Abstract
Stromal interaction molecule (STIM) proteins play a crucial role in store-operated calcium entry (SOCE) as endoplasmic reticulum Ca2+ sensors. In neurons, STIM2 was shown to have distinct functions from STIM1. However, its role in brain activity and behavior was not fully elucidated. The present study analyzed behavior in zebrafish (Danio rerio) that lacked stim2a. The mutant animals had no morphological abnormalities and were fertile. RNA-sequencing revealed alterations of the expression of transcription factor genes and several members of the calcium toolkit. Neuronal Ca2+ activity was measured in vivo in neurons that expressed the GCaMP5G sensor. Optic tectum neurons in stim2a−/− fish had more frequent Ca2+ signal oscillations compared with neurons in wildtype (WT) fish. We detected an increase in activity during the visual–motor response test, an increase in thigmotaxis in the open field test, and the disruption of phototaxis in the dark/light preference test in stim2a−/− mutants compared with WT. Both groups of animals reacted to glutamate and pentylenetetrazol with an increase in activity during the visual–motor response test, with no major differences between groups. Altogether, our results suggest that the hyperactive-like phenotype of stim2a−/− mutant zebrafish is caused by the dysregulation of Ca2+ homeostasis and signaling.
Highlights
In any cell, the precise regulation of Ca2+ flow is possible because of the existence of different branches of calcium signaling that allow Ca2+ influx into the cytosol and into Ca2+ depots, including the endoplasmic reticulum (ER), mitochondria, and cytosolic Ca2+-binding proteins
The main proteins that are involved in store-operated calcium entry (SOCE) are stromal interaction molecule (STIM) proteins, Orai and transient receptor potential (TRP) channels
This test focuses on spatial memory function, which depends on neuronal function in the hippocampus, a brain region where STIM2 levels are high
Summary
The precise regulation of Ca2+ flow is possible because of the existence of different branches of calcium signaling that allow Ca2+ influx into the cytosol and into Ca2+ depots, including the endoplasmic reticulum (ER), mitochondria, and cytosolic Ca2+-binding proteins One such pathway is store-operated Ca2+ entry (SOCE), which is responsible for restoring Ca2+ levels in the ER, the largest store of Ca2+ [1]. In Stim2−/− mice that were younger than 8 weeks of age, cognitive deficits were observed in the Morris water maze compared with wildtype (WT) littermates This test focuses on spatial memory function, which depends on neuronal function in the hippocampus, a brain region where STIM2 levels are high. We identified some candidate genes that could be responsible for such changes
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