Cortex commands the performance of skilled movement

Mammalian cerebral cortex is accepted as being critical for voluntary motor control, but what functions depend on cortex is still unclear. Here we used rapid, reversible optogenetic inhibition to test the role of cortex during a head-fixed task in which mice reach, grab, and eat a food pellet. Sudden cortical inhibition blocked initiation or froze execution of this skilled prehension behavior, but left untrained forelimb movements unaffected. Unexpectedly, kinematically normal prehension occurred immediately after cortical inhibition, even during rest periods lacking cue and pellet. This ‘rebound’ prehension was only evoked in trained and food-deprived animals, suggesting that a motivation-gated motor engram sufficient to evoke prehension is activated at inhibition’s end. These results demonstrate the necessity and sufficiency of cortical activity for enacting a learned skill.

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Corticospinal vs Rubrospinal Revisited: An Evolutionary Perspective for Sensorimotor Integration

Frontiers in Neuroscience ◽

10.3389/fnins.2021.686481 ◽

2021 ◽

Vol 15 ◽

Author(s):

Rafael Olivares-Moreno ◽

Paola Rodriguez-Moreno ◽

Veronica Lopez-Virgen ◽

Martín Macías ◽

Moisés Altamira-Camacho ◽

...

Keyword(s):

Spinal Cord ◽

Cerebral Cortex ◽

Sensorimotor Integration ◽

Motor Deficits ◽

Cns Injury ◽

Evolutionary Perspective ◽

Skilled Movement ◽

Spinal Cord Level ◽

Behavioral Evidence

The knowledge about how different subsystems participate and interplay in sensorimotor control is fundamental to understand motor deficits associated with CNS injury and movement recovery. The role of corticospinal (CS) and rubrospinal (RS) projections in motor control has been extensively studied and compared, and it is clear that both systems are important for skilled movement. However, during phylogeny, the emerging cerebral cortex took a higher hierarchical role controlling rubro-cerebellar circuits. Here, we present anatomical, neurophysiological, and behavioral evidence suggesting that both systems modulate complex segmental neuronal networks in a parallel way, which is important for sensorimotor integration at spinal cord level. We also highlight that, although specializations exist, both systems could be complementary and potentially subserve motor recovery associated with CNS damage.

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Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

Scientific Reports ◽

10.1038/s41598-021-91872-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Igor Lavrov ◽

Timur Latypov ◽

Elvira Mukhametova ◽

Brian Lundstrom ◽

Paola Sandroni ◽

...

Keyword(s):

Neuropathic Pain ◽

Cerebral Cortex ◽

Motor Cortex ◽

Initial Assessment ◽

Motor Cortex Stimulation ◽

Chronic Neuropathic Pain ◽

Long Term Effect ◽

Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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The Fourth IOCDC

CNS Spectrums ◽

10.1017/s1092852900024950 ◽

2000 ◽

Vol 5 (S4) ◽

pp. 4-4

Author(s):

Eric Hollander ◽

Joseph Zohar ◽

Donatella Marazziti

Keyword(s):

Obsessive Compulsive Disorder ◽

Brain Stimulation ◽

Current Knowledge ◽

Active Role ◽

Cortical Inhibition ◽

Obsessive Compulsive ◽

Future Directions ◽

Compulsive Disorder ◽

Ablative Surgery

The Fourth International Obsessive Compulsive Disorder Conference (IOCDC) was held February 10–12, 2000, on the beautiful island of St. Thomas. The IOCDC is an annual meeting which brings together the world's leading experts in obsessive-compulsive disorder (OCD) and related disorders in a small workshop setting to present recent research advances, discuss gaps in our current knowledge, and plan or international approaches that address these knowledge gaps. The IOCDC meetings have been held on islands on both sides of the Atlantic—Capri, Guadeloupe, Madeira, and now St. Thomas.The International Organizing Committee consists of Eric Hollander, MD (USA), Joseph Zohar, MD (Israel), and Donatella Marazziti, MD (Italy). The proceedings are generously supported by an unrestricted educational grant from Solvay Pharmaceuticals Inc. and Solvay Pharmaceuticals, and we would like to acknowledge the very important contributions of Chantal Vekens and Mary Blangiardo of Solvay. Also, an mportant part of the success of these meetings stems from the very active role of the chairpersons and cochairpersons of the workshops who lead the discussions, who synthesize the future directions and prepare the manuscripts that result from these discussions that appear in this academic supplement.The meeting led off with a state-of-the-art plenary address by Mark George, MD (USA), describing how new methods of brain stimulation are improving research and therapy in OCD and promise to revolutionize neuropsychiatric research and herapy over the next decade. He describes how transcranial magnetic stimulation (TMS) is used to test the circuits in OCD and test electrophysiologic evaluations of cortical inhibition n OCD. Newer techniques that are less invasive than ablative surgery and appear promising in OCD therapy include vagus nerve stimulation and deep brain stimulation.

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Role of Cerebral Cortex in Voluntary Movements

Physical Therapy ◽

10.1093/ptj/65.5.624 ◽

1985 ◽

Vol 65 (5) ◽

pp. 624-635 ◽

Cited By ~ 28

Author(s):

Paul D. Cheney

Keyword(s):

Cerebral Cortex ◽

Voluntary Movements

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Brain-Specific SNAP-25 Deletion Leads to Elevated Extracellular Glutamate Level and Schizophrenia-Like Behavior in Mice

Neural Plasticity ◽

10.1155/2017/4526417 ◽

2017 ◽

Vol 2017 ◽

pp. 1-11 ◽

Cited By ~ 12

Author(s):

Hua Yang ◽

Mengjie Zhang ◽

Jiahao Shi ◽

Yunhe Zhou ◽

Zhipeng Wan ◽

...

Keyword(s):

Cerebral Cortex ◽

Mouse Model ◽

Glutamate Release ◽

Critical Role ◽

Conditional Knockout ◽

Snare Complex ◽

Extracellular Glutamate ◽

Glutamate Level

Several studies have associated reduced expression of synaptosomal-associated protein of 25 kDa (SNAP-25) with schizophrenia, yet little is known about its role in the illness. In this paper, a forebrain glutamatergic neuron-specific SNAP-25 knockout mouse model was constructed and studied to explore the possible pathogenetic role of SNAP-25 in schizophrenia. We showed that SNAP-25 conditional knockout (cKO) mice exhibited typical schizophrenia-like phenotype. A significantly elevated extracellular glutamate level was detected in the cerebral cortex of the mouse model. Compared with Ctrls, SNAP-25 was dramatically reduced by about 60% both in cytoplasm and in membrane fractions of cerebral cortex of cKOs, while the other two core members of SNARE complex: Syntaxin-1 (increased ~80%) and Vamp2 (increased ~96%) were significantly increased in cell membrane part. Riluzole, a glutamate release inhibitor, significantly attenuated the locomotor hyperactivity deficits in cKO mice. Our findings provide in vivo functional evidence showing a critical role of SNAP-25 dysfunction on synaptic transmission, which contributes to the developmental of schizophrenia. It is suggested that a SNAP-25 cKO mouse, a valuable model for schizophrenia, could address questions regarding presynaptic alterations that contribute to the etiopathophysiology of SZ and help to consummate the pre- and postsynaptic glutamatergic pathogenesis of the illness.

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Role of thalamic nuclei in the modulation of Fos expression within the cerebral cortex during hypertonic saline-induced muscle nociception

Neuroscience ◽

10.1016/j.neuroscience.2015.07.027 ◽

2015 ◽

Vol 304 ◽

pp. 36-46 ◽

Cited By ~ 5

Author(s):

Y. Xiao ◽

J. Lei ◽

G. Ye ◽

H. Xu ◽

H.-J. You

Keyword(s):

Cerebral Cortex ◽

Hypertonic Saline ◽

Thalamic Nuclei ◽

Fos Expression

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P4-164: Neuroprotective role of ATP dependent potassium channel regulators following ischemia-reperfusion in parietal cerebral cortex of rat

Alzheimer s & Dementia ◽

10.1016/j.jalz.2006.05.1903 ◽

2006 ◽

Vol 2 ◽

pp. S564-S564

Author(s):

Mehdi Mehdizadeh ◽

Mansoureh Slimany ◽

Hammid Pasouki ◽

Mohammad Taghi Joghataei

Keyword(s):

Cerebral Cortex ◽

Potassium Channel ◽

Ischemia Reperfusion

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Case Reports: The Influence of Selective Voluntary Motor Control on Gait After Hamstring Lengthening Surgery

Clinical Orthopaedics and Related Research ◽

10.1007/s11999-011-2028-2 ◽

2011 ◽

Vol 470 (5) ◽

pp. 1320-1326 ◽

Cited By ~ 12

Author(s):

Evan J. Goldberg ◽

Eileen G. Fowler ◽

William L. Oppenheim

Keyword(s):

Motor Control ◽

Case Reports ◽

Voluntary Motor

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The role of Ca2+ in the protoveratrine-induced release of γ-aminobutyrate from rat brain slices

Biochemical Journal ◽

10.1042/bj1900333 ◽

1980 ◽

Vol 190 (2) ◽

pp. 333-339 ◽

Cited By ~ 19

Author(s):

M C W Minchin

Keyword(s):

Cerebral Cortex ◽

Rat Brain ◽

Dose Response ◽

Transmitter Release ◽

Response Curve ◽

Brain Slices ◽

Veratrum Alkaloids ◽

Similar Dose ◽

22Na Uptake

1. Protoveratrine A increased the release of gamma-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 microM. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 microM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for gamma-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated gamma-aminobutyrate release also inhibited 22Na+ uptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced gamma-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.

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