Acute ischemic and brain injury is triggered by excitotoxic elevation of intraneuronal Ca2+
followed by reoxygenation-dependent oxidative stress, metabolic failure, and cell death …

Following a hypoxic-ischemic insult, the collapse of ion gradients results in the inappropriate
release of excitatory neurotransmitters. Although excitatory amino acids such as glutamate …

Mitochondria play critical roles in cerebral energy metabolism and in the regulation of
cellular Ca2+ homeostasis. They are also the primary intracellular source of reactive oxygen …

Mitochondrial uptake of calcium in excitotoxicity is associated with subsequent increase in
reactive oxygen species (ROS) generation and delayed cellular calcium deregulation in …

Mitochondrial oxidative stress has been reported as the result of respiratory complex
anomalies, genetic defects, or insufficient oxygen or glucose supply. Although Ca2+ has no …

Excitotoxic mechanisms contribute to the degeneration of hippocampal pyramidal neurons
after recurrent seizures and brain ischemia. However, susceptibility differs, with CA1 …

Calcium is an extraordinarily versatile signaling ion, encoding cellular responses to a wide
variety of external stimuli. In neurons, mitochondria can accumulate enormous amounts of …

It is becoming increasingly clear that mitochondrial Ca2+ uptake from and release into the
cytosol has important consequences for neuronal and glial activity. Ca2+ regulates …

Loss of Ca2+ homeostasis, often in the form of cytoplasmic increases, leads to cell injury.
Depending upon cell type and the intensity of Ca2+ toxicity, the ensuing pathology can be …

Traumatic brain injury (TBI) is associated with primary and secondary injury. A thorough
understanding of secondary injury will help to develop effective treatments and improve …