2-deoxyglucose-induced long-term potentiation in CA1 is not prevented by intraneuronal chelator

In hippocampal slices, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose is followed by marked and very sustained potentiation of EPSPs (2-DG LTP). To investigate its mechanism, we examined 2-DG's effect in CA1 neurons recorded with sharp 3 M KCI electrodes containing a strong c helator, 50 or 100 mM ethylene glycol-bis(beta-aminoethyl ether)-N, N,N',N' -tetraacetic acid (EGTA). In most cases, field EPSPs were simultaneously re corded and conventional LTP was also elicited in some cells by tetanic stim ulation of stratum radiatum. 2-DG potentiated intracellular EPSP slopes by 48 +/-: 5.1% (SE) in nine cells recorded with plain KCI electrodes and by 5 2 +/- 6.2% in seven cells recorded with EGTA-containing electrodes. In four of the latter cells, tetanic stimulation (twice 100 Hz for 1 s) failed to evoke LTP (2 +/- 1.1%), although field EPSPs were clearly potentiated (by 2 8 +/- 6.9%). Thus unlike tetanic LTP, 2-DG LTP is not readily prevented by postsynaptic intraneuronal injection of EGTA. These findings agree with oth er evidence that the rise in postsynaptic (somatic) [Ca2+](i) caused by 2-D G is not the principal trigger for the subsequent 2-DG LTP and that it may be a purely presynaptic phenomenon.