Abstract
Synaptic plasticity is assumed as the cellular basis of memory. Long-termplasticity that lasts for days/weeks has not been fully analyzed, mainlybecause of the lack of model system. We found previously that the repeatedinduction of LTP in cultured hippocampal slice caused a long-lastingsynaptic enhancement accompanied by the formation of new synapses, which wasseparate from LTP itself. We found recently that the repeated induction ofLTD by mGluR activation in the same specimen caused a long-lasting decreasein synaptic strength accompanied by the elimination of synapses. Thus wepropose that these repetition-dependent synaptic changes can serve as themodel system for the analysis of long-term plasticity. Here we addfollowing findings that support this proposal. 1) The synapse eliminationis independent of the means of LTD induction, since LTD induced not only byDHPG (dihydroxyphenylglycine, a class I mGluR agonist) but also by a lowdose of NMDA (N-methyl-D-aspartate, an NMDAR agonist) or by DHO(dihydroouabain, a Na/K-ATPase inhibitor) led to the equivalent synapticelimination, when repeated three times (as monitored by electrophysiologicaland morphological indices). 2) The elimination required protein synthesis,since the application of anisomycin (an inhibitor of mRNAs translation toproteins) suppressed the development of synapse elimination. [J Physiol Sci. 2006;56 Suppl:S169]
