Glutamate-induced delayed neurotoxicity has been proposed to account for the selective
loss of hippocampal pyramidal neurons after an ischemic period. We have studied the …

Excitatory dicarboxylic amino acid neurotransmitters, particularly glutamate, have been
implicated in mediating neuronal cell injury in brain ischemia-anoxia, epilepsy, and stroke …

Microdialysis was used to apply 1 mM N-methyl-D-aspartate (NMDA) for 20 min to the
hippocampus of rabbits, control and pre-treated with GM1 ganglioside (im injections of 30 …

The neurotoxic effects of l-aspartate were evaluated in rat cerebellar granule cell cultures.
Acute (15 min) exposure to l-aspartate produced a time-dependent, delayed degeneration of …

Abstract Immature hippocampal neurons (E-18) were maintained in defined medium for up
to 3 weeks and their susceptibility to N-methyl-d-aspartic acid (NMDA)-induced cell death …

In some animal models of reversible ischemia, there is a therapeutic window during early
recovery when glutamate receptor antagonists can rescue neurons from injury. We have …

Exposure of cultured cerebellar granule cells to glutamate results in a concentration-
dependent (EC50= 22.7+/-0.4 microM) and delayed (24-72 hr) neurotoxicity, which is …

Rat hippocampal pyramidal neurons in culture, exposed 30 min to Mg 2+-free, glycine-
supplemented medium undergo a selective (about 35%) degeneration over the next 24 h …

Monosialoganglioside GM1 prevents excitatory amino acid (EAA)-related neuronal death in
cultured central nervous system (CNS) neurons and reduces the severity of acute brain …

The neurodegenerative action of the excitatory amino acid neurotransmitter (glutamate) and
its exogenous (N-methyl-D-aspartate, kainate) or endogenous (quinolinate) analogues were …