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Synaptic release of excitatory amino acid neurotransmitter mediates anoxic neuronal death.

Paper summary

Anoxic cultured hippocampal neurons are protected by blocking excitatory amino-acid signaling. Parallel physiological tests support transmitter-mediated depolarization as a causal contributor to neuronal death under oxygen deprivation.

Relevance to the project

A mechanism lead showing that death may depend on interactions as well as resource absence. Future neuron lifecycle models would need to distinguish those causes explicitly.

Biological neuronsBrain energy useSynaptic communication

A specific injury mechanism is not normal developmental turnover.

Source record

Reference ID
pmid-6737044
Archived version
PMC article HTML; manuscript/publication label retained in source
Summary provenance
reference-library/papers/pmid-6737044/metadata.json · summary
Review status
initial orientation summary; not a critical full-paper review
Reading scope
Selected abstract/opening and available closing discussion/conclusion passages in the preserved text extract; broader project notes provide context. No reproduction of experiments, exhaustive methods review, or equation/figure audit.