Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca2+ Signals in Dendritic Spines to Regulate Working and Associative Memory | Zendy

Mohammad Mehdi Maneshi | Zendy; Anna B. Toth | Zendy; Toshiyuki Ishii | Zendy; Kotaro Hori | Zendy; Shogo Tsujikawa | Zendy; Andrew Shum | Zendy; Nisha Shrestha | Zendy; Megumi Yamashita | Zendy; Richard J. Miller | Zendy; Jelena Raduloviç | Zendy; Geoffrey T. Swanson | Zendy; Murali Prakriya | Zendy

Open Access

Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca2+ Signals in Dendritic Spines to Regulate Working and Associative Memory

Author(s) -

Mohammad Mehdi Maneshi,

Anna B. Toth,

Toshiyuki Ishii,

Kotaro Hori,

Shogo Tsujikawa,

Andrew Shum,

Nisha Shrestha,

Megumi Yamashita,

Richard J. Miller,

Jelena Raduloviç,

Geoffrey T. Swanson,

Murali Prakriya

Publication year - 2020

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2020.108464

Subject(s) - neuroscience , dendritic spine , schaffer collateral , long term potentiation , excitatory postsynaptic potential , synaptic plasticity , glutamate receptor , biology , hippocampal formation , dendritic filopodia , hippocampus , metabotropic glutamate receptor , nmda receptor , receptor , biochemistry , inhibitory postsynaptic potential

SUMMARY Store-operated Orai1 calcium channels function as highly Ca 2+ -selective ion channels and are broadly expressed in many tissues including the central nervous system, but their contributions to cognitive processing are largely unknown. Here, we report that many measures of synaptic, cellular, and behavioral models of learning are markedly attenuated in mice lacking Orai1 in forebrain excitatory neurons. Results with focal glutamate uncaging in hippocampal neurons support an essential role of Orai1 channels in amplifying NMDA-receptor-induced dendritic Ca 2+ transients that drive activity-dependent spine morphogenesis and long-term potentiation at Schaffer collateral-CA1 synapses. Consistent with these signaling roles, mice lacking Orai1 in pyramidal neurons (but not interneurons) exhibit striking deficits in working and associative memory tasks. These findings identify Orai1 channels as essential regulators of dendritic spine Ca 2+ signaling, synaptic plasticity, and cognition.

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