LONG-TERM POTENTIATION IN HIPPOCAMPAL SLICES INDUCED BY TEMPORARY SUPPRESSION OF GLYCOLYSIS

1. Temporary suppression of glycolysis by 2-deoxy-D-glucose (2-DG)-lon g enough to abolish CA1 population spikes (PSs) and reduce field excit atory postsynaptic potentials (EPSPs) by two-thirds-is followed by a s ustained rebound of EPSPs and PSs (both up by 70-150%). 2. Post 2-DG l ong-term potentiation (2-DG-LTP) is prevented by block of N-methyl-D-a spartate (NMDA) receptors (NMDARs). Though ZDG-LTP is normally express ed by other receptors, in presence of picrotoxin 2-DG causes similar L TP of NMDAR-mediated EPSPs. 3. Stimulation at 1 s(-1) fully depotentia tes 2-DG-LTP. 4. Unlike tetanic LTP, 2-DG-LTP is not pathway-specific, is not occluded by a preceding tetanic LTP (or vice Versa) and is ins ensitive to block of NO synthesis. 5. Hypoglycemic states may have lon g-lasting after-effects on cerebral synaptic function.