Role of intercellular interactions in heterosynaptic long-term depression

Abstract

BIDIRECTIONAL control of synaptic strength is thought to be important for the development of neuronal circuits and information storage. The demonstration of homosynaptic long-term depression¹ greatly enhances the usefulness of the synapse as a mnemonic device, but theoreticians have also seen the need for heterosynaptic decreases in synaptic efficacy, both in neuronal development^2–4 and information storage⁵. Indeed, induction of long-term potentiation in one population of synapses can be associated with a modest depression at neighbouring inactive synapses in the same population of cells^6–10. Here we report that in the CA1 region of the hippocampus this heterosynaptic long-term depression has the property that its sites of induction and expression occur in different populations of cells and thus requires the spread of a signal between neurons. Such a mechanism ensures a widespread distribution of this form of plasticity.