Localized loss of Ca2+ homeostasis in neuronal dendrites is a downstream consequence of metabolic compromise during extended NMDA exposures
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Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?Interactive HIV-1 Tat and morphine-induced synaptodendritic injury is triggered through focal disruptions in Na⁺ influx, mitochondrial instability, and Ca²⁺ overload.Excessive Na+/H+ exchange in disruption of dendritic Na+ and Ca2+ homeostasis and mitochondrial dysfunction following in vitro ischemiaCytosolic zinc release and clearance in hippocampal neurons exposed to glutamate--the role of pH and sodium.Calcium-dependent mitochondrial function and dysfunction in neurons.Evolution of neuronal and astroglial disruption in the peri-contusional cortex of mice revealed by in vivo two-photon imaging.Intracellular Zn2+ accumulation contributes to synaptic failure, mitochondrial depolarization, and cell death in an acute slice oxygen-glucose deprivation model of ischemia.Intracellular Zn2+ increases contribute to the progression of excitotoxic Ca2+ increases in apical dendrites of CA1 pyramidal neuronsCoupling diverse routes of calcium entry to mitochondrial dysfunction and glutamate excitotoxicityContributions of Ca2+ and Zn2+ to spreading depression-like events and neuronal injury.Differential Vulnerability of CA1 versus CA3 Pyramidal Neurons After Ischemia: Possible Relationship to Sources of Zn2+ Accumulation and Its Entry into and Prolonged Effects on Mitochondria.Zinc: new clues to diverse roles in brain ischemia.Two sides of the same coin: sodium homeostasis and signaling in astrocytes under physiological and pathophysiological conditions.The nuclear calcium signaling target, activating transcription factor 3 (ATF3), protects against dendrotoxicity and facilitates the recovery of synaptic transmission after an excitotoxic insult.Intramitochondrial Zn2+ accumulation via the Ca2+ uniporter contributes to acute ischemic neurodegeneration.Functional NMDA receptors in rat erythrocytes.Sustained NMDA receptor activation by spreading depolarizations can initiate excitotoxic injury in metabolically compromised neurons.Sequential changes in neuronal activity in single neocortical neurons after spreading depression.Best time window for the use of calcium-modulating agents to improve functional recovery in injured peripheral nerves-An experiment in rats.
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P2860
Localized loss of Ca2+ homeostasis in neuronal dendrites is a downstream consequence of metabolic compromise during extended NMDA exposures
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on May 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Localized loss of Ca2+ homeost ...... during extended NMDA exposures
@en
Localized loss of Ca2+ homeost ...... uring extended NMDA exposures.
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type
label
Localized loss of Ca2+ homeost ...... during extended NMDA exposures
@en
Localized loss of Ca2+ homeost ...... uring extended NMDA exposures.
@nl
prefLabel
Localized loss of Ca2+ homeost ...... during extended NMDA exposures
@en
Localized loss of Ca2+ homeost ...... uring extended NMDA exposures.
@nl
P2093
P2860
P1476
Localized loss of Ca2+ homeost ...... during extended NMDA exposures
@en
P2093
C William Shuttleworth
John A Connor
Thomas A Vander Jagt
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P304
P356
10.1523/JNEUROSCI.5069-07.2008
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P577
2008-05-01T00:00:00Z