Abstract

In a series of past experiments where we measured the rate of oxygen disappearance with ischemic onset during seizure induced by penthylentetrazole (PTZ), we noted occasions where during major discharges in the EEG the tissue PO2 was driven to zero and remained there for more than thirty seconds. This was intriguing, and we wondered about those neurons at the locus of PO2 measurement, and how they would respond to the hypoxia together with the metabolic demand of the seizure state. Recently, we have acquired the capability to simultaneously measure PO2 and unit activity from the same PO2 microelectrode, and thus the opportunity was presented to perform experiments to address this question.

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