In this study Mongolian gerbils were submitted to a normothermic bilateral carotid
ligation lasting 5 min. A noncompetitive antagonist of
NMDA receptors,
MK-801, 0.8 mg/kg, was injected i.p. 30 min before
ischemia, or the
ganglioside GM1, 30 mg/kg, was given i.p. for 3 days, twice a day. The morphology of the hippocampal CA1 neurones and the brain content of
cyclooxygenase metabolites of
arachidonic acid:
prostaglandin 6-keto
PGF1 alpha and
thromboxane Tx B2 were studied. Untreated
ischemia induced the accumulation in brain of the 6-keto
PGF1 alpha and Tx B2 immunoreactive materials, and resulted in a lesion of 70% of CA1 neurones. In the MK-801- and GM1-pretreated groups the postischemic levels of Tx B2 were significantly decreased. However
MK-801 and GM1 did not prevent damage to the CA1 neurones in gerbils normothermic after
ischemia, whereas a partial neuroprotection was observed in hypothermic,
MK-801 treated gerbils. The results of this study indicate that
NMDA receptors may participate in the mechanism of postischemic release of
eicosanoids in brain. They also confirm a potential modulatory role of
gangliosides. These results are discussed in terms of the involvement of
cyclooxygenase metabolites of
arachidonic acid in the mechanism of a selective delayed neuronal damage to the hippocampus CA1 after
ischemia.