INHIBITION OF RELEASE OF GLUTAMATE FROM ISCHÆMIC BRAIN BY THE κ-AGONIST ENADOLINE (CI-977)

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Abstract
After permanent occlusion of the middle cerebral artery in the rat the onset of “early infarction" of cortical neurones bears a temporal relationship to the increase (up to 5-fold) in the recovery by dialysis of glutamate from the penumbral (“salvageable") cortex. The neuroprotective effect of the Kagonist enadoline (CI-977, 1 mg/kg s.c.) 30 min prior to occlusion (42–45% reduction in cortical damage) was confirmed in this study, but we have now shown that with this treatment the increase in release of glutamate is blocked. The effect of enadoline to inhibit the release of glutamate in the cortex may not be merely a consequence of the increase in the number of viable neurones, secondary to the neuroprotective effect, but may be causal; in the caudate nucleus, where a neuroprotective effect is not obtained, the effect to reduce release of glutamate is observed nevertheless.

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