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

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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Subcortical circuits mediate communication between primary sensory cortical areas in mice

Nature Communications ◽

10.1038/s41467-021-24200-x ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Michael Lohse ◽

Johannes C. Dahmen ◽

Victoria M. Bajo ◽

Andrew J. King

Keyword(s):

Cortical Neurons ◽

Common Property ◽

Primary Auditory Cortex ◽

Facilitatory Effect ◽

Thalamic Nuclei ◽

Auditory Midbrain ◽

Cortical Areas ◽

Auditory Responses ◽

Evoked Activity

AbstractIntegration of information across the senses is critical for perception and is a common property of neurons in the cerebral cortex, where it is thought to arise primarily from corticocortical connections. Much less is known about the role of subcortical circuits in shaping the multisensory properties of cortical neurons. We show that stimulation of the whiskers causes widespread suppression of sound-evoked activity in mouse primary auditory cortex (A1). This suppression depends on the primary somatosensory cortex (S1), and is implemented through a descending circuit that links S1, via the auditory midbrain, with thalamic neurons that project to A1. Furthermore, a direct pathway from S1 has a facilitatory effect on auditory responses in higher-order thalamic nuclei that project to other brain areas. Crossmodal corticofugal projections to the auditory midbrain and thalamus therefore play a pivotal role in integrating multisensory signals and in enabling communication between different sensory cortical areas.

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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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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 ADENOSINE A2A RECEPTORS IN THE NEUROLEPTIC-INDUCED c-Fos EXPRESSION

Behavioural Pharmacology ◽

10.1097/00008877-199808001-00221 ◽

1998 ◽

Vol 9 (Supplement) ◽

pp. S93

Author(s):

J. Wardasa ◽

A. Pinna ◽

A. Cozzolino ◽

M. Morellib

Keyword(s):

Adenosine A2a Receptors ◽

A2a Receptors ◽

Fos Expression ◽

Adenosine A2a

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Fos expression in the rostral thalamic nuclei and associated cortical regions in response to different spatial memory tests

Neuroscience ◽

10.1016/s0306-4522(00)00288-8 ◽

2000 ◽

Vol 101 (4) ◽

pp. 983-991 ◽

Cited By ~ 82

Author(s):

S.D Vann ◽

M.W Brown ◽

J.P Aggleton

Keyword(s):

Spatial Memory ◽

Thalamic Nuclei ◽

Memory Tests ◽

Fos Expression ◽

Cortical Regions

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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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