Abstract
Long-term depression (LTD) in pairs of cultured rodent hippocampal neurons was examined to study the molecular basis of this form of synaptic plasticity. We have previously characterized two components of transmitter release: a synchronous, fast phase that requires synaptotagmin I, and an asynchronous, slow component that persists in the absence of synaptotagmin I. Are these two release components differentially affected by the presynaptic changes of LTD, or is the mechanism of plasticity common to both? We find that LTD is expressed as parallel changes in the fast and slow components of release, and that this form of synaptic plasticity is still seen in the absence of functional synaptotagmin I. Any alterations in the presynaptic release machinery observed during LTD thus involve mechanisms shared by both modes of release.
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