Excessive activation of excitatory amino acid receptors has been implicated in the neuronal
degeneration caused by ischemia, hypoglycemia, and prolonged seizures. We have …

The mechanisms associated with the neurotoxic response caused by kainate(KA) were
examined in cerebellar granule cell cultures. Under the conditions studied, millimolar …

We assessed the effect of a broad spectrum glutamatergic receptor antagonist, kynurenic
acid (500 mg/kg) on ischemia-induced hippocampal glutamate release and neuronal …

The perfusion of slices of rat hippocampus with solutions containing N-methyl-dl-aspartic
acid (NMA), kainic acid, ibotenic acid or quinolinic acid produced a reduction in the size of …

Immunocytochemistry was used to study the distribution of the kainate receptors GluR1,
GluR2/3 and GluR4 and of the N-methyl-d-aspartate (NMDA) receptor NMDAR1 as well as …

The toxic effects of glutamate exposure on neurons were first recognized nearly half a
century ago, when Lucas and Newhouse observed that subcutaneous administration of …

The effects of l-glutamate on the potency of kainate for stimulating guanosine 3', 5'-cyclic
monophosphate (cyclic GMP) accumulation and for killing neurones in incubated slices of …

The neuronal damage induced by systemic administration of kainic acid reproduces the
cellular and regional pattern of damage produced by repeated seizures, The ability of kainic …

Intra‐hippocampal kainate injection induces an epileptiform activity termed status
epilepticus. We examined the emergence of this activity with extracellular and intracellular …

Evidence from animal stroke models suggests that the proximate cause of neuronal
degeneration after ischemia is massive release of glutamate and activation of NMDA …