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Changes in Extracellular Amino Acids and Spontaneous Neuronal Activity During Ischemia and Extended Reflow in the CA1 of the Rat Hippocampus
Author(s) -
Andiné Peter,
Orwar Owe,
Jacobson Ingemar,
Sandberg Mats,
Hagberg Henrik
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb02119.x
Subject(s) - extracellular , taurine , ischemia , glutamate receptor , hippocampus , amino acid , excitatory postsynaptic potential , chemistry , medicine , anesthesia , endocrinology , pharmacology , biochemistry , inhibitory postsynaptic potential , receptor
This study addresses the possible involvement of an agonist‐induced postischemic hyperactivity in the delayed neuronal death of the CA1 hippocampus in the rat. In two sets of experiments, dialytrodes were implanted into the CA1 either acutely or chronically (24 h of recovery). During 20 min of cerebral ischemia (four‐vessel occlusion model) and 8 h of reflow, we followed extracellular amino acids and multiple‐unit activity. Multiple‐unit activity ceased within 20 sec of ischemia and remained zero during the ischemic insult and for the following 1 h of reflow. During ischemia, extracellular aspartate, glutamate, taurine, and ‐γ‐aminobutyric acid increased in both acute and chronic experiments (seven‐to 26‐fold). Multiple‐unit activity recovered to preischemic levels following 4–6 h of reflow. In the group with dialytrodes implanted acutely, the continuous increase in multiple‐unit activity reached 110% of basal at 8 h of reflow. In the group with dialytrodes implanted chronically, multiple‐unit activity recovered faster and reached 140% of control at 8h, paralleled by an increase in extracellular aspartate (5.5‐fold) and glutamate (twofold). In conclusion, the postischemic increase of excitatory amino acids and the recovery of the neuronal activity may stress the CA1 pyramidal cells, which could be detrimental in combination with, e.g., postsynaptic impairments.