Abstract
Hippocampal synaptic plasticity includes both long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength, and has been implicated in shaping place field representations that form upon initial exposure to a novel environment. However, direct evidence causally linking either LTP or LTD to place fields remains limited. Here, we show that hippocampal LTD regulates the acute formation and maintenance of place fields using electrophysiology and blocking specifically LTD in freely-moving rats. We also show that exploration of a novel environment produces a widespread and pathway specific de novo synaptic depression in the dorsal hippocampus. Furthermore, disruption of this pathway-specific synaptic depression alters both the dynamics of place field formation and the stability of the newly formed place fields, affecting spatial memory in rats. These results suggest that activity-dependent synaptic depression is required for the acquisition and maintenance of novel spatial information.
Highlights
Hippocampal synaptic plasticity includes both long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength, and has been implicated in shaping place field representations that form upon initial exposure to a novel environment
Novelty triggers pathway-specific synaptic depression. Stimulation at both stratum radiatum and stratum oriens evoked canonical post-synaptic field potentials that were maintained for 1-h recording sessions across at least 3 days
Calculating an average proportion of channels above or below 1 standard deviation (SD) on a per animal basis demonstrated that a specific decrease in a subset of radiatum evoked fEPSPs was a consistent feature across animals relative to oriens evoked fEPSPs after exposure to the novel environment (Fig. 1H, I; FEpoch(2,8) = 16.17, p < 0.001, FGroup(1,8) = 5.81, p = 0.04, FEpoch*Group(2,8) = 5.49, p = 0.02 interaction, follow-up pairwise comparisons oriens vs radiatum t0–30(8) = 0.55, p = 0.59, t30–60(8) = 1.89, p = 0.09, t60–90(8) = 2.67, p = 0.02)
Summary
The de novo shift in fEPSP responses observed at radiatum sites was prevented by GluA23Y relative to Scrambled control after novel environment exploration (Fig. 2E, F; ks30–60 = 0.27, p = 0.18, ks60–90 = 0.49, p < 0.001) This distribution change was reflected in the per-animal proportion of channels below 1 SD of baseline (Fig. 2G, H; FEpoch(2,7) = 3.21, p = 0.07, FGroup(1,7) = 8.11, p = 0.02, FEpoch*Group(2,7) = 3.60, p = 0.05; follow-up pairwise comparisons Scrambled vs GluA23Y t0–30(7) = 1.08, p = 0.32, t30–60(7) = 2.41, p = 0.047, t60–90(7) = 2.38, p = 0.049).
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