Ischemic neuronal injury in the rat hippocampus following transient forebrain ischemia: evaluation using in vivo microdialysis.

Neuronal vulnerability to ischemia in the rat hippocampus was investigated by the measurement of high potassium evoked overflow of neurotransmitters using in vivo microdialysis. Changes in the extracellular level of amino acids caused by high potassium (100 mM) stimulation were measured on the 5th day after 20 min of forebrain ischemia, and the ratio of stimulated to basal levels or the peak concentration following the stimulation were correlated to neuronal activities. The responses to high potassium stimulation of glutamate and aspartate were reduced to 35-40% of the control values on the 5th day after 20 min ischemia, whereas the responses of gamma-aminobutyric acid (GABA) and taurine were not reduced on the 5th day after the ischemia. These results suggest that excitatory amino acid neurons (glutamatergic and aspartatergic) are more vulnerable than inhibitory amino acid neurons (GABAergic and taurinergic) in the hippocampus. Histologically, hippocampal CA1 pyramidal cells, which are believed to be glutamatergic or aspartatergic, demonstrated a marked neuronal necrosis on the 5th days after 20 min ischemia. Biochemical features revealed by high potassium stimulation may be an expression of 'delayed neuronal death' in the hippocampal CA1 area.