STIM1 Ca 2+ Sensor Control of L-type Ca 2+ -Channel-Dependent Dendritic Spine Structural Plasticity and Nuclear Signaling

• Published in: Cell reports (Cambridge) Vol. 19; no. 2; pp. 321 - 334
• Main Authors: Dittmer, Philip J., Wild, Angela R., Dell’Acqua, Mark L., Sather, William A.
• Format: Journal Article
• Language: English
• Published: United States 01.04.2017
• Subjects: Animals; Calcium Channels, L-Type - biosynthesis; Calcium Channels, L-Type - genetics; Calcium Signaling - genetics; Dendritic Spines - genetics; Dendritic Spines - metabolism; Endoplasmic Reticulum - genetics; Endoplasmic Reticulum - metabolism; Glutamic Acid - metabolism; Hippocampus - metabolism; Humans; Neurons - metabolism; NFATC Transcription Factors - genetics; NFATC Transcription Factors - metabolism; Primary Cell Culture; Protein Aggregates - genetics; Rats; Receptors, N-Methyl-D-Aspartate - biosynthesis; Receptors, N-Methyl-D-Aspartate - genetics; Stromal Interaction Molecule 1 - biosynthesis; Stromal Interaction Molecule 1 - genetics; structural plasticity; nuclear factor of activated T cells; cytoplasmic Ca(2+); L-type Ca(2+) channel; N-methyl-D-aspartate receptor; dendritic spine; stromal interaction molecule 1; endoplasmic reticulum; glutamate; voltage-gated Ca(2+) channel

Potentiation of synaptic strength relies on postsynaptic Ca signals, modification of dendritic spine structure, and changes in gene expression. One Ca signaling pathway supporting these processes routes through L-type Ca channels (LTCC), whose activity is subject to tuning by multiple mechanisms. He...