REMOVAL OF EXTRACELLULAR CALCIUM AFTER CONDITIONING STIMULATION DISRUPTS LONG-TERM POTENTIATION IN THE CA1 REGION OF RAT HIPPOCAMPAL SLICES

During a conditioning stimulus, the influx of Ca2+ into neurons appear s to be crucial for the induction of long-term potentiation at CA1 hip pocampal synapses. We report here that extracellular Ca2+ is also requ ired for full production of long-term potentiation during a critical p eriod following the conditioning stimulus. In control slices, removal of extracellular Ca2+ (0 mM Ca2+/10 mM Mg2+) for 15 min eliminated syn aptic transmission. Following reintroduction of normal extracellular s olution, synaptic responses recovered fully within 15 min. However, re moval of extracellular Ca2+ 15-30 min after theta burst stimulation si gnificantly decreased the magnitude of long-term potentiation. A time window seems to exist for this effect, since either earlier or later C a2+ removal was less effective. The effect of the 0 mM Ca2+/10 mM Mg2 solution was observed in the absence of afferent stimulation, suggest ing that evoked synaptic activity is not required. Perfusion with an e xtracellular solution containing Cd2+ (40 mu M), a broad spectrum inhi bitor of voltage-dependent Ca2+ channels, or a low concentration (50 m u M) of Ni2+, which preferentially blocks T-type, low-voltage-activate d Ca2+ channels, also caused a significant decrease in potentiation, w hereas an inhibitor of L-type, high voltage-activated Ca2+ channel, ni fedipine (20 mu M), had no effect. These results suggest that the pres ence of extracellular Ca2+ during a specific period after high-frequen cy synaptic activity is necessary for the maintenance of long-term pot entiation, and that voltage-gated Ca2+ channels play a role in the sta bilization of synaptic plasticity. Copyright (C) 1996 IBRO. Published by Elsevier Science Ltd.