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At least 253 records · Page 14Linked to original sources

PubMed1998

Adenosinergic modulation of ethanol-induced motor incoordination in the rat motor cortex.

1. On going work in our laboratory has shown that adenosine modulates ethanol-induced motor incoordination (EIMI) when given systemically as well as directly into the cerebral ventricles, cerebellum and corpus striatum of the rat and/or mouse. 2. The objective of this study was to determine what effect adenosine agonists and antagonists would have within the rat motor cortex on EIMI. 3. The participation of the motor cortex in EIMI was suggested when microinfusion of the anti-ethanol compound, Ro15-4513, an inverse agonist of the benzodiazepine binding site, directly into the motor cortex significantly attenuated EIMI. Further, the adenosine agonists N6-cyclohexyladenosine (CHA) and 2-p-(2-carboxyethyl)-phenethylamino-5'-N-carboxaminoadenosine++ + hydrochloride (CGS-21680) significantly accentuated EIMI in a dose-related manner. The adenosine A1 receptor-selective agonist, CHA, appeared most potent in this modulatory effect when compared to the A2-selective agonist, CGS-21680. 4. The extent of diffusion of the adenosine drugs within the cortical tissue after their microinfusion was also checked by measuring the dispersion of microinfused [3H]CHA. The [3H]CHA dispersion study indirectly confirmed that the results of the present investigation were based on the effect of adenosine drugs within the motor cortex only. 5. Accentuation by the A1- and A2-selective adenosine agonists was significantly attenuated by the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) but not by the A2 receptor-selective antagonist 8-(3-chlorostyryl)caffeine (CSC) further suggesting modulation mainly by the A1-subtype. 6. Pretreatment of the motor cortex with pertussis toxin (PT) significantly reduced the capacity of both A1- and A2-selective adenosine agonists to accentuate EIMI suggesting the involvement of a PT-sensitive Gi/Go protein. 7. These data support earlier work which showed that adenosine modulates EIMI within the central nervous system (CNS), most likely via the A1 receptor, and moreover, extend that work by including the motor cortex as a brain area participating in the adenosinergic modulation of ethanol-induced motor impairment.

Adenosine↗

PubMed1995

Transcranial magnetic coil stimulation of motor cortex in patients with central pain.

We report two patients with deafferentation pain secondary to central nervous system lesions who were evaluated by noninvasive magnetic coil stimulation of the motor cortex followed by electrical motor cortex stimulation with epidural electrode array implantation. Magnetic coil stimulation was very useful to estimate the effect of electrical stimulation. Our first patient was a 52-year-old man who experienced a left putamenal hemorrhage at the age of 48. Two years later, he had paresthesias and intractable pain in the extremities and face on the right side. Pain was resistant to barbiturates but responded to magnetic coil stimulation of the motor cortex. Electrical motor cortex stimulation provided excellent relief from the pain. The second patient was a 43-year-old man who was suffering from congenital cerebral palsy for which left thalamotomy was performed two times, at the ages of 9 and 13. He began to experience intractable pain on the right side 20 years later. Although barbiturate administration was effective for pain relief, neither magnetic coil stimulation nor electrical stimulation of the motor cortex gave relief from pain.

Adult↗

PubMed2007

Role of hyperactive cerebellum and motor cortex in Parkinson's disease.

Previous neuroimaging studies have found hyperactivation in the cerebellum and motor cortex and hypoactivation in the basal ganglia in patients with Parkinson's disease (PD) but the relationship between the two has not been established. This study examined whether cerebellar and motor cortex hyperactivation is a compensatory mechanism for hypoactivation in the basal ganglia or is a pathophysiological response that is related to the signs of the disease. Using a BOLD contrast fMRI paradigm PD patients and healthy controls performed automatic and cognitively controlled thumb pressing movements. Regions of interest analysis quantified the BOLD activation in motor areas, and correlations between the hyperactive and hypoactive regions were performed, along with correlations between the severity of upper limb rigidity and BOLD activation. There were three main findings. First, the putamen, supplementary motor area (SMA) and pre-SMA were hypoactive in PD patients. The left and right cerebellum and the contralateral motor cortex were hyperactive in PD patients. Second, PD patients had a significant negative correlation between the BOLD activation in the ipsilateral cerebellum and the contralateral putamen. The correlation between the putamen and motor cortex was not significant. Third, the BOLD activation in the motor cortex was positively correlated with the severity of upper limb rigidity, but the BOLD activation in the cerebellum was not correlated with rigidity. Further, the activation in the motor cortex was not correlated with upper extremity bradykinesia. These findings provide new evidence supporting the hypothesis that hyperactivation in the ipsilateral cerebellum is a compensatory mechanism for the defective basal ganglia. Our findings also provide the first evidence from neuroimaging that hyperactivation in the contralateral primary motor cortex is not a compensatory response but is directly related to upper limb rigidity.

Aged↗

PubMed2003

Reduced muscle selectivity during individuated finger movements in humans after damage to the motor cortex or corticospinal tract.

We investigated how damage to the motor cortex or corticospinal tract affects the selective activation of finger muscles in humans. We hypothesized that damage relatively restricted to the motor cortex or corticospinal tract would result in unselective muscle activations during an individuated finger movement task. People with pure motor hemiparesis attributed to ischemic cerebrovascular accident were tested. Pure motor hemiparetic and control subjects were studied making flexion/extension and then abduction/adduction finger movements. During the abduction/adduction movements, we recorded muscle activity from 3 intrinsic finger muscles: the abductor pollicis brevis, the first dorsal interosseus, and the abductor digit quinti. Each of these muscles acts as an agonist for only one of the abduction/adduction movements and might therefore be expected to be active in a highly selective manner. Motor cortex or corticospinal tract damage in people with pure motor hemiparesis reduced the selectivity of finger muscle activation during individuated abduction/adduction finger movements, resulting in reduced independence of these movements. Abduction/adduction movements showed a nonsignificant trend toward being less independent than flexion/extension movements in the affected hands of hemiparetic subjects. These changes in the selectivity of muscle activation and the consequent decrease in individuation of movement were correlated with decreased hand function. Our findings imply that, in humans, spared cerebral motor areas and descending pathways that remain might activate finger muscles, but cannot fully compensate for the highly selective control provided by the primary motor cortex and the crossed corticospinal system.

Adult↗

PubMed2004

Functional recovery in a primate model of Parkinson's disease following motor cortex stimulation.

A concept in Parkinson's disease postulates that motor cortex may pattern abnormal rhythmic activities in the basal ganglia, underlying the genesis of observed motor symptoms. We conducted a preclinical study of electrical interference in the primary motor cortex using a chronic MPTP primate model in which dopamine depletion was progressive and regularly documented using 18F-DOPA positron tomography. High-frequency motor cortex stimulation significantly reduced akinesia and bradykinesia. This behavioral benefit was associated with an increased metabolic activity in the supplementary motor area as assessed with 18-F-deoxyglucose PET, a normalization of mean firing rate in the internal globus pallidus (GPi) and the subthalamic nucleus (STN), and a reduction of synchronized oscillatory neuronal activities in these two structures. Motor cortex stimulation is a simple and safe procedure to modulate subthalamo-pallido-cortical loop and alleviate parkinsonian symptoms without requiring deep brain stereotactic surgery.

Animals↗

PubMed1990

Functional organization of the direct and indirect projection via the reticularis thalami nuclear complex from the motor cortex to the thalamic nucleus ventralis lateralis.

The projection systems which arise from the motor cortex to reach the nucleus ventralis lateralis (VL) were investigated in the rat. They included a direct as well as an indirect projection via the reticularis thalami nuclear complex (RT). The investigation was performed in two steps: i) the former concerned the projection to the VL as well as to the RT from individual cortical foci electrophysiologically identified by the motor effects evoked by electrical stimulation; the second step concerned the projection from the RT to functionally defined regions of the VL. The direct projection from the motor cortex to the VL is somatotopically arranged. The projection reciprocates the fiber system directed from the VL to the motor cortex. Thus cortical zones controlling the motor activity of the proximal segments of the limbs project onto the regions of the VL that project back to these same cortical areas. With regard to cortical zones controlling the motor activity of the distal segments of the limbs, they not only project to the region of the VL specifically related to them, but also to the region of the VL associated with the cortical areas responsible for movements of the proximal parts of the same limb. In that case fiber terminals were more dense in the VL region controlling the proximal segment than in the region controlling the distal segment of the same limb. This organization suggests that proximal adjustments may be automatically provided by the motor activity of the distal segments of the same limb. The motor cortex projects to the rostral region of the RT with a precise topographical organization. In particular, the projection shows a dorsoventral organization in the RT in relation to the caudorostral body representation in the motor cortex. The projection which arises from the rostral region of the RT also reaches the VL with a topographical arrangement. It discloses a rostrocaudal organization in the VL in relation to a dorsoventral displacement in the RT. Comparing the projection from the motor cortex to the RT and that from this nuclear complex to the VL it was shown that the regions of the VL and their receptive cortical areas were associated with the same regions of the RT. It was therefore concluded that the motor cortical projection to the VL relayed by the RT is somatotopically organized. In both direct and relayed pathways the projections from "hind-" and "forelimb" motor area are segregated, whereas the "head" projection overlaps, at least partially, the "forelimb" terminal field.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Activation of the primary motor cortex by somatosensory stimulation in adult rats is mediated mainly by associational connections from the somatosensory cortex.

In anaesthetized adult rats, facial nerve injury causes a disinhibition of the interhemispheric connections between homotopic representation fields in the primary motor cortex with a latency of 4 min (Toldi et al., 1996, Neurosci Lett. 203, 179-182). One possible explanation for the induction of such rapid changes is an alteration of the somatosensory input to the motor cortex. To test this hypothesis, unit activity in primary motor cortex was recorded during electrical stimulation of trigeminal afferents in the contralateral whisker-pad. About one-third of all recorded primary motor cortex neurons responded with latencies shorter than in the ventrolateral and posterior nuclei of the thalamus. Responses failed at stimulation frequencies > or = 10 Hz and after elimination or inactivation of the somatosensory cortex. Within primary motor cortex, the activatable neurons displayed a bilaminar distribution and were identified as pyramidal neurons by neurobiotin labelling. The results suggest that trigeminal afferents participate in modulation of the activity of primary motor cortex output neurons via primary somatosensory cortex-to-primary motor cortex associational connections, even under anaesthesia.

Afferent Pathways↗

PubMed1995

An investigation of the late excitatory potential in the hand following magnetic stimulation of the motor cortex.

Magnetic stimulation of the motor cortex gives rise to a motor evoked potential (MEP) followed by a silent period (SP) during which a late excitatory potential (LEP) may occur in the surface EMG. To elucidate the mechanism of the LEP we investigated the effect of muscle contraction, stimulus intensity and stimulation site on the LEP recorded from the abductor pollicis brevis muscle. The amplitude of the LEP increased with increasing levels of muscle contraction and decreased with increasing stimulus intensity. There was no direct relationship between the amplitude of the LEP and the MEP, but there was an inverse relationship between LEP amplitude and SP duration. The latency of the LEP was unaffected by the level of muscle contraction, but increased with increasing stimulus intensity. Topographic mapping with stimulation at multiple scalp sites yielded a LEP at sites partially encircling but not including the centre of the APB motor area. These results are consistent with the LEP being due to reflex alpha motoneurone firing as a result of gamma motoneurone activation or with a period of disinhibition at cortical level allowing breakthrough of voluntary activity.

Adult↗

PubMed1996

Tactile experience determines the organization of movement representations in rat motor cortex.

We mapped movement representations in motor cortex of rats that had their mystacial vibrissae (whiskers) clipped continually for various periods during their development. In animals clipped since birth, and in adult animals clipped for 5 days, there was a significant reduction in the ratio of whisker to forelimb representation areas. Allowing the whiskers to regrow for at least 72 h resulted in normal-appearing representation patterns. The plasticity of motor representations induced by whisker clipping, and that following whisker regrowth, were not age dependent. These findings indicate that a relatively innocuous procedure that restricts sensory and motor functions results in pronounced, and reversible, changes in the functional organization of the motor cortex.

Age Factors↗

PubMed1999

Topographical organization of projections to cat motor cortex from nucleus interpositus anterior and forelimb skin.

1. The activation of the motor cortex from focal electrical stimulation of sites in the forelimb area of cerebellar nucleus interpositus anterior (NIA) was investigated in barbiturate-anaesthetized cats. Using a microelectrode, nuclear sites were identified by the cutaneous climbing fibre receptive fields of their afferent Purkinje cells. These cutaneous receptive fields can be identified by positive field potentials reflecting inhibition from Purkinje cells activated on natural stimulation of the skin. Thereafter, the sites were microstimulated and the evoked responses were systematically recorded over the cortical surface with a ball-tipped electrode. The topographical organization in the motor cortex of responses evoked by electrical stimulation of the forelimb skin was also analysed. 2. Generally, sites in the forelimb area of NIA projected to the lateral part of the anterior sigmoid gyrus (ASG). Sites in the hindlimb area of NIA also projected to lateral ASG and in addition to a more medial region. Sites in the face area of NIA, however, projected mainly to the middle part of the posterior sigmoid gyrus (PSG). 3. For sites in the forelimb area of NIA, the topographical organization and strength of the projections varied specifically with the cutaneous climbing fibre receptive field of the site. The largest cortical responses were evoked from sites with receptive fields on the distal or ventral skin of the forelimb. 4. Microelectrode recordings in the depth of the motor cortex revealed that responses evoked by cerebellar nuclear stimulation were due to an excitatory process in layer III. 5. Short latency surface responses evoked from the forelimb skin were found in the caudolateral part of the motor cortex. At gradually longer latencies, responses appeared in sequentially more rostromedial parts of the motor cortex. Since the responses displayed several temporal peaks that appeared in specific cortical regions for different areas of the forelimb skin, several somatotopic maps were seen. 6. The cerebellar and cutaneous projections activated mainly different cortical regions and had topographical organizations that apparently were constant between animals. Their patterns of activation may constitute a frame of reference for investigations of the functional organization of the motor cortex.

Afferent Pathways↗

PubMed1993

Input organization of distal and proximal forelimb areas in the monkey primary motor cortex: a retrograde double labeling study.

The present double-labeling study was designed to demonstrate the morphological framework for motor control in coordinated distal and proximal forelimb movements, which may partly, at least, depend on corticocortical and thalamocortical inputs to the forelimb area in the primary motor cortex. After intracortical microstimulation mapping of the forelimb area in the primary motor cortex of four macaque monkeys, a retrograde tracing study with fluorescent dyes was attempted to label simultaneously neurons in cortical and subcortical sites projecting to the distal forelimb representation area and those projecting to the proximal representation area of the primary motor cortex. Neurons projecting to distal and proximal forelimb parts of the primary motor cortex were largely separate in the following areas: the premotor area, primary somatosensory area, secondary somatosensory area, area 5, and thalamus. In contrast, there was no precise topographic organization of labeled projection neurons in the following areas: the supplementary motor area, cingulate motor area, primary motor cortex adjacent to the injection sites, claustrum, and basal nucleus of Meynert. The present study revealed that the forelimb area of the primary motor cortex receives both segregated and intermixed inputs from cortical and subcortical sources. In particular, the fact that the forelimb area of the primary motor cortex receives topographically organized inputs from the premotor area and nontopographically organized inputs from the supplementary motor area and cingulate motor area indicates possible different functional roles of frontal premotor areas in control of coordinated distal and proximal forelimb movements.

Animals↗

PubMed1983

Amphetamine and apomorphine restore tactile placing after motor cortex injury in the cat.

Unilateral motor cortex injury in the cat results in a prolonged loss of tactile placing in the forelimb contralateral to the injury. Amphetamine (5 mg/kg) temporarily reverses this tactile placing deficit as early as 4 days following the injury. Racemic amphetamine was found to produce a significantly more prolonged restoration of placing than the d isomer, which was significantly more effective than the l isomer. Haloperidol (0.4 mg/kg) blocked the amphetamine-induced recovery of placing responses and also blocked placing in nondrugged cats showing partial spontaneous recovery. This dosage of haloperidol had no effect on tactile placing in normal cats. Apomorphine at moderate dosages (0.25 and 0.5 mg/kg) produced a weak restoration of tactile placing in motor cortex-injured animals. These pharmacological data suggest that the loss of tactile placing after motor cortex injury is due to a depression of catecholaminergic function, which is temporarily reversible by catecholaminergic stimulation.

Amphetamine↗

PubMed2003

Context-related representation of timing processes in monkey motor cortex.

Precise timing is essential for motor performance, though the neuronal representation of time is unknown. To explore neuronal correlates of timing processes during movement preparation and execution, we compared the activities of neurons recorded in monkey motor cortex during the performance of two tasks requiring correct time estimation in different contextual situations. Despite the fact that both tasks had many common features (e.g. same movements, same time intervals to estimate), they involved different degrees of spatial and temporal uncertainty. Our findings indicate that time is indeed represented in neuronal activity of the motor cortex, albeit strongly dependent on context and not in an invariant manner as a distinct process per se.

Animals↗

PubMed1998

Decreased N-acetylaspartate in motor cortex and corticospinal tract in ALS.

The primary objectives of this study were to test whether 1) N-acetylaspartate (NAA), a neuronal marker, is reduced in motor cortex and corticospinal-tract (CST) brain regions of ALS patients; and 2) motor cortex NAA correlates to a clinical measurement of upper motor neuron function in ALS patients. Ten probable or definite ALS patients and nine neurologically normal control subjects were studied. Three axial planes of two-dimensional 1H MRSI data were collected, using a single spin-echo multislice sequence (TE140/TR2000). Two of the 1H MRSI planes were positioned superior to the lateral ventricles, and one plane was positioned at the level of the internal capsule. Spectroscopy voxels were selected from motor cortex, frontal cortex, parietal cortex, medial gray matter, centrum semiovale white matter, anterior internal capsule, and posterior internal capsule. Peak integrals were obtained for the three major 1H MRSI singlet resonances, NAA, creatine and phosphocreatine (Cr), and cholines (Cho). Maximum finger-tap rate was used as a clinical measurement of upper motor neuron function. In ALS, brain NAA/(Cho+Cr) was reduced 19% (p=0.024) in the motor cortex and 16% (p=0.021) in the CST (centrum semiovale and posterior internal capsule) regions. NAA/ (Cho+Cr) was not reduced in frontal cortex, parietal cortex, medial gray matter, or anterior internal capsule. There was a significant relation between ALS motor cortex NAA/(Cho+Cr) and maximum finger-tap rate (r=0.80; p=0.014). NAA/(Cho+Cr) was reduced in motor cortex and CST regions and unchanged in other brain regions of ALS patients when compared with controls. These findings are consistent with the known distribution of neuronal loss in ALS. The positive correlation between motor cortex NAA/(Cho+Cr) and maximum finger-tap rate suggests that reduced NAA/(Cho+Cr) is a surrogate marker of motor cortex neuron loss in ALS. These findings support the study of 1H MRSI NAA measurement as an objective and quantitative measurement of upper motor neuron dysfunction in ALS.

Adult↗

PubMed2003

Motor cortex excitability in Alzheimer's disease: a transcranial magnetic stimulation study.

Motor deficits affect patients with Alzheimer's disease only at later stages. Recent studies demonstrate that the primary motor cortex is affected by neuronal degeneration accompanied by the formation of amyloid plaques and neurofibrillary tangles. It is conceivable that neuronal loss is compensated by reorganization of the neural circuitries occurring along the natural course of the disease, thereby maintaining motor performances in daily living. Cortical motor output to upper limbs was tested via motor-evoked potentials from forearm and hand muscles elicited by transcranial magnetic stimulation of motor cortex in 16 patients with mild Alzheimer's disease without motor deficits. Motor cortex excitability was increased, and the center of gravity of motor cortical output, as represented by excitable scalp sites, showed a frontal and medial shift, without correlated changes in the site of maximal excitability (hot-spot). This may indicate functional reorganization, possibly after the neuronal loss in motor areas. Hyperexcitability might be caused by a dysregulation of the intracortical GABAergic inhibitory circuitries and selective alteration of glutamatergic neurotransmission. Such findings suggest that motor cortex hyperexcitability and reorganization allows prolonged preservation of motor function during the clinical course of Alzheimer's disease.

Aged↗

PubMed2003

The alpha2-adrenergic agonist guanfacine reduces excitability of human motor cortex through disfacilitation and increase of inhibition.

OBJECTIVE: To test the acute effects of the alpha2-adrenoceptor agonist guanfacine (GFC) on motor excitability in intact humans. METHODS: Eight healthy right-handed adults received a single oral dose of 2 mg of GFC. Motor cortex excitability was tested by focal transcranial magnetic stimulation of the hand area of the left motor cortex. Motor evoked potentials (MEP) were recorded from the right abductor pollicis brevis muscle. In addition, spinal and neuromuscular excitability were tested. All measures were obtained immediately before GFC intake (baseline), and 2, 6, and 24 h later. RESULTS: GFC decreased the slope of the MEP intensity curve, increased paired-pulse short-interval intracortical inhibition, and decreased paired-pulse intracortical facilitation and I-wave facilitation. These effects were maximal at 2-6 h and returned to baseline at 24 h. Motor threshold, cortical silent period, and the measures of spinal (peripheral silent period, F waves) and neuromuscular excitability (maximum M wave) remained unaffected. CONCLUSIONS: This is the first study on the effects of an anti-noradrenergic drug on human motor cortex excitability. GFC reduced cortical excitability by disfacilitation and increased inhibition. These findings support the idea that anti-noradrenergic drugs are detrimental for cortical plasticity and learning which are down-regulated by disfacilitation or increased inhibition.

Adrenergic alpha-Agonists↗

PubMed1994

Neostriatal modulation of motor cortex excitability.

The influence of the basal ganglia motor loop on motor cortex function was examined by pharmacologically altering neostriatal activity while monitoring the electrical stimulation thresholds for eliciting movements of the ipsilateral and contralateral motor cortex in ketamine anesthetized rats. Repeated unilateral intraneostriatal infusions (1-3) of the glutamate agonist, kainic acid (0.1 microliter, 75 ng), or glutamate (0.3 microliter, 1.65 micrograms) reliably increased ipsilateral but not contralateral cortical thresholds. Single infusions of kainic acid (0.3 microliter, 150 or 225 ng) elevated ipsilateral cortical thresholds for 30-45 min; with glutamate (0.3 microliter, 1.65 micrograms), the change lasted less than 10 min. Antidromically identified striatonigral projection neurons (n = 8) located approximately 500 microM from the infusion cannula, showed either increased firing (n = 4) for less than 10 min following glutamate infusion or no change from their non-firing state (n = 4). Non-antidromically activated neurons (n = 3) were all excited by the infusion, although an interval of inhibition preceded or followed the excitation in two cases. Infusions (0.3 microliter) of inhibitory agents (GABA, 31 and 310 ng; muscimol 34.2 ng; and DNQX 34.2 ng) did not alter cortical threshold, nor did saline vehicle. Lesion of the ventrolateral but not ventromedial thalamic nucleus prevented the modulation of cortical thresholds following intraneostriatal infusion of 225 ng kainic acid. Thus the neostriatal alteration of cortical thresholds indicates a modulation of cortical excitability via thalamic projections and not the outcome of competing descending cortical and neonstriatal influences converging on motorneurons. These results suggest that tonic feedforward modulation of the motor cortex and the pyramidal tract by the basal ganglia can be inhibitory.

Animals↗

PubMed1975

Afferent-efferent linkages in motor cortex for single forelimb muscles.

1. In locally anesthetized cats, extracellular recordings were made from single neurons in the lateral cruciate gyrus of cerebral cortex. These neurons responded to natural activation of stretch receptors in single, contralateral, forelimb wrist muscles, typically with phasic excitation. Low-velocity stretches, which activate primary endings of muscle spindles, excited one set of neurons at a mean latency of 11 ms; high-velocity stretches, which principally activate Golgi tendon organs and/or secondary spindle endings, excited a second set at 18 ms. The cortical neurons showing threshold responses to low-velocity stretches were found exclusively within restricted columns, 0.5-2.0 mm in diameter, which were spatially separate for each muscle. Neurons exhibiting threshold responses to high-velocity stretches were present in high density within the same columns and were also distributed, although more sparsely, outside the columns. 2. These afferent columns were located in cytoarchitectonic area 4gamma, and were shown by intracortical microstimulation to coincide with the efferent columns for contraction of the same muscle from which in input rose. Discrete afferent columns were also found for single muscles in the peridimple region of sensory cortex (area 3a), spatially separate from the columns in motor cortex. The excitation of the columns in motor cortex by these inputs from muscle was independent of that in sensory cortex. 3. The role of the cerebellum in controlling these feedback systems to motor cortex was investigated by selective cooling of interpositus and dentate nucleus, respectively. Cooling of interpositus markedly reduced transmission in the high-threshold system; cooling of dentate had a similar effect on the low-threshold system. 4. The latency, threshold, and cooling data indicated that the low-threshold system to motor cortex utilizes extracerebellar pathways including medial lemniscus and is facilitated by dentate nucleus. The high-threshold system involves a transcerebellar pathway including interpositus nucleus. Both systems transmit velocity-related information, with each showing different and complementary sensitivity and dynamic range. 5. The results are discussed with reference to the cortical load-compensation mechanism postulated by Phillips (37-38).

Animals↗