Glutamate-mediated excitotoxicity in schizophrenia: A review

Cholesterol loss during glutamate-mediated excitotoxicity.

The deregulation of brain cholesterol metabolism is typical in acute neuronal injury (such as stroke, brain trauma and epileptic seizures) and chronic neurodegenerative diseases (Alzheimer's disease). Since both conditions are characterized by excessive stimulation of glutamate receptors, we have here investigated to which extent excitatory neurotransmission plays a role in brain cholesterol ho...

Glutamate excitotoxicity in the cerebellum mediated by IL-1β.

Na-K-Cl cotransporter contributes to glutamate-mediated excitotoxicity.

We hypothesized that cation-dependent Cl- transport protein Na-K-Cl cotransporter isoform 1 (NKCC1) plays a role in the disruption of ion homeostasis in cerebral ischemia. In the current study, a role for NKCC1 in neuronal death was elucidated in neurotoxicity induced by glutamate and oxygen and glucose deprivation (OGD). Incubation of cortical neurons cultured for 14-15 d in vitro (DIV) with 1...

Pictorial review of glutamate excitotoxicity: fundamental concepts for neuroimaging.

Neuroradiologists may encounter, on a daily basis, a challenging diversity of neurologic disorders, including stroke, trauma, epilepsy, and even neurodegenerative conditions, such as Huntington disease, AIDS dementia complex, and amyotrophic lateral sclerosis (1), but this spectrum of disease is not usually thought of as sharing the same mechanism of neuronal injury and death. These and a growi...

Glutamate excitotoxicity in transient global cerebral ischemia.

The glutamate excitotoxicity hypothesis of ischemic cell damage holds that cell damage caused by transient cerebral ischemia is triggered by glutamate, released during ischemia from the intracellular compartment into the synaptic cleft: high extracellular glutamate levels activate ionotropic glutamate receptors, thus inducing an overflow of calcium ions into the neurones and a calcium-induced a...