Abstract
In hippocampal pyramidal cells, a small subset of dendritic spines contain endoplasmic reticulum (ER). In large spines, ER frequently forms a spine apparatus, while smaller spines contain just a single tubule of smooth ER. Here we show that the ER visits dendritic spines in a non-random manner, targeting spines during periods of high synaptic activity. When we blocked ER motility using a dominant negative approach against myosin V, spine synapses became stronger compared to controls. We were not able to further potentiate these maxed-out synapses, but long-term depression (LTD) was readily induced by low-frequency stimulation. We conclude that the brief ER visits to active spines have the important function of preventing runaway potentiation of individual spine synapses, keeping most of them at an intermediate strength level from which both long-term potentiation (LTP) and LTD are possible.
Highlights
IntroductionA small subset of dendritic spines contain endoplasmic reticulum (ER)
In hippocampal pyramidal cells, a small subset of dendritic spines contain endoplasmic reticulum (ER)
We assessed the presence of ER in dendritic spines of CA1 pyramidal cells expressing the red fluorescent protein tdimer[2] in the cytoplasm and EGFP in the ER (Fig. 1a)
Summary
A small subset of dendritic spines contain endoplasmic reticulum (ER). We conclude that the brief ER visits to active spines have the important function of preventing runaway potentiation of individual spine synapses, keeping most of them at an intermediate strength level from which both long-term potentiation (LTP) and LTD are possible. Spines containing ER express different forms of synaptic depression compared to ER-lacking spines on the same dendrite[10]. ER forms a specialized organelle, the spine apparatus[7,9], which is readily identified by the presence of synaptopodin. The frequency of spine entry events increased when synapses were active and ER motility was blocked by a MyoVa-based dominant-negative construct. Blocking ER motility in individual neurons led to strengthening of synapses and prevented further potentiation by a long-term potentiation (LTP) protocol. Transient ER visits appear to limit runaway potentiation of these synapses
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