Synaptic plasticity at thalamocortical synapses in developing rat somatosensory cortex: LTP, LTD, and silent synapses

Thalamocortical synaptic transmission in the rat's primary somatosensory (S 1) cortex is modified by sensory experience during a critical period early in life. Despite the importance of such plasticity for the maturation of th alamocortical circuits, the synaptic basis of this plasticity is unknown. H ere, we review evidence suggesting that long-term potentiation and depressi on (LTP and LTD) of thalamocortical synaptic transmission may be involved i n this plasticity. In an in vitro slice preparation, thalamocortical synapt ic responses exhibit N-methyl-D-aspartate (NMDA) receptor-dependent LTP and LTD during a developmental period similar to the critical period in vivo. The inability to induce LTP and LTD after the critical period may result in part from a developmental reduction in the duration of NMDA receptor curre nts. In addition, during the critical period many thalamocortical synapses exhibit NMDA receptor currents but no detectable AMPA receptor currents, an d thus may be functionally silent at resting membrane potentials, LTP conve rts silent synapses to functional ones by causing the rapid appearance of A MPA currents. These observations suggest that thalamocortical synapses may be formed as silent synapses which are subsequently made functional by LTP. LTP and LTD may then regulate the efficacy of these functional synapses an d thereby contribute to experience dependent changes in S1 thalamocortical circuits. (C) 1999 John Wiley & Sons. Inc.