In contrast to its known anti-apoptotic activity in sympathetic neurons, immortal neuronal cell lines, and primary cultured immature neurons of the central nervous system (CNS), the role of Bcl-2 in CNS neurons in the adult brain is poorly understood. In the present study, we examined effects of overexpression of Bcl-2 on selective neuronal death of the hippocampal CA1 neurons and the dentate g...

Acidosis is a rapid and inevitable event accompanying cerebral ischemia or trauma. We used hippocampal slice cultures to examine an immediate effect of acidosis, synaptic depression; and a delayed effect, neuronal loss. Exposure to low bicarbonate artificial cerebral spinal fluid (aCSF), pH 6.70 for 30 min at 32 degrees C, acidified intracellular pH from 7.31+/-0.12 to 6.53+/-0.08. Accompanying...

Murine neocortical cell cultures were transiently deprived of both oxygen and glucose, producing widespread neuronal swelling in less than 60 min, followed by neuronal degeneration over the ensuing several hours, despite return to normal medium. Cultured glia (> 95% astrocytes) were irreversibly injured only by oxygen-glucose deprivation exposures exceeding 4-6 hr. Replacing either Na+ or Cl- w...

introduction: dna damage, as an important initiator of neuronal cell death, has been implicated in numerous neurodegenerative conditions. previously we have delineated several pathways that control embryonic cortical neuronal cell death evoked by the dna-damaging agent, camptothecin. the camptothecin, topoisomerase ι inhibitor, has been shown to induce cortical neuronal cell death in a reproduc...

In brain ischemia, gating of postsynaptic glutamate receptors and other membrane channels triggers intracellular Ca2+ overload and cell death. In excitotoxic settings, the initial Ca2+ influx through glutamate receptors is followed by a second uncontrolled Ca2+ increase that leads to neuronal demise. Here we report that the major plasma membrane Ca2+ extruding system, the Na+/Ca2+ exchanger (NC...