B. Djuricic et al., PROTEIN-SYNTHESIS AND ENERGY-METABOLISM IN HIPPOCAMPAL SLICES DURING EXTENDED (24 HOURS) RECOVERY FOLLOWING DIFFERENT PERIODS OF ISCHEMIA, Metabolic brain disease, 9(4), 1994, pp. 377-389
Hippocampal slices were successfully maintained for 24 hours in vitro
in a flow-through chamber by using a modified artificial CSF (amino ac
ids included). Measurement of energy metabolism parameters (adenine nu
cleotides) and the slice response to KCl-induced depolarization (relea
se of GABA and aspartate) indicated that hippocampal slices were metab
olically stable for at least 24 hours. The preparation was used to stu
dy recovery of protein synthesis after different periods of in vitro i
schemia (5, 10, or 15 min). Protein synthesis inhibition was only part
ly reversed after 15 min of ischemia, but fully reversible after 5- or
10-min ischemia at 24 hours of recovery. Furthermore, the model was u
sed to study a possible role of glutamate in postischemic inhibition o
f protein synthesis. Glutamate receptor agonists (glutamate or quinoli
nic acid) or antagonist (kynurenic acid) were applied during ischemia.
Neither treatment affected the late (24 hours) outcome of ischemia, a
rguing 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.