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PubMed2000

Functional MRI at 4.7 tesla of the rat brain during electric stimulation of forepaw, hindpaw, or tail in single- and multislice experiments.

Stimulation of peripheral nerves activates corresponding regions in sensorimotor cortex. We have applied functional magnetic resonance imaging (fMRI) techniques to monitor activated brain regions by means of measuring changes of blood oxygenation level-dependent contrast during electric stimulation of the forepaw, hindpaw, or tail in rats. During alpha-chloralose anesthesia, artificial respiration, and complete muscle relaxation, stimulations were delivered at 3 Hz via subcutaneous bipolar electrodes with 500-microseconds-current pulses of 0.2-2.0 mA. Single- or multislice gradient echo images were collected during recording sessions consisting of five alternating rest and stimulation periods. Stimulation of the right and left forepaws and hindpaws repeatedly led to robust activation of the contralateral sensorimotor cortex. There was a significant correlation (P < 0.05) between current pulse strength and amount of activation of the sensory cortex during forepaw stimulation. The center of the main cortical representation of the forepaw was situated 3.4 mm lateral to the midline and 5 mm posterior to the rhinal fissure. The main representation of the hindpaw was 2.0 mm lateral to the midline and 6 mm posterior to the rhinal fissure. Tail stimulation gave rise to a strikingly extended bilateral cortical activation, localized along the midline in medial parietal and frontal cortex 4 and 5 mm posterior to the rhinal fissure. In conclusion, the experiments provide evidence that peripheral nerve stimulation induces a fMRI signal in the respective division of the somatosensory cortex in a stimulus-related manner. The marked cortical activation elicited by tail stimulation underlines the key importance of the tail.

Afferent Pathways↗
PubMed1980

An ultrastructural investigation of afferent connections of the red nucleus in the rat.

The pattern and mode of termination of afferents to the red nucleus of the rat were investigated with the electron microscope. Lesions were placed by electrocautery in the sensorimotor cortex or were placed electrolytically in the deep cerebellar nuclei and brachium conjunctivum using a stereotaxic approach. With both types of lesion, degenerating fibres of passage, preterminal axons, and synaptic terminals were observed in greatest numbers on the third post-operative day. Following cerebellar lesions, degenerating terminals occurred on the cell bodies and proximal dendrites of large, multipolar neurons in the magnocellular portion of the red nucleus, and on intermediate and small dendrites in the parvocellular portion. It is concluded that the former are interpositus terminals while the latter are dentate (lateralis) terminals ending on rubrospinal and rubrobulbar neurons respectively. Following lesions of the sensorimotor cortex, small degenerating terminals were observed on the distal dendrites and dendritic spines of parvocellular, rubrobulbar neurons. Large terminals containing round vesicles did not undergo degeneration following either type of lesion. These findings suggest the existence of an interpositorubro-spinal pathway in which the interpositus terminals exert a strong influence on the large, caudally placed rubrospinal neurons. The background excitability of the rostrally located rubrobulbar neurons is probably regulated by the distal cortical input while the more proximally located dentate terminals probably exert a stronger discrete influence over their activity.

Afferent Pathways↗
PubMedDate not supplied

Lateralization of brain trauma in female Wistar rats determines the immune and neurological status of offspring.

Unilateral trauma to the sensorimotor cortex in ambidextrous maternal female rats decreased the resistance of their offspring, as indicated by a reduction in the functional activity of natural killer cells. Offspring rats showed T-cell immunodeficiency regardless of the lateralization of the trauma in their mothers; this was more severe after right-sided trauma (both mature and immature T-lymphocytes were affected). The EMG pattern of evoked responses in offspring rats changed according to the lesions evoked by unilateral trauma in their mothers (in the muscles responsible for postural asymmetry). Cruder movement disturbances were also seen in offspring after right-sided trauma in mothers. Right-sided organic damage to the sensorimotor cortex in mothers evoked marked increases in negative emotionality and decreases in the motivation of orientational-investigative behavior in one-month-old offspring rats in the "open field" test.

Algorithms↗
PubMed1997

Chronic intractable epilepsy associated with a tumor located in the central region: functional mapping data and postoperative outcome.

Out of 57 patients operated for intractable epilepsy of the central region, 8 harbored an indolent glioma (7 dysembryoplastic neuroepithelial tumors, 1 ganglioglioma). Mapping of the sensorimotor area with depth electrodes implanted for stereoelectroencephalographic exploration demonstrated no or abnormal motor responses after low-frequency stimulation, and variable sensory responses to high-frequency stimulation, suggesting reorganization of the sensorimotor cortex representation around the tumor and absence of functional tissue within the neoplastic volume. After lesionectomy (3 cases) or corticectomy including the tumor (5 cases), 6 (75%) patients were seizure-free (class I of Engel) at the time to follow-up. No permanent motor or sensory deficit was observed in 6 cases. In 2, a mild facial (in 1) and arm (in 1) deficit persisted. It is concluded that the resection of intrinsic low-grade tumors associated with long-standing epilepsy and located in the central region can be associated with excellent seizure outcome and no or minimal postoperative deficit because of functional reorganization of the sensorimotor cortex.

Adolescent↗
PubMed2006

Salvianolic acid B improves motor function after cerebral ischemia in rats.

In a previous short-term study, salvianolic acid B was reported to have a protective effect on cerebral ischemia. Here, we investigated whether salvianolic acid B improves the recovery of motor function after cerebral ischemia in a 14-day investigation. Cerebral ischemia was induced by middle cerebral artery occlusion in rats. Motor function was evaluated with beam-walking performance. Neural cell injury in both the sensorimotor cortex and CA1 of the hippocampus ipsilateral to ischemia was studied by Nissl stain with methylene blue. The integrity of cerebral microvessels was monitored by immunoglobulin extravasations. Neurogenesis in the subgranular zone in the dentate gyrus of the hippocampus was detected with 5'-bromo-2'-deoxyuridine incorporation. Animals receiving salvianolic acid B at a dose of 10 mg/kg had a more rapid recovery of beam-walking performance than vehicle-treated ischemia animals, and the improvement became significant at 10 and 14 days after ischemia (P<0.05). Treatment with salvianolic acid B at a dose of 10 mg/kg also significantly prevented neural cell loss in CA1 of the hippocampus. Neural cells in the sensorimotor cortex were also preserved in animals that received salvianolic acid B at a high dose of 10 mg/kg. Salvianolic acid B (10 mg/kg) also improved the integrity of microvessels after ischemia. We observed a slight increase in 5'-bromo-2'-deoxyuridine-positive cells in the subgranular zone of the hippocampus in the animals treated with salvianolic acid B at a dose of 10 mg/kg. These data indicate that salvianolic acid B could improve the recovery of motor function after cerebral ischemia in rats.

Animals↗
PubMed2005

Combining EEG and fMRI to investigate the post-movement beta rebound.

The relationship between synchronous neuronal activity as measured with EEG and the blood oxygenation level dependent (BOLD) signal as measured during fMRI is not clear. This work investigates the relationship by combining EEG and fMRI measures of the strong increase in beta frequency power following movement, the so-called post-movement beta rebound (PMBR). The time course of the PMBR, as measured by EEG, was included as a regressor in the fMRI analysis, allowing identification of a region of associated BOLD signal increase in the sensorimotor cortex, with the most significant region in the post-central sulcus. The increase in the BOLD signal suggests that the number of active neurons and/or their synaptic rate is increased during the PMBR. The duration of the BOLD response curve in the PMBR region is significantly longer than in the activated motor region, and is well fitted by a model including both motor and PMBR regressors. An intersubject correlation between the BOLD signal amplitude associated with the PMBR regressor and the PMBR strength as measured with EEG provides further evidence that this region is a source of the PMBR. There is a strong intra-subject correlation between the BOLD signal amplitude in the sensorimotor cortex during movement and the PMBR strength as measured by EEG, suggesting either that the motor activity itself, or somatosensory inputs associated with the motor activity, influence the PMBR. This work provides further evidence for a BOLD signal change associated with changes in neuronal synchrony, so opening up the possibility of studying other event-related oscillatory changes using fMRI.

Adult↗
PubMed2001

The existence of two sources in rolandic epilepsy: confirmation with high resolution EEG, MEG and fMRI.

In benign rolandic epilepsy seizure semiology suggests that the epileptic focus resides in the lower sensorimotor cortex. Previous studies involving dipole modeling based on 32 channel EEG have confirmed this localization. These studies have also suggested that two distinct dipole sources are required to adequately describe the typical interictal spikes. Since in benign epilepsy invasive validation is prohibited, this study tries to further establish these results using a multi-modal approach, involving 32 channel EEG, high resolution 84 channel EEG, 151 channel MEG and fMRI. From one patient interictal spikes were recorded and analyzed using the MUSIC algorithm in a realistic volume conductor model. In an fMRI experiment the same patient performed voluntary tongue movements, thus mimicking a typical seizure. Results show that EEC, MEG and fMRI localization converge on the same area in the lower part of the sensorimotor cortex, and that high resolution EEG clearly reveals two distinct sources, one in the post- and one in the pre-central cortex.

Brain Mapping↗
PubMed1997

Frequency-dependent changes of regional cerebral blood flow during finger movements: functional MRI compared to PET.

To evaluate the effect of the repetition rate of a simple movement on the magnitude of neuronal recruitment in the primary sensorimotor cortex, we used a blood flow-sensitive, echo planar functional magnetic resonance imaging (fMRI) sequence in six normal volunteers. Three of the volunteers also had [15O]water positron emission tomography (PET) studies using the same paradigm. Previous PET studies had shown an increase in regional CBF (rCBF) with movement frequencies up to 2 Hz and then a plateau of regional cerebral blood flow (rCBF) at faster frequencies. To evaluate the extent of the activation, the correlation coefficient (cc) of the Fourier-transformed time-signal intensity change with the Fourier-transformed reference function was calculated pixel by pixel. The degree of activation was measured as the signal percent change of each region of interest with a cc > 0.5. The left primary sensorimotor cortex was constantly activated at 1, 1.5, 2, and 4 Hz, while there was only inconsistent activation at 0.25 and 0.5 Hz. Percent change in signal intensity linearly increased from 1 to 4 Hz. Area of activation increased up to 2 Hz and showed a tendency to decrease at higher frequencies. Individual analysis of PET data showed activation in the same location as that revealed by fMRI. The combination of progressively increasing signal intensity with an area that increases to 2 Hz and declines at faster frequencies explains the PET finding of plateau of rCBF at the faster frequencies. Functional magnetic resonance imaging shows similar results to PET, but is better able to dissociate area and magnitude of change.

Adult↗
PubMed2005

Reduced basal activity and increased functional homogeneity in sensorimotor and striatum of a Parkinson's disease rat model: a functional MRI study.

Functional neuro-imaging studies of Parkinson's disease (PD) patients and animal models show inconsistent cortical responses to sensory stimulation: some present increased sensorimotor cortex activation contradicting classical basal ganglia-cortex circuitry models, whereas others show decreased activation. As functional neuro-imaging activation is defined as the signal difference between stimulation ON and stimulation OFF, reduced 'activation' can point to either increased neuronal activity during stimulation ON or to decreased basal neuronal activity during stimulation OFF. A unique non-invasive method that uses the temporal and the spatial variances of functional magnetic resonance imaging signal is employed here to compare basal neuronal activity levels and 'functional homogeneity' between groups. Based on the assumption that the temporal variance reflects average neuronal activity, the variance of activity within a predefined region is defined as the region's 'functional homogeneity', which is assumed to estimate neuronal synchronization. Comparison of temporal and spatial variances of the sensorimotor cortex and the striatum in the 6-hydroxydopamine (6-OHDA) PD rat model and a control rat group show bilaterally decreased temporal and spatial variances in the 6-OHDA rat group, suggesting bilateral reduction of basal neuronal activity levels together with an increase in local neuronal synchronization in line with classical basal ganglia-cortex circuit models.

Adrenergic Agents↗
PubMed2003

Parametric analysis of rate-dependent hemodynamic response functions of cortical and subcortical brain structures during auditorily cued finger tapping: a fMRI study.

A multitude of functional imaging studies revealed a mass activation effect at the level of the sensorimotor cortex during repetitive finger-tapping or finger-to-thumb opposition tasks in terms of either a stepwise or a monotonic relationship between movement rate and hemodynamic response. With respect to subcortical structures of the centralmotor system, there is, by contrast, some preliminary evidence for nonlinear rate/response functions within basal ganglia and cerebellum. To further specify these hemodynamic mechanisms, functional magnetic resonance imaging (fMRI) was performed during a finger-tapping task in response to acoustic stimuli (six different frequencies: 2.0, 2.5, 3.0, 4.0, 5.0 and 6.0 Hz; applied via headphones). Passive listening to the same auditory stimuli served as a control condition. Statistical evaluation of the obtained data considered two approaches: categorical and parametric analysis. As expected, the magnitude of the elicited hemodynamic response within left sensorimotor cortex (plateau phase at frequencies above 4 Hz) and mesiofrontal cortex paralleled movement rate. The observed bipartite mesial response pattern, most presumably, reflects functional compartmentalization of supplementary motor area (SMA) in a rostral component (pre-SMA) and in a caudal (SMA proper) component. At the level of the cerebellum, two significant hemodynamic responses within the hemisphere ipsilateral to the hand engaged into finger tapping (anterior/posterior quadrangular lobule and posterior quadrangular lobule) could be observed. Both activation foci exhibited a stepwise rate/response function. In accordance with clinical data, these data indicate different cerebellar contributions to motor control at frequencies below or above about 3 Hz, respectively. Caudate nucleus, putamen, and external pallidum of the left hemisphere displayed, by contrast, a negative linear rate/response relationship. The physiological significance of these latter findings remains to be clarified.

Adult↗
PubMed1981

Development of the pyramidal tract in the hamster. I. A light microscopic study.

The development of the pyramidal tract and other projections from the sensorimotor cortex was studied in the postnatal hamster with both (3H) proline and horseradish peroxidase (HRP) as anterograde tracers. In the 1-day-old animal labeled axons extend as far as the pons. Other corticofugal fibers have penetrated into the corpus striatum and the thalamus. By 2 days postnatally, the pyramidal tract has grown to midmedullary levels and there is substantial retrograde (HRP) and anterograde labeling in the thalamus. The pyramidal decussation is formed at 3 days of age and by 4 days the pyramidal tract has descended in the dorsal funiculus as far as midcervical spinal cord. Corticofugal fibers invade the pontine nuclei at 4 days and both the dorsal column nuclei and the superior colliculus at 6 days of age. At 6 days the pyramidal tract can be traced to mid-thoracic levels of the spinal cord, by 8 days the tract reaches lumbar levels, and by 14 days it has completed its caudal growth to the coccygeal spinal cord. Fibers first penetrate the gray matter of a given spinal cord level approximately 2 days after the tract has grown past that level in the dorsal funiculus. Pyramidal fibers continue their lateral growth into the dorsal horn at all levels of the cord throughout the third postnatal week such that by 21 days of age the pyramidal tract appears similar to that of the adult. The projections from sensorimotor cortex to the pontine nuclei, the superior colliculus, and the dorsal column nuclei appear to have a pattern similar to that of the adult soon after the fibers grown into these structures. There is a consistent delay of 2 to 3 days between the arrival of the pyramidal tract axons in the white matter adjacent to target structures and their innervation of a given terminal field. The pyramidal tract grows more quickly through the dorsal funiculus of the spinal cord than it does along the ventral surface of the medulla. Extensive elongation of pyramidal tract axons is achieved long before the growth and differentiation of the sensorimotor cortical neurons from which they originate. Finally, the pyramidal tract appears to grow as a compact bundle and not by the addition of temporally staggered groups of fibers. The relatively protracted period of innervation of the spinal cord by the pyramidal tract coupled with the immaturity of the cortical neurons at birth may be factors contributing to the significant regrowth of pyramidal tract axons severed early in development.

Aging↗
PubMed1983

Infant lesion effect: III. Anatomical correlates of sparing and recovery of function after spinal cord damage in newborn and adult cats.

We have demonstrated that sparing of tactile placing occurs after neonatal but not adult spinal cord damage and that the spared tactile placing of one limb depends on the corresponding (contralateral) sensorimotor cortex. In order to determine whether anatomical reorganization of the corticospinal or brainstem-spinal pathways also occurred which might account for the sparing of the tactile placing response, we used retrograde transport of horseradish peroxidase to map supraspinal neurons which project caudal to a spinal hemisection made either neonatally or in adulthood. The pattern of HRP labeling in the brainstem was identical in both the neonatal and adult operates. Neonatal operates, however, showed severe retrograde cell loss in brainstem nuclei which projected to the damaged side of the cord. This massive retrograde cell loss was not seen when lesions were made in the adult. In contrast, sparing of corticospinal projections and anatomical reorganization of the corticospinal tract were found after neonatal, but not adult spinal cord lesions. In adult operates, this lesion abolished HRP labeling in the contralateral sensorimotor cortex, while in all of the neonatal operates, HRP labeled cells were found throughout these cortical areas. The labeled cells had many characteristics in common with those of the normal CST. They were located in lamina V of cytoarchitectonic areas 4, 3, 1-2, and 5. Although the range of cell diameter was normal, the mean diameter of these spared neurons was below normal. Although the 'spared' CST may share many characteristics with the normal CST, its axons must have reached caudal segments of the cord by an abnormal pathway, since the normal route for the CST was destroyed by the lesion. The results indicate that two different regions of the CNS responded differently to the same neonatal lesion. Growing CST axons exhibited anatomical plasticity, contrasting with the retrograde death of the brainstem spinal tracts. We suggest that this difference between the two classes of pathways is due to the difference in time of their development. Only the latest developing pathways displayed anatomical sparing. The difference may also be seen in terms of the behavioral results. Only late-developing motor patterns were spared after neonatal lesions.

Age Factors↗
PubMed1981

Late muscular responses to arm perturbations persist during supraspinal dysfunctions in monkeys.

This study was conducted to determine which supraspinal structures, if any, are essential for generation of late (M2 and M3) EMG responses to perturbations. EMGs were recorded during active arm movements made by Cebus monkeys trained to resist perturbations applied to a handle and/or during passive movements imposed on sedated or anesthetized animals. EMGs were tested during active movements after ablation of the arm areas of the sensory and caudal motor cortices, during cooling part of the sensorimotor cortex along the central sulcus, and during cooling the arm area in the ventral lateral (VL) thalamus. EMG responses to passive movements were tested after decerebration and decerebellation, after lesions of the motor and/or sensory cortices, during surface cooling the same, and during cooling the VL arm area and the cerebellar dentate nucleus. M1, M2, and M3 were not abolished in any monkey. Decreases in the magnitudes of these responses occurred in some animals, but no reproducible changes in the sizes of M2 and M3 (in comparison to M1) were observed following any procedure. The effects of cortical lesions on M1, M2, and M3 responses to passive movements were found to depend on the level of arousal of the animal. These results demonstrate that M1, M2, and M3 can be produced in the primate spinal cord and brainstem and that the sensorimotor cortex can facilitate these responses.

Animals↗
PubMed2006

[Effects of transcranial magnetic stimulation on recovery of neural functions and changes of synaptic interface and dendritic structure in the contralateral brain area after cerebral infarction: experiment with rats].

OBJECTIVE: To evaluate the effects of transcranial magnetic stimulation (TMS) on the brain plasticity and its role in functional outcome in cerebral infarction. METHODS: Twenty male SD rats underwent suture of the unilateral middle cerebral artery (MCA) so as to establish focal cerebral infarction models and then were randomly divided into 2 equal groups: model group, to be reared in the original living state, and TMS group, given in addition TMS treatment 1 day after infarction 2 times per day and 30 pulses per time for 4 weeks. Twenty-eight days after the rats were killed. Four rats from each group underwent microscopy of the brain to measure the dendritic structure of the pyramidal cells quantitatively. Other 4 rats from each group underwent electron microscopy of the brain to measure the parameters of synaptic interface in the sensorimotor cortex. Neural function scoring was conducted 24 hours after the establishment of model and before being killed. RESULTS: There was no significant difference in the neural function 24 h after the establishment of models, however, 28 days after the score of neural function of the TMA group was 0.58 +/- 0.49, significantly lower than that of the model group (0.92 +/- 0.28, P < 0.05). The total dendritic length, number of dendritic branching points, and dendritic density in layer V pyramidal cells within the undamaged motor cortex of the TMS group were 898 microm +/- 127 microm, 6.6 +/- 1.5, and 0.75/microm +/- 0.19/microm, all significantly higher than those of the model group (788 microm +/- 112 microm, 5.8 +/- 1.5, and 0.60/microm +/- 0.16/microm, P < 0.05 or < 0.01). Electron microscopy showed that the synaptic curvatures and post-synaptic density of the TMS group were 1.06 +/- 0.08 and 64 +/- 13 respectively, both significantly higher than those of the model group (1.02 +/- 0.06 and 54 +/- 12 nm respectively, P < 0.05 and P < 0.01), and the synapse cleft width of the TMS group was 19.5 +/- 2.1, significantly narrower than that of the model group (23.3 +/- 2.3, P < 0.01). CONCLUSION: TMS promotes the improvement of neural functions of the rats with cerebral ischemia by the potential mechanism that TMS strengthen the compensatory roles of the synaptic interface and dendritic structure in the undamaged sensorimotor cortex area and increase synaptic plasticity.

Animals↗
PubMedDate not supplied

[Somatosensory evoked potentials during natural and learned patterns of postural adjustment, accompanying limb movements in dogs].

A goal of the study was to investigate cortical reorganization corresponding to inhibition of innate motor patterns during motor learning. Functional changes in the sensorimotor cortex during learned rearrangement of the natural diagonal pattern of postural adjustment (PA) accompanying a hindlimb movement into a new one, the so-called unilateral pattern, were studied in dogs by testing somatosensory evoked potentials (SEP) in response to stimulation of a forelimb during PA immediately before the limb movement onset. During PA the latency and the amplitude of several SEP components decreased. In general, changes in SEP were less pronounced in the learned unilateral pattern of postural adjustment in comparison with the innate diagonal pattern, but the difference was significant only for some SEP components. The SEP late positivity in the learned postural pattern was replaced by a negativity. The SEP changes were similar independently of whether the test stimulus was applied on the forelimb loaded or unloaded during postural adjustment. The data suggest that changes in interrelations between different neuronal populations in the sensorimotor cortex during formation and realization of a learned motor program can be reflected in SEP changes.

Animals↗
PubMed2005

Single-dose ketamine administration induces apoptosis in neonatal mouse brain.

UNLABELLED: The activity of N-methyl-D-aspartate (NMDA) receptors is critical for neuronal survival in the immature brain. Studies have reported that chronic blockage of these receptors mediates apoptosis in neonatal animals. We investigated the apoptotic effect of a clinically relevant single dose of ketamine, an NMDA receptor antagonist, in the brain of neonatal mice. Seven-day-old ICR mice were injected with ketamine (1.25, 2.5, 5, 10, 20, and 40 mg/kg body weight, subcutaneously in 0.9% NaCl) or with 0.9% NaCl alone as control. Righting reflex testing was performed and mouse brains were examined at 24, 48, and 72 h and 7 days after injection. The number of degenerating neurons was measured using silver staining. Apoptosis was confirmed by DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling). We observed in the sensorimotor cortex and cerebellum of ketamine-treated mice extensive apoptosis, which was clearly dose-dependent and present even after a low dose of ketamine (5 mg/kg). The most prominent apoptotic damage was detected 72 h post-injection (P < 0.001 vs control), at doses ranging from 10 to 40 mg/kg. After 7 d the number of neurodegenerative neurons, at doses ranging from 5 to 40 mg/kg, remained significantly high. The brain weight was comparable to that of untreated control mice and no gross neurobehavioral effects in the righting reflex test or alteration in the pattern of behavior was observed. The results indicate that the administration of ketamine in a clinically relevant single dose triggers long-lasting neuronal apoptosis in certain brain areas of neonatal mice. IMPLICATIONS: The administration of ketamine in a clinically relevant single dose to 7-d-old mice induced apoptosis in the sensorimotor cortex and cerebellum. This effect was dose-dependent and long lasting.

Animals↗
PubMedDate not supplied

The effects of sodium nitrite on neocortical neuron activity during performance of defensive and inhibitory conditioned reflexes.

Administration of the NO-generating substance sodium nitrite to conscious non-immobilized rabbits at a dose of 11 mg/kg (s.c.) decreased the intensity and duration of the short-latency "modality-specific" components of the responses of neurons in the visual cortex (to flashes of light) and sensorimotor cortex (to pain reinforcement). Decreases in neuron activation in the visual cortex in response to flashes of light occurred independently of their biological significance. i.e., as the signal for a defensive reflex and on the background of conditioned inhibition. The long-latency activatory components of the response of sensorimotor and visual cortex neurons to pain reinforcement, the inhibitory pause in the responses of visual cortex neurons to flashes of light, and the disinhibitory effect of pain reinforcement showed smaller changes after sodium nitrite. The results obtained here support the suggestion that different neuromediators are involved in transmitting "modality-specific" and "modality-non-specific" influences to neocortical neurons during learning, and provide the basis for suggesting that sodium nitrite has a neurotropic action when given systemically.

Animals↗
PubMed2005

Activation of the stress-activated MAP kinase, p38, but not JNK in cortical motor neurons during early presymptomatic stages of amyotrophic lateral sclerosis in transgenic mice.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder, characterized by the degeneration of upper and lower motor neurons (MNs). Central nervous system features include a loss of Betz cells and other pyramidal cells from sensorimotor cortex. The intrinsic mechanism underlying this selective motor neuron loss has not been identified. A recent in vitro study has provided evidence of a novel programmed cell death (PCD) pathway that is unique to spinal cord MNs and is exacerbated by superoxide dismutase (SOD) mutations. This PCD pathway is triggered through the Fas receptor and involves the apoptosis signal-regulating kinase 1 (ASK1), the p38 MAP kinase, and the neuronal form of nitric oxide synthase (nNOS). Previously, we found significant increases in the numbers of ventral horn MNs immunopositive for these enzymes in the spinal cords of mutant SOD transgenic (G93A) mice as early as 60 days of age, suggesting that this pathway may be active in vivo. Since the upper MNs of ALS patients and G93A mice are also known to degenerate, the purpose of the present study was to investigate the possible activation of this PCD pathway in the MNs of the sensorimotor cortex of G93A transgenic mice. Compared to non-transgenic littermates, the G93A mice showed significant increases in the numbers of MNs immunopositive for the active (phosphorylated) forms of ASK1, p38, MKK3/6 (the known activator of p38), and also active caspase-3, as early as 60 days of age. Another stress-activated protein kinase, c-Jun N-terminal kinase (JNK), commonly activated in other neurodegenerative disorders such as Alzheimer's disease, showed no increases in G93A mice at any age. These results suggest that, not only has a PCD pathway been activated in the cortical MNs, but one that may be unique to ALS. Moreover, these findings suggest that earlier diagnosis and therapeutic intervention may be possible for successful treatment of ALS. Consequently, these enzymes may provide the biochemical markers to enable earlier diagnosis of ALS and molecular targets for the development of new therapeutic compounds.

Amyotrophic Lateral Sclerosis↗