Role of Cerebral Cortex in Voluntary Movements

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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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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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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Role of the basal ganglia and cerebral cortex in tardive dyskinesia: evidence from cerebrovascular accident.

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp.50.3.367 ◽

1987 ◽

Vol 50 (3) ◽

pp. 367-368 ◽

Cited By ~ 1

Author(s):

A S Walters ◽

M Katchen ◽

J Fleishman ◽

S Chokroverty ◽

R Duvoisin

Keyword(s):

Cerebral Cortex ◽

Basal Ganglia ◽

Tardive Dyskinesia ◽

Cerebrovascular Accident

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Role of adenosine in NMDA receptor modulation in the cerebral cortex of an anoxia-tolerant turtle (Chrysemys picta belli).

Journal of Experimental Biology ◽

10.1242/jeb.198.7.1621 ◽

1995 ◽

Vol 198 (7) ◽

pp. 1621-1628 ◽

Cited By ~ 4

Author(s):

L T Buck ◽

P E Bickler

Keyword(s):

Cerebral Cortex ◽

Nmda Receptor ◽

Nmda Receptors ◽

Control Level ◽

Chrysemys Picta ◽

Receptor Modulation ◽

A1 Receptor ◽

Excitatory Neurotransmission ◽

Similar Decrease

Accumulation of the neuromodulator adenosine in the anoxia-tolerant turtle brain may play a key role in a protective decrease in excitatory neurotransmission during anoxia. Since excitatory neurotransmission is mediated largely by Ca2+ entry through N-methyl-D-aspartate (NMDA) receptors, we measured the effect of adenosine on NMDA-mediated Ca2+ transients in normoxic and anoxic turtle cerebrocortical sheets. Intracellular [Ca2+] was measured fluorometrically with the Ca2+-sensitive dye Fura-2. Baseline intracellular [Ca2+] and [ATP] were also measured to assess cortical sheet viability and potential toxic effects of NMDA. Baseline [Ca2+] did not change significantly under any condition, ranging from 109 +/- 22 to 187 +/- 26 nmoll-1. Throughout normoxic and 2h anoxic protocols, and after single and multiple NMDA exposures, [ATP] did not change significantly, ranging from 16.0 +/- 1.9 to 25.3 +/- 4.9 nmol ATP mg-1 protein. Adenosine caused a reduction in the normoxic NMDA-mediated increase in [Ca2+] from a control level of 287 +/- 35 to 103 +/- 22 nmoll-1 (64%). This effect is mediated by the A1 receptor since 8-phenyltheophylline (a specific A1 antagonist) effectively blocked the adenosine effect and N6-cyclopentyladenosine (a specific A1 agonist) elicited a similar decrease in the NMDA-mediated response. Cortical sheets exposed to anoxia alone exhibited a 52% decrease in the NMDA-mediated [Ca2+] rise, from 232 +/- 30 to 111 +/- 9 nmoll-1. The addition of adenosine had no further effect and 8-phenyltheophylline did not antagonize the observed decrease. Therefore, the observed down-regulation of NMDA receptor activity during anoxia must involve additional, as yet unknown, mechanisms.

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