Disease relevance of Motor Cortex

• According to the basal ganglia-thalamocortical circuit model, dopamine depletion in the nigrostriatal system leads to hypoactivation in the supplementary motor area (SMA) and the primary motor cortex (M1) in Parkinson's disease [1].
• Alumina cream-induced focal motor epilepsy in cats. IV. Thickness and cellularity of layers in the perilesional motor cortex [2].
• Monoamine oxidase-B in motor cortex: changes in amyotrophic lateral sclerosis [3].
• In contrast, the anticonvulsant effects on light-induced generalized seizures are more pronounced when GABA is infused into the RMC than when it is infused into the motor cortex [4].
• It is suggested that the stimulus-sensitive myoclonus arose because input into this region from peripheral sensory afferents produced an abnormal discharge which was fed forwards via cortico-cortical connections to the precentral motor cortex, to produce a reflex muscle jerk [5].

Psychiatry related information on Motor Cortex

• Synaptogenesis and Fos expression in the motor cortex of the adult rat after motor skill learning [6].
• In conclusion, these findings from reaction time tasks in patients with primary dystonia provide evidence of abnormal pre-movement motor cortex excitability [7].
• Here, we specifically asked whether in the motor cortex short intracortical inhibition (SICI) and facilitation (ICF) can be elicited at all in sleep using the paired-pulse TMS protocol, and if so, how SICI and ICF vary across sleep stages [8].
• The dopamine modulation of microiontophoretic application of antagonists of glutamate metabotropic synaptic transmission was studied in the sensory motor cortex of awake cats during instrumental conditioned reflex [9].
• Motor activity induced by disinhibition of the primary motor cortex of the rat is blocked by a non-NMDA glutamate receptor antagonist [10].

High impact information on Motor Cortex

• We report a marked decrease of CNTF in the ventral horn of spinal cord in ALS, with no change in cerebral motor cortex [11].
• Thresholds and latencies for motor cortex stimulation to excite thumb flexor muscles and the resulting fast mechanical responses were the same in both ON and OFF conditions, even though the patients were unable to execute fast thumb flexion movements voluntarily when OFF [12].
• Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex injury [13].
• As long as 150 years ago, when Fritz and Hitzig demonstrated the electrical excitability of the motor cortex, scientists and fiction writers were considering the possibility of interfacing a machine with the human brain [14].
• In addition, the injection of muscimol, a GABA agonist, into motor cortex resulted in an increase in the error rate during sequence production, without concomitant effects on nonsequenced motor performance [15].

Chemical compound and disease context of Motor Cortex

• Stimulation of the motor cortex induced: (1). hypotension and a significant decrease in plasma noradrenaline levels, and (2). a significant increase in the number of the double-labelled neurones in the rostral ventrolateral medulla projecting to T2 [16].
• A gamma-aminobutyric acid (GABA) agonist, muscimol (MUS; 1-5 microgram), and an antagonist, bicuculline methiodide (BMI, 1-10 micrograms), were injected at various sites in the precentral motor cortex (MC), at which single-unit activity was related to the manual aspects of the performance of the reaction-time task [17].
• Forty minutes after intraperitoneal injection of ethanol or saline, the rats received a pneumatic piston-induced contusion injury of the left primary motor cortex [18].
• The focal seizures were induced by injecting potassium penicillin G into the face-hand area in the right motor cortex [19].
• Secondarily generalized convulsive status epilepticus was induced by intraperitoneal (i.p.) injection of D,L-homocysteine thiolactone to rats with actively epileptogenic cobalt lesions in motor cortex [20].

Biological context of Motor Cortex

• Plastic changes in the motor cortex contralateral to deafferentation were probed with TMS, measuring motor threshold (MT), motor evoked-potential (MEP) size, and intracortical inhibition (ICI) and facilitation (ICF) to the biceps brachii muscle proximal to the level of deafferentation [21].
• As stimuli were applied in the axilla, over the C7 vertebral level, and over the arm area of the motor cortex, recordings were made of muscle action potentials of forearm flexor muscles [22].
• Contrary to this, chronic intermittent stimulation of the motor cortex down-regulated cocaine-induced gene expression in the striatum, but enhanced striatal gene expression induced by a full D1 receptor agonist (SKF 81297) and did not change the early-gene response elicited by a D2 receptor antagonist (haloperidol) [23].
• We have examined the expression and subcellular distribution of G(1) to S phase cell-cycle regulators in the spinal cord, motor cortex, and sensory cortex from clinically and neuropathologically diagnosed sporadic ALS cases and age-matched controls [24].
• NMDA receptor antagonists impair learning and memory in animal models, presumably by inhibiting long-term potentiation in the motor cortex [25].

Anatomical context of Motor Cortex

• Currents mediated by a glutamate transporter cloned from human motor cortex were measured in Xenopus oocytes [26].
• 2. At PND 8, many of these neurons--in particular, those in lamina Va of the barrel field area--project simultaneously across the corpus callosum and to the ipsilateral motor cortex [27].
• Functional imaging of the brain in primary dystonia has suggested reduced pallidal inhibition of the thalamus with consequent overactivity of medial and prefrontal cortical areas and underactivity of the primary motor cortex during movements [28].
• The contributions of motor cortex, nigrostriatal dopamine and caudate-putamen to skilled forelimb use in the rat [29].
• We used [11C]raclopride and PET to measure changes in extracellular dopamine concentration following rTMS of the motor cortex in six healthy human subjects. rTMS of the left primary motor cortex caused a reduction in [11C]raclopride binding in the left putamen compared with rTMS of the left occipital cortex [30].

Associations of Motor Cortex with chemical compounds

• 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 [31].
• This finding demonstrates a cortico-cortical mechanism subserving the transformation from the geometrical properties of an object to the outputs from motor cortex before grasp that is specific for object-driven movements [32].
• In these studies we sought to extend our understanding of glutamate transporters in ALS by examining the mRNA for each transporter subtype in ALS motor cortex [33].
• We conclude that the changes in intracortical excitability are caused by GABA-controlled interneuronal circuits in the motor cortex while changes in motor threshold are dependent on ion channel conductivity and may reflect membrane excitability [34].
• The effects of repeated cocaine administration were not mimicked by repeated injections of the local anesthetic lidocaine and were not observed in neurons within the motor cortex, indicating that they did not result from local anesthetic actions of cocaine [35].

Gene context of Motor Cortex

• The highest MMP-9 (100-kDa) activities in ALS were found in the motor cortex and thoracic and lumbar cord specimens [36].
• We found a specific reduction of TrkB receptors in transgenic exon-1 and full-length knock-in HD mouse models and also in the motor cortex and caudate nucleus of HD brains [37].
• In 12 brains of individuals without neurological disease glial cells showing moderate immunoreactivity for both GFAP and S-100 protein were uniformly distributed in the primary motor cortex in the upper regions of layer I and layer II [38].
• Thus, the activation of PKA and the ERK1/2 cascade are required for two forms of chemically induced long-lasting increases of synaptic efficacy in slices of rat motor cortex [39].
• BDNF levels were progressively decreased by 1 Hz rTMS in healthy subjects; there was no effect of 1 Hz rTMS on BDNF plasma levels in ALS patients, an effect probably due to the loss of motor cortex pyramidal cells [40].

Analytical, diagnostic and therapeutic context of Motor Cortex

• In this issue of Neuron, Huang et al. show that a version of the classic theta burst stimulation protocol used to induce LTP/LTD in brain slices can be adapted to a transcranial magnetic stimulation (TMS) protocol to rapidly produce long lasting (up to an hour), reversible effects on motor cortex physiology and behavior [41].
• In the motor cortex group, microdialysis revealed no local change in dopamine in any of the animals, despite large local cocaine increase and strong rCBV response, indicating that the central hemodynamic response following acute iv cocaine challenge is not driven directly by local dopamine changes in the motor cortex [42].
• 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 [43].
• We evaluated (3H) beta-Alanine uptake by reactive astrocytes proliferating within scar of epileptogenic foci induced in rat motor cortex by microinjections of 100 mM ferric chloride [44].
• The differential effect of ketamine on responses evoked by magnetic and electric stimulation demonstrates that subanaesthetic doses of ketamine enhance the recruitment of excitatory cortical networks in motor cortex [45].

References