Katsumori H, Baldwin R A, Wasterlain C G
Epilepsy Research Laboratory, Veterans Affairs Medical Center, Sepulveda, CA, USA.
Brain Res. 1999 Feb 20;819(1-2):160-4. doi: 10.1016/s0006-8993(98)01352-3.
We studied the source of extracellular glutamate released by hippocampal slices obtained from P14 or adult rats, during 50 mM K+ depolarization by using two potent inhibitors of Na+-dependent glutamate transport: l-trans-pyrrolidine-2,4-dicarboxylate (PDC), which is a relatively non-selective inhibitor of various glutamate transporter subtypes and dihydrokainic acid (DHK), a specific inhibitor of the glial transporter, GLT-1. Most depolarization-induced glutamate release was Ca2+-dependent in adults, while in P14 slices most glutamate release was Ca2+-independent. PDC decreased depolarization-induced glutamate release in P14 slices but not in adults. DHK increased glutamate release in adults but not in P14 slices. These data suggest that most depolarization-induced glutamate release in immature hippocampal slices is due to reversal of transport through a PDC-sensitive Na+-dependent glutamate transporter, presumably acting on presynaptic or cytoplasmic neuronal pools, and is not due to exocytosis from vesicular pools.
