Effect of chemically induced mGluR-dependent long-term depression on dendritic spine volume

Abstract

Based on extracellular field recordings and stimulations at the Schaeffer collateral-CA1 synapse, the synaptic tagging and capture (STC) model has hypothesized that at synapses that express any form of LTP and LTD (long-term potentiation and depression, respectively) are tagged in a protein synthesis-independent manner, the induction of LLTP/ L-LTD leads to protein synthesis, and all tagged synapses can use the resulting plasticity-related products to express L-LTP/L-LTD. Several models have hypothesized that STC works through somatically synthesized plasticity-related protein products available to synapses throughout the neuron, suggesting that, at the single neuronal level, memory engrams are formed at synapses throughout the dendritic arbor. However, the Clustered Plasticity Hypothesis suggests that neurons store long-term memory engrams at synapses that tend to be spatially clustered within dendritic branches, as opposed to dispersed throughout the dendritic arbor. This hypothesis suggests that the dendritic branch, as opposed to the synapse, is the primary unit for long-term memory storage. Evidence for this hypothesis has come from studies of LTP, however, and there is no such data for LTD. This thesis establishes a single-synapse marker for LTD, namely spine length changes, that can be used to study the role of LTD and dendritic branch-specific plasticity.