L-type Ca²⁺ channel activation of STIM1-Orai1 signaling remodels the dendritic spine ER to maintain long-term structural plasticity.

ABSTRACT: Learning and memory require coordinated structural and functional plasticity at neuronal glutamatergic synapses located on dendritic spines. Here, we investigated how the endoplasmic reticulum (ER) controls postsynaptic Ca²⁺ signaling and long-term potentiation of dendritic spine size, i.e., sLTP that accompanies functional strengthening of glutamatergic synaptic transmission. In most ER-containing (ER+) spines, high-frequency optical glutamate uncaging (HFGU) induced long-lasting sLTP that was accompanied by a persistent increase in spine ER content downstream of a signaling cascade engaged by N-methyl-D-aspartate receptors (NMDARs), L-type Ca²⁺ channels (LTCCs), and Orai1 channels, the latter being activated by stromal interaction molecule 1 (STIM1) in response to E

SUBMITTER: Dittmer PJ 

PROVIDER: S-EPMC11363309 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature