (29 months) animals by 36% whereas numerical density of neurons does not change between these ages, resulting in a decline in the ratio of presumptive inhibitory synapses per neuron in this cortical area. This study demonstrates a deficit in the intrinsic inhibitory circuitry of the aging neocortex, which suggests an anatomical substrate for age-related cognitive impairment.

Aging↗

PubMed1996

Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats.

Thalamic neuronal degeneration after neocortical lesions involve both anterograde and retrograde components. This study deals with the thalamic microglial response after neocortical aspiration lesions, using fluorogold fluorescent prelabeling, to identify retrogradely degenerating thalamocortical neurons, combined with histochemical or immunohistochemical staining of microglial cells. Adult male Wistar rats were injected with the retrograde fluorescent tracer fluorogold, in the right sensorimotor cortex (forepaw area) in order to retrogradely label thalamic neurons projecting to this area. After 1 week, the fluorogold injection site was removed by aspiration, axotomizing at the same time the thalamic projection neurons now retrogradely labeled with fluorogold. After 3, 7, 14, and 28 days the animals were killed and processed for nucleoside diphosphatase histochemistry or complement type 3 receptor immuno-histochemistry and class I and II major histocompatibility complex immunohistochemistry using OX42, OX18, and OX6 antibodies. The histological analysis showed a prominent and progressive nucleoside diphosphatase-, OX42-, and OX6-positive microglial cell response in the ventrolateral, posterior, and ventrobasal thalamic nuclei with ongoing retrograde and anterograde neuronal degeneration. Initially the reactive microglia had a bushy morphology and were succeeded by ameboid microglia and microglial cluster cells as the reaction progressed. However, in the reticular thalamic nucleus, which suffered exclusively anterograde neuronal degeneration, a different picture was seen with only bushy microglia. The neurons undergoing retrograde degeneration in the ventrolateral, posterior, and ventrobasal thalamic nuclei were retrogradely labeled by the fluorogold tracer. Individual nucleoside diphosphatase-, OX42-, or OX6-positive microglial cells extended long cytoplasmic processes surrounding fluorogold-labeled neurons and had in some cases apparently phagocytized these. Several microglial cells were thus double-labeled with nucleoside diphosphatase or OX42 and fluorogold. In addition, small nucleoside diphosphatase-positive, fluorogold-labeled perivascular cells were observed in the neocortex near the fluorogold-injected and ablated neocortical areas and in the ipsilateral thalamus. This study demonstrates: (1) that the microglial response to thalamic degeneration after neocortical lesion is graded with a limited reaction to the well-known massive anterograde axonal degeneration and a more extended reaction to the axotomy-induced retrograde cell death; and (2) that also perivascular cells and possibly macrophages may contribute to this reaction, as seen by uptake of fluorogold from axotomized neurons in the degenerating thalamic nuclei.

Acid Anhydride Hydrolases↗

PubMed2007

Abnormal plasticity of the sensorimotor cortex to slow repetitive transcranial magnetic stimulation in patients with writer's cramp.

Previous studies demonstrated functional abnormalities in the somatosensory system, including a distorted functional organization of the somatosensory cortex (S1) in patients with writer's cramp. We tested the hypothesis that these functional alterations render S1 of these patients more susceptible to the "inhibitory" effects of subthreshold 1 Hz repetitive transcranial magnetic stimulation (rTMS) given to S1. Seven patients with writer's cramp and eight healthy subjects were studied. Patients also received rTMS to the motor cortex hand area (M1). As an outcome measure, short-latency afferent inhibition (SAI) was tested. SAI was studied in the relaxed first dorsal interosseous muscle using conditioning electrical stimulation of the index finger and TMS pulses over the contralateral M1. Baseline SAI did not differ between groups. S1 but not M1 rTMS reduced SAI in patients. rTMS had no effects on SAI in healthy subjects. Because SAI is mediated predominantly at a cortical level in the sensorimotor cortex, we conclude that there is an abnormal responsiveness of this area to 1 Hz rTMS in writer's cramp, which may represent a trait toward maladaptive plasticity in the sensorimotor system in these patients.

Adult↗

PubMed2003

Long-term potentiation of polysynaptic responses in layer V of the sensorimotor cortex induced by theta-patterned tetanization in the awake rat.

Although the neocortex in awake, adult animals is resistant to the induction of long-term potentiation (LTP), synaptic potentiation may be enhanced by rhythmic patterns of activation that evoke short- term synaptic facilitation effects. The effectiveness of stimulation patterned after the theta (4-12 Hz) EEG rhythm for the induction of LTP of sensorimotor cortex responses to corpus callosum stimulation was assessed in vivo by inducing LTP using either high- frequency (300 Hz) trains or paired trains delivered at a 100 ms (10 Hz) interval. High-frequency trains caused a reduction of the early field potential component, reflecting a potentiation of direct layer V activation, and a potentiation of the late component, reflecting enhanced polysynaptic activation in layer V. Paired trains resulted in a much larger potentiation of polysynaptic responses than was observed following 300 Hz trains. To determine if short-term facilitation effects contributed to the enhanced LTP induction by theta-patterned trains, facilitation effects induced by the trains were challenged with NMDA receptor antagonists. NMDA-receptor antagonism reduced responses to single pulses, and also reduced facilitated responses evoked by theta-patterned stimulation. The effectiveness of theta-patterned stimulation for the induction of LTP of layer V polysynaptic responses is therefore likely due to frequency-dependent synaptic facilitation effects that enhance NMDA receptor activation.

Animals↗

PubMed1999

Scanning electron microscopy of the floor of the fourth ventricle in rats subjected to graded impact injury to the sensorimotor cortex.

OBJECT: Respiratory dysfunction including apnea frequently follows head injury in humans. The purpose of this study was to identify any structural alterations in the region of brainstem respiratory nuclei that might account for immediate postinjury respiratory abnormalities in anesthetized experimental animals. METHODS: Using scanning electron microscopy, the authors examined the floor of the fourth ventricle in injured rats after a piston strike to the sensorimotor cortex that depressed the dura 1, 2, or 4 mm. The rats were killed within minutes of injury. Cortical impact depths measuring either 1 or 2 mm (eight rats) produced no respiratory abnormalities, and the structural integrity of the ependymal lining of the ventricular floor in these animals was not compromised. Thirteen rats were subjected to impact to a 4-mm depth and 10 of these exhibited immediate temporary or permanent apnea. The medullae of nine of these rats were studied using scanning electron microscopy, and the fourth ventricular floors of all nine rats showed tears. Four rats that exhibited immediate, permanent apnea had tears in the caudal fourth ventricle floor near the obex, whereas five rats with no or only transient apnea had tears located more anteriorly, near the aqueduct or laterally. Changes in cerebrospinal fluid flow or pressure dynamics may have caused these tears. Light microscopy, focused near the area postrema, revealed a shearing defect through the ependyma of the fourth ventricular floor into the subjacent neuropil with a disruption of axonal pathways. CONCLUSIONS: Respiratory neuronal network components lying within 2 mm of the area postrema may well have been disrupted by the caudal tears producing permanent apnea. A similar phenomenon could account for the transient or permanent postinjury apnea seen in humans with severe head injury.

Animals↗

PubMed2005

On the human sensorimotor-cortex beta rhythm: sources and modeling.

Cortical oscillations in the beta band (13-35 Hz) are known to be modulated by the GABAergic agonist benzodiazepine. To investigate the mechanisms generating the approximately 20-Hz oscillations in the human cortex, we administered benzodiazepines to healthy adults and monitored cortical oscillatory activity by means of magnetoencephalography. Benzodiazepine increased the power and decreased the frequency of beta oscillations over rolandic areas. Minimum current estimates indicated the effect to take place around the hand area of the primary sensorimotor cortex. Given that previous research has identified sources of the beta rhythm in the motor cortex, our results suggest that these same motor-cortex beta sources are modulated by benzodiazepine. To explore the mechanisms underlying the increase in beta power with GABAergic inhibition, we simulated a conductance-based neuronal network comprising excitatory and inhibitory neurons. The model accounts for the increase in the beta power, the widening of the spectral peak, and the slowing down of the rhythms with benzodiazepines, implemented as an increase in GABAergic conductance. We found that an increase in IPSCs onto inhibitory neurons was more important for generating neuronal synchronization in the beta band than an increase in IPSCs onto excitatory pyramidal cells.

Adult↗

PubMedDate not supplied

Localization of sensorimotor cortex in neurosurgery by recording of somatosensory evoked potentials.

The current method of localizing somatosensory and motor cortex during neurosurgical removal of abnormal tissue is Penfield's method of cortical stimulation. While useful, this method has drawbacks, in particular the need to operate under local anesthesia. Another method of localization, described here, involves intra-operative recording of short-latency somatosensory evoked potentials to stimulation of the contralateral median nerve, from electrodes placed directly on central cortex. Proper localization involves identification of potentials which invert in polarity across the central sulcus, identification of other potentials which are largest in the medial portion of the hand area of somatosensory cortex and do not polarity invert, and determination of the region of maximal potential amplitude. This method of localization works equally well whether the patient is under local or general anesthesia, but it occasionally fails in patients with tumors abutting or invading the hand area of sensorimotor cortex.

Anesthesia↗

PubMedDate not supplied

[The effect of dilantin on the neuronal reactions of the sensorimotor cortex and hippocampus during learning].

After dilantin (D) administration in a dose which reduced posttetanic potentiation (according to the data of literature), probability of movements to light flashes (conditioned signal of a defensive reflex) did not change. Weak but stable disinhibition of motor reactions to flashes was observed when they were presented at the background of continuous light as a conditioned inhibitor. Activation of neurons of the sensorimotor cortex in response to reinforced and non-reinforced light flashes increased under D action (as it had been earlier observed in neurons of the visual cortex), and activatory reactions to pain reinforcement decreased. In hippocampal neurons increase of the rate of impulsation in response to reinforced flashes under the action of D disappeared. On the basis of the data obtained it can be concluded that PTP in the neocortex does not participate in long-term memory storage of the biological significance of activating stimulus.

Animals↗

PubMed2002

Bilateral overactivation of the sensorimotor cortex in the unilateral rodent model of Parkinson's disease - a functional magnetic resonance imaging study.

Functional magnetic resonance imaging (fMRI) is used to investigate the basal ganglia (BG)-cortex circuit using a rat model of Parkinson's disease (PD). The model involves a unilateral destruction of the right substantia nigra by intranigral injection of the dopaminergic neurotoxin 6-hydroxydopamine. Volume of cortical activity was measured by the blood oxygenation level-dependent contrast method while applying electrical forepaw stimulation. The main findings are the following. (i) Contrary to the predictions of the classic model but in line with recent experimental results (positron emission tomography, fMRI and electrophysiology), an increased cortical activity in the sensorimotor cortex of PD rats compared with sham-operated or normal rats was found. (ii) A diffuse neuronal activity at large cortical areas that were not related directly to the stimulation used, was observed. (iii) No difference was found between the lesion and the nonlesion hemispheres when the left or the right forepaw was stimulated; both cortices show significant overactivation of the sensorimotor cortices in addition to diffuse cortical activation. The last finding could be explained by either corticocortical connections or by bilateral BG-cortex connections. These finding suggest that the mutual influence of the two hemispheres is important in the pathophysiology of the BG-cortex circuit and might be crucial in predicting treatments.

Animals↗

PubMed1997

Adrenoceptor-mediated elevation of ambient GABA levels activates presynaptic GABA(B) receptors in rat sensorimotor cortex.

At inhibitory synapses in the mature neocortex and hippocampus in vitro, spontaneous action-potential-dependent and -independent release of gamma-aminobutyric acid (GABA) activates postsynaptic GABA(A) receptors but not pre- or postsynaptic GABA(B) receptors. Elevation of synaptic GABA levels with pharmacological agents or electrical stimulation can cause activation of GABA(B) receptors, but the physiological conditions under which such activation occurs need further elucidation. In rodent sensorimotor cortex, epinephrine produced a depression in the amplitude of evoked monosynaptic inhibitory postsynaptic currents (IPSCs) and a concomitant, adrenoceptor-mediated increase in the frequency of spontaneous IPSCs. Blockade of GABA(B) receptors prevented the depression of evoked IPSC amplitude by epinephrine but did not affect the increase in spontaneous IPSC frequency. These data show that adrenoceptor-mediated increases in spontaneous IPSCs can cause activation of presynaptic GABA(B) receptors and indirectly modulate impulse-related GABA release, presumably through elevation of synaptic GABA levels.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMedDate not supplied

Influence of dilantin on the reactions of neurons of the sensorimotor cortex and hippocampus during learning.

The probability of movements in response to light flashes, the conditional signal of a defense reflex, did not alter against the background of the action of dilantin (D) in a dose which, according to published data, attenuates posttetanic potentiation (PTP). A weak but stable disinhibition of the motor reaction was observed in response to flashes turned on against the background of conditional inhibition, continuous light. The activation of neurons of sensorimotor cortex in response to reinforced and nonreinforced light flashes against the background of D was intensified in the same way as was observed previously as exemplified by the reactions of neurons of the visual cortex [3], while it was diminished in response to painful reinforcement. The acceleration of impulses in response to reinforced light flashes under the influence of D became weaker in the hippocampus, by contrast with neurons of the new cortex. It can be concluded on the basis of the data obtained that PTP does not participate in the storage in the new cortex of long-term memory of the biological significance of an activating stimulus.

Acoustic Stimulation↗

PubMed2003

Model of recovery of locomotor ability after sensorimotor cortex injury in rats.

Animal models of locomotor recovery after brain injury provide tools for understanding the basic neurobiological processes that may underlie recovery after stroke in humans. Measurement of the ability of rats to traverse a narrow elevated beam has proven to be a particularly useful test of locomotor function. Repeated measurement of this behavior over time provides a simple method for quantifying the rate and degree of a rat's locomotor recovery after sensorimotor cortex injury and constitutes a tool for studying its mechanisms and possible treatment strategies. The model has proven particularly useful in predicting the effects of drugs on poststroke recovery in humans.

Animals↗

PubMed2004

N-methyl-D-aspartate receptor-independent long-term depression and depotentiation in the sensorimotor cortex of the freely moving rat.

Bidirectional modifications in synaptic efficacy are central components in recent models of cortical learning and memory, and we previously demonstrated both long-term synaptic potentiation (LTP) and long-term synaptic depression (LTD) in the neocortex of the unanaesthetized adult rat. Here, we have examined the effects of N-methyl-D-aspartate receptor (NMDAR) blockade on the induction of LTD, LTP, and depotentiation of field potentials evoked in sensorimotor cortex by stimulation of the white matter in the adult, freely moving rat. High frequency (300 Hz) stimulation (HFS) was used to induce LTP and prolonged, low-frequency (1 Hz) stimulation was used to induce either depotentiation or LTD. LTD was expressed as a reduction in the amplitude of the short and long-latency field potential components, while depotentiation was expressed as a decrease in the amplitude of a previously enhanced late component. Under NMDAR blockade, HFS failed to induce LTP and instead produced a depression effect similar to LTD. Following washout of the drug, HFS induced a normal LTP effect. Unlike LTP, LTD and depotentiation were found to be NMDAR-independent in the neocortex of the freely moving rat.

Animals↗

PubMed2002

Repetitive concentric wave-ring spread of oligemia/hyperemia in the sensorimotor cortex accompanying K(+)-induced spreading depression in rats and cats.

Vascular changes accompanying spreading depression (SD) remain controversial. We examined dynamic alterations of local cerebral blood volume (CBV) during SD by observing light transmission at an isosbestic point of hemoglobin (550 nm) in seven rats and five cats under alpha-chloralose/urethane anesthesia. The two species were used for comparison between the lissencephalic and gyrencephalic brains. We found that a concentrated K(+) solution microinjected into the sensorimotor cortex provoked CBV changes that appeared as a repetitive propagation of concentric wave-rings of ischemia followed by hyperemia expanding peripherally from the injection site at speeds of 1.9-3.2 mm/min. The dynamic CBV changes continued repeatedly every 1-5 min for more than 30 min in three rats, ceased within 30 min in three rats and remained at the site of K(+) injection in one rat. Similar repeated CBV changes occurred in two out of five cats.

Animals↗