Protein synthesis and energy metabolism in hippocampal slices during extended (24 hours) recovery following different periods of ischemia.
Hippocampal slices were successfully maintained for 24 hours in vitro in a flow-through chamber by using a modified artificial CSF (amino acids included). Measurement of energy metabolism parameters (adenine nucleotides) and the slice response to KCl-induced depolarization (release of GABA and aspartate) indicated that hippocampal slices were metabolically stable for at least 24 hours. The preparation was used to study recovery of protein synthesis after different periods of in vitro ischemia (5, 10, or 15 min). Protein synthesis inhibition was only partly reversed after 15 min of ischemia, but fully reversible after 5- or 10-min ischemia at 24 hours of recovery. Furthermore, the model was used to study a possible role of glutamate in postischemic inhibition of protein synthesis. Glutamate receptor agonists (glutamate or quinolinic acid) or antagonist (kynurenic acid) were applied during ischemia. Neither treatment affected the late (24 hours) outcome of ischemia, arguing against the critical role of glutamate in ischemic cell damage. The present approach allows use of the hippocampal slice preparation in the study of delayed effects of ischemia of different duration.
Djuricic
B
B
Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, Germany.
Berger
R
R
Paschen
W
W
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology; D004734:Energy Metabolism; D018698:Glutamic Acid; D006624:Hippocampus / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000378:metabolism; D051381:Rats; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D009419:Nerve Tissue Proteins; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D000255:Adenosine Triphosphate