Absence of tolerance to the aversive stimulus properties of ethanol following oral ethanol self-administration

Aluminum has been reported to inhibit long-term potentiation (LTP) following 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 hippocampus, we examined the effects of aluminum chloride (AlCl3) on depolarization-induced glutamate release and LTP in rat hippocampal slices. The effects of AlCl3 on [14C]glutamate release were examined by incubation of slices in depolarizing (56 mM)K+ buffer solution in the absence or presence of 2 mM CaCl2. After 15 min depolarization, AlCl3 (100-1000 microM) did not significantly affect Ca(2+)-dependent [14C]glutamate release from slices, whereas a known Ca2+ channel blocker (100 microM CdCl2) decreased Ca(2+)-dependent [14C]glutamate release by approximately 50%. In contrast to a previous report, acute exposure to AlCl3 was without effect on depolarization-dependent glutamate release. LTP of the population spike (PS) in CA1 of hippocampus was induced by the delivery of stimulus trains to the stratum radiatum. LTP of the PS was observed in both control slices and slices bathed in solution containing 100 microM 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 hippocampus.