Arachidonic acid participates in the anoxia-induced increase in mEPSC frequency in CA1 neurons of the rat hippocampus.

Patch clamp in the whole cell configuration was used to examine the effects of a variety of agents that influence arachidonic acid metabolism on vesicular glutamate release in CA1 neurons of rat hippocampal slices. As previously demonstrated, anoxia induced a significant increase in the frequency of spontaneous glutamate-mediated miniature excitatory postsynaptic currents (mEPSCs) during the first 5 min following anoxia. This increase in frequency was almost completely abolished if slices were preincubated in artificial cerebral spinal fluid (ACSF) containing the phospholipase C/A2 inhibitor, bromophenacyl-bromide (BPB; 20 microM) or the cyclooxygenase inhibitors, indomethacin (20 microM) and piroxicam (10 microM). This observation may be important to our understanding of the neuroprotective action of these agents. These data suggest that arachidonic acid (AA) and its cyclooxygenase products or by-products (oxygen free radicals) contribute to vesicular glutamate release during the early phase of anoxia.