quisqualic acid/necrosis

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The glutamate analogue quisqualic acid is neurotoxic in striatum and hippocampus of immature rat brain.

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To assess the neurotoxic properties of the glutamate agonist quisqualic acid (QA) in immature brain, we injected this compound (100 nmol QA/1 microliter) directly into the striatum of 7-day-old rats. QA produced neuronal necrosis and glial infiltration in 14 pups and reduced the size of the striatum

Both apoptosis and necrosis occur following intrastriatal administration of excitotoxins.

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To learn about the mechanisms of excitotoxic cell death in vivo, three different excitatory amino acid receptor agonists (kainic acid, quinolinic acid or quisqualic acid) were injected in the left striatum of adult rats. Brains were examined at 24 and 48 h after injection. Morphological and

Spinal and supraspinal changes in tumor necrosis factor-alpha expression following excitotoxic spinal cord injury.

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The role of tumor necrosis factor-alpha (TNF-alpha) after spinal cord injury (SCI) is well characterized in the cord, but the impact of this inflammatory process on supraspinal levels is unknown. This study examines TNF-alpha mRNA and protein levels in the brains and spinal cords of mice after SCI.

Effects of interleukin-10 (IL-10) on pain behavior and gene expression following excitotoxic spinal cord injury in the rat.

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Intraspinal injection of quisqualic acid (QUIS) produces excitotoxic injury with pathophysiological characteristics similar to those associated with ischemic and traumatic spinal cord injury (SCI). Responses to QUIS-induced injury include an inflammatory component, as well as the development of

Selective destruction of nitric oxide synthase neurons with quisqualate reduces damage after hypoxia-ischemia in the neonatal rat.

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The vulnerability of the developing CNS to hypoxia-ischemia (H-I) differs from that of the mature brain and is due in part to release of nitric oxide (NO) from parenchymal neurons. If NO is important in the generation of excitotoxic injury after H-I in the developing CNS, then selective destruction

Systemic administration of MK-801 protects against N-methyl-D-aspartate- and quisqualate-mediated neurotoxicity in perinatal rats.

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MK-801, a non-competitive antagonist of N-methyl-D-aspartate-type glutamate receptors, was tested for its ability to antagonize excitotoxic actions of N-methyl-D-aspartate or quisqualic acid injected into the brains of seven-day-old rats. Stereotaxic injection of N-methyl-D-aspartate (25 nmol/0.5

Neonatal excitotoxic brain injury. Physiologic, metabolic, and pathologic findings.

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The mechanism of brain injury caused by excitotoxins has been explored in detail in the adult, but not the developing animal. To better define the cerebral physiologic. metabolic and pathological effects of excitotoxic damage, quisqualic acid (QA), a glutamate analogue, was injected into the

Mechanism based neurotoxicity of mGlu5 positive allosteric modulators--development challenges for a promising novel antipsychotic target.

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Previous work has suggested that activation of mGlu5 receptor augments NMDA receptor function and thereby may constitute a rational approach addressing glutamate hypofunction in schizophrenia and a target for novel antipsychotic drug development. Here, we report the in vitro activity, in vivo

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