IN-VITRO EXPOSURE TO ALUMINUM DOES NOT ALTER LONG-TERM POTENTIATION OR GLUTAMATE RELEASE IN RAT HIPPOCAMPAL SLICES

Aluminum has been reported to inhibit long-term potentiation (LTP) fol lowing in vivo administration and decrease glutamate release following in vitro exposure. Because glutamate release is critical for synaptic transmission and the development and maintenance of LTP in the hippoc ampus, we examined the effects of aluminum chloride (AlCl3) on depolar ization-induced glutamate release and LTP in rat hippocampal slices. T he effects of AlCl3 on [C-14]glutamate release were examined by incuba tion of slices in depolarizing (56 mM) K+ buffer solution in the absen ce or presence of 2 mM CaCl2. After 15 min depolarization, AlCl3 (100- 1000 mu M) did not significantly affect Ca2+-dependent [C-14]glutamate release from slices, whereas a known Ca2+ channel blocker (100 mu M C dCl2) decreased Ca2+-dependent [C-14]glutamate release by approximatel y 50%. In contrast to a previous report, acute exposure to AlCl3 was w ithout effect on depolarization-dependent glutamate release. LTP of th e population spike (PS) in CAI of hippocampus was induced by the deliv ery of stimulus trains to the stratum radiatum. LTP of the PS was obse rved in both control slices and slices bathed in solution containing 1 00 mu M AlCl3. Neither the magnitude nor longevity (measured up to 1 h posttrain) of LTP distinguished control from aluminum-exposed slices. The lack of sensitivity in rat to the encephalopathic changes induced by aluminum, or methodological differences in exposure conditions may account for the lack of effect of aluminum on in vitro LTP in rat hip pocampus.