Ischemic incubation significantly increased
amino acid release from rat striatal slices. Reoxygenation (REO) of the ischemic slices, however, enhanced only
taurine and
citrulline levels in the medium.
Ischemia-induced increases in
glutamate,
taurine and
GABA outputs were accompanied with a similar amount of decline in their tissue levels. Tissue final
aspartic acid level, however, was doubled by
ischemia.
Lactate dehydrogenase (LDH) leakage was not altered by
ischemia, but enhanced during REO. Presence of tetrodotoxine (TTX) during ischemic period caused significant decline in
ischemia-induced
glutamate output, but not altered REO-induced LDH leakage. Although omission of extracellular
calcium ions from the medium during ischemic period protected the slices against REO-induced LDH leakage, this treatment failed to alter
ischemia-induced
glutamate and
GABA outputs. The release of other
amino acids, however, declined 50% in
calcium-free medium. Blockade of the
glutamate uptake transporter by L-trans-PDC, on the other hand, doubled
ischemia induced
glutamate and
aspartic acid outputs. These results indicate that more than one mechanisms probably support the
ischemia-evoked accumulation of
glutamate and other
amino acids in the extracellular space. Although LDH leakage enhanced during REO, processes involved in this increment were found to be dependent on extracellular
calcium ions during
ischemia but not REO period.