Abstract

A comparison has been made of the effects of carbon monoxide (CO) or nitrogen (N 2) exposure on synaptic transmission in the hippocampal slice. CA1 field potentials, evoked by Schaffer collateral stimulation, were unaffected by superfusion of slices with artificial cerebral spinal fluid (ACSF) equilibrated with either 15% CO or 15% N 2 for 120 min. However, superfusion with hypoxic ACSF equilibrated with either 85% CO or 85% N 2 caused a rapid depression of synaptic transmission. Reperfusion with control ACSF following 30 min hypoxia led to recovery of evoked responses and a slight hyperexcitability. In the hippocampal slice, synaptic transmission, as assessed by input/output curves, was not different during or following hypoxia induced by exposure to CO or N 2. In the short term, CO is not toxic.

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