Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain. - Wikidata - wikimedia - TriplyDB

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

http://www.wikidata.org/entity/Q35229769

about

Ionotropic glutamate receptors and voltage-gated Ca²⁺ channels in long-term potentiation of spinal dorsal horn synapses and pain hypersensitivity Cell signaling and mitochondrial dynamics: Implications for neuronal function and neurodegenerative disease Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity Use of Capsaicin to Treat Pain: Mechanistic and Therapeutic Considerations Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts.Carbonic anhydrase-8 regulates inflammatory pain by inhibiting the ITPR1-cytosolic free calcium pathway.Induction of long-term potentiation and long-term depression is cell-type specific in the spinal cord.Ca2+-mediated mitochondrial reactive oxygen species metabolism augments Wnt/β-catenin pathway activation to facilitate cell differentiation.Drp1-mediated mitochondrial abnormalities link to synaptic injury in diabetes model.Mechanisms of G protein-coupled estrogen receptor-mediated spinal nociception.HSV vector-mediated GAD67 suppresses neuropathic pain induced by perineural HIV gp120 in rats through inhibition of ROS and Wnt5a Involvement of reactive oxygen species in cocaine-taking behaviors in rats Sex differences in opioid analgesia and addiction: interactions among opioid receptors and estrogen receptors.Oxidative Stress as a Physiological Pain Response in Full-Term Newborns Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma.Deconstructing the neuropathic pain phenotype to reveal neural mechanisms.Neuronal calcium signaling in chronic pain.Reactive oxygen species affect spinal cell type-specific synaptic plasticity in a model of neuropathic pain.Mitochondrial dynamics in neuronal injury, development and plasticity.MnSOD mediated by HSV vectors in the periaqueductal gray suppresses morphine withdrawal in rats.Pharmacological Modulation of the Mitochondrial Electron Transport Chain in Paclitaxel-Induced Painful Peripheral Neuropathy.Miro1-dependent mitochondrial positioning drives the rescaling of presynaptic Ca2+ signals during homeostatic plasticity.The role of TRPM2 in hydrogen peroxide-induced expression of inflammatory cytokine and chemokine in rat trigeminal ganglia.Reactive oxygen species (ROS) modulate AMPA receptor phosphorylation and cell-surface localization in concert with pain-related behavior.Gene therapy with HSV encoding p55TNFR gene for HIV neuropathic pain: an evidence-based mini-review.Phosphorylated CCAAT/Enhancer Binding Protein β Contributes to Rat HIV-Related Neuropathic Pain: In Vitro and In Vivo Studies.Sciatic nerve ligation causes impairment of mitochondria associated with changes in distribution, respiration, and cardiolipin composition in related spinal cord neurons in rats.

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P2860

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

http://www.wikidata.org/entity/Q35229769

description

2011 nî lūn-bûn

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2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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type

label

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

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JNEUROSCI.3093-11.2011

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Journal of Neuroscience

P1476

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

@en

P2093

Hee Young Kim

http://www.w3.org/2001/XMLSchema#string

Jigong Wang

http://www.w3.org/2001/XMLSchema#string

Jin Mo Chung

http://www.w3.org/2001/XMLSchema#string

Kwan Yeop Lee

http://www.w3.org/2001/XMLSchema#string

Kyungsoon Chung

http://www.w3.org/2001/XMLSchema#string

Lian Cui

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Sang Jeong Kim

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Ying Lu

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P2860

Free radicals in the physiological control of cell function

Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia

Neuronal plasticity: increasing the gain in pain

Calcium, ATP, and ROS: a mitochondrial love-hate triangle

Privileged access to mitochondria of calcium influx through N-methyl-D-aspartate receptors.

Visualization of NMDA receptor-induced mitochondrial calcium accumulation in striatal neurons.

Involvement of reactive oxygen species in long-term potentiation in the spinal cord dorsal horn.

Disturbed Ca2+ signaling and apoptosis of medium spiny neurons in Huntington's disease.

Calcium channel blockers and pain therapy.

Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain.

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10.1523/JNEUROSCI.3093-11.2011

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21900577

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