A normobar hypoxia (9% oxygen) of 8 h reduces the neurotoxicity of a s
ubcutaneous injection of 10 mg/kg kainic acid given one week later. Bo
th seizures and degenerative changes, including cell death of hippocam
pal and cortical neurons are markedly decreased by hypoxia. It is also
shown that hypoxia also markedly reduced the extensive depletion of z
inc from messy fiber terminals normally induced by kainic acid. This s
uggests that a protective mechanism induced by hypoxia may affect the
glutamatergic transmission in these synapses and prevent excessive syn
aptic excitation. The possible involvement of adenosine and/or GABA in
this protective mechanism is discussed.