Fluid-percussion-induced traumatic brain injury model in rats.

Traumatic brain injury (TBI) is a major cause of mortality and morbidity. Various attempts have been made to replicate clinical TBI using animal models. The fluid-percussion model (FP) is one of the oldest and most commonly used models of experimentally induced TBI.

Roscovitine reduces neuronal loss, glial activation, and neurologic deficits after brain trauma.

Traumatic brain injury (TBI) causes both direct and delayed tissue damage. The latter is associated with secondary biochemical changes such as cell cycle activation, which leads to neuronal death, inflammation, and glial scarring. Flavopiridol--a cyclin-dependent kinase (CDK) inhibitor that is neither specific nor selective--is neuroprotective.

Glutamate-mediated excitotoxicity in neonatal hippocampal neurons is mediated by mGluR-induced release of Ca++ from intracellular stores and is prevented by estradiol.

Hypoxic/ischemic (HI) brain injury in newborn full-term and premature infants is a common and pervasive source of life time disabilities in cognitive and locomotor function. In the adult, HI induces glutamate release and excitotoxic cell death dependent on NMDA receptor activation. In animal models of the premature human infant, glutamate is also released following HI, but neurons are largely insensitive to NMDA or AMPA/kainic acid (KA) receptor-mediated damage.

Estradiol modulation of kainic acid-induced calcium elevation in neonatal hippocampal neurons.

The developing hippocampus of both males and females is exposed to high levels of the gonadal steroid estradiol. The impact of this estradiol exposure on developing hippocampal neurons is essentially unknown. In the rat, the newborn hippocampus is relatively insensitive to excitotoxic brain injury, which in adults is associated with the release of amino acids, in particular glutamate, resulting in a significant increase in intracellular calcium and eventual cell death.

Simultaneous glutamate and GABA(A) receptor agonist administration increases calbindin levels and prevents hippocampal damage induced by either agent alone in a model of perinatal brain injury.

Perinatal brain injury is associated with the release of amino acids, principally glutamate and GABA, resulting in massive increases in intracellular calcium and eventual cell death. We have previously demonstrated that independent administration of kainic acid (KA), an AMPA/kainate receptor agonist, or muscimol, a GABA(A) receptor agonist, to newborn rats results in hippocampal damage [Hilton, G.D.

Neuroprotective effects of estradiol in newborn female rat hippocampus.

Perinatal brain injury, consequent to hypoxic/ischemic events, is associated with the release of excess excitatory neurotransmitters, including glutamate. We have previously shown that administration of a glutamate receptor agonist, kainic acid (KA), to postnatal day 0 (PN0) and PN1 rats results in damage selective to the dentate gyrus of females. Pretreatment with the gonadal steroid estradiol prevents KA-induced damage to the female dentate gyrus.