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5 results on '"Swanson, Geoffrey T."'

1. Orai1 channels are essential for amplification of glutamate-evoked Ca2+ signals in dendritic spines to regulate working and associative memory

Author

Maneshi, Mohammad Mehdi, primary, Toth, Anna B., additional, Ishii, Toshiyuki, additional, Hori, Kotaro, additional, Tsujikawa, Shogo, additional, Shum, Andrew K., additional, Shrestha, Nisha, additional, Yamashita, Megumi, additional, Miller, Richard J., additional, Radulovic, Jelena, additional, Swanson, Geoffrey T., additional, and Prakriya, Murali, additional

Published
2021
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2. Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca2+ Signals in Dendritic Spines to Regulate Working and Associative Memory

Author

Maneshi, Mohammad Mehdi, primary, Toth, Anna B., additional, Ishii, Toshiyuki, additional, Hori, Kotaro, additional, Tsujikawa, Shogo, additional, Shum, Andrew K., additional, Shrestha, Nisha, additional, Yamashita, Megumi, additional, Miller, Richard J., additional, Radulovic, Jelena, additional, Swanson, Geoffrey T., additional, and Prakriya, Murali, additional

Published
2020
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4. Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca2+Signals in Dendritic Spines to Regulate Working and Associative Memory

Author

Maneshi, Mohammad Mehdi, Toth, Anna B., Ishii, Toshiyuki, Hori, Kotaro, Tsujikawa, Shogo, Shum, Andrew K., Shrestha, Nisha, Yamashita, Megumi, Miller, Richard J., Radulovic, Jelena, Swanson, Geoffrey T., and Prakriya, Murali

Abstract

Store-operated Orai1 calcium channels function as highly Ca2+-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 Ca2+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 Ca2+signaling, synaptic plasticity, and cognition.

Published
2020
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5. Orai1 Channels Are Essential for Amplification of Glutamate-Evoked Ca 2+ Signals in Dendritic Spines to Regulate Working and Associative Memory.

Author

Maneshi MM, Toth AB, Ishii T, Hori K, Tsujikawa S, Shum AK, Shrestha N, Yamashita M, Miller RJ, Radulovic J, Swanson GT, and Prakriya M

Subjects
Animals, Hippocampus metabolism, Memory, Mice, ORAI1 Protein, Pyramidal Cells metabolism, Signal Transduction, Calcium metabolism, Calcium Signaling, Dendritic Spines metabolism, Glutamic Acid metabolism
Abstract

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., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2020
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