Relationships between glutamate release, blood flow and spreading depression: real-time monitoring using an electroenzymatic dialysis electrode

Spreading depression (SD) in a flow-restricted area of the brain may be pro longed and may become potentially harmful by releasing glutamate. We induce d SD in an oligemia model and examined the subsequent glutamate release. In 18 anesthetized male Fischer rats, a laser Doppler flowmeter, an electroen zymatic electrode for continuous measurement of glutamate, and a calomel el ectrode for measuring DC potential were placed through a cranial window pos itioned 3 mm away from a second window where KCl-soaked cotton was placed t o initiate SD. The left carotid artery or both the common carotid arteries were ligated to suppress reactive hyperemia of SD. SD produced an increase in glutamate from 24.8 +/- 13.8 to 33.5 +/- 25.3 mu M (peak value) (P < 0.0 001). After ligation of both carotid arteries, the duration of SD increased from 1.5 +/- 0.6 min (before ligation) to 6.4 +/- 5.1 min (P < 0.05). Glut amate reached a peak level of 63.9 +/- 72.3 mu M, then quickly returned to the control value. However, there was no positive correlation between the d uration of SD and glutamate concentration. It is concluded that prolonged S D is not accompanied by a progressive increase in glutamate. Therefore, glu tamate release induced by SD may not exert harmful effects on neurons. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.