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Postsynaptic p47phox regulates long-term depression in the hippocampus.


ABSTRACT: It is well documented that reactive oxygen species (ROS) affects neurodegeneration in the brain. Several studies also implicate ROS in the regulation of synapse function and learning and memory processes, although the precise source of ROS generation within these contexts remains to be further explored. Here we show that postsynaptic superoxide generation through PKC?-activated NADPH oxidase 2 (NOX2) is critical for long-term depression (LTD) of synaptic transmission in the CA1-Shaffer collateral synapse of the rat hippocampus. Specifically, PKC?-dependent phosphorylation of p47phox at serine 316, a NOX2 regulatory subunit, is required for LTD but is not necessary for long-term potentiation (LTP). Our data suggest that postsynaptic p47phox phosphorylation at serine 316 is a key upstream determinant for LTD and synapse weakening.

SUBMITTER: Yi JH 

PROVIDER: S-EPMC6110736 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Postsynaptic p47phox regulates long-term depression in the hippocampus.

Yi Jee Hyun JH   Kim Dong Hyun DH   Piers Thomas M TM   Piers Thomas M TM   Kim Seung Chan SC   Whitcomb Daniel J DJ   Regan Philip P   Cho Kwangwook K  

Cell discovery 20180828


It is well documented that reactive oxygen species (ROS) affects neurodegeneration in the brain. Several studies also implicate ROS in the regulation of synapse function and learning and memory processes, although the precise source of ROS generation within these contexts remains to be further explored. Here we show that postsynaptic superoxide generation through PKCζ-activated NADPH oxidase 2 (NOX2) is critical for long-term depression (LTD) of synaptic transmission in the CA1-Shaffer collatera  ...[more]

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