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Selective role of the translin/trax RNase complex in hippocampal synaptic plasticity

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dc.contributor.authorPark, Alan Jung-
dc.contributor.authorShetty, Mahesh Shivarama-
dc.contributor.authorBaraban, Jay M.-
dc.contributor.authorAbel, Ted-
dc.date.accessioned2024-05-20T00:39:40Z-
dc.date.available2024-05-20T00:39:40Z-
dc.date.created2024-05-17-
dc.date.issued2020-11-
dc.identifier.citationMOLECULAR BRAIN, Vol.13 No.1-
dc.identifier.urihttps://hdl.handle.net/10371/203356-
dc.description.abstractActivity-dependent local protein synthesis is critical for synapse-specific, persistent plasticity. Abnormalities in local protein synthesis have been implicated in psychiatric disorders. We have recently identified the translin/trax microRNA-degrading enzyme as a novel mediator of protein synthesis at activated synapses. Additionally, translin knockout (KO) mice, which lack translin/trax, exhibit some of the behavioral abnormalities found in a mouse model of fragile X syndrome (fragile X mental retardation protein-FMRP-KO mice). Therefore, identifying signaling pathways interacting with translin/trax to support persistent synaptic plasticity is a translationally relevant goal. Here, as a first step to achieve this goal, we have assessed the requirement of translin/trax for multiple hippocampal synaptic plasticity paradigms that rely on distinct molecular mechanisms. We found that mice lacking translin/trax exhibited selective impairment in a form of persistent hippocampal plasticity, which requires postsynaptic protein kinase A (PKA) activity. In contrast, enduring forms of plasticity that are dependent on presynaptic PKA were unaffected. Furthermore, these mice did not display exaggerated metabotropic glutamate receptor-mediated long-term synaptic depression (mGluR-LTD), a hallmark of the FMRP KO mice. On the contrary, translin KO mice exhibited deficits in N-methyl-d-aspartate receptor (NMDAR) dependent LTD, a phenotype not observed in the FMRP knockouts. Taken together, these findings demonstrate that translin/trax mediates long-term synaptic plasticity that is dependent on postsynaptic PKA signaling and suggest that translin/trax and FMRP play distinct roles in hippocampal synaptic plasticity.-
dc.language영어-
dc.publisherBMC-
dc.titleSelective role of the translin/trax RNase complex in hippocampal synaptic plasticity-
dc.typeArticle-
dc.identifier.doi10.1186/s13041-020-00691-5-
dc.citation.journaltitleMOLECULAR BRAIN-
dc.identifier.wosid000593935600001-
dc.identifier.scopusid2-s2.0-85095755555-
dc.citation.number1-
dc.citation.volume13-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorPark, Alan Jung-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusLONG-TERM DEPRESSION-
dc.subject.keywordPlusD-ASPARTATE RECEPTOR-
dc.subject.keywordPlusPROTEIN-SYNTHESIS-
dc.subject.keywordPlusTRANSLATIONAL CONTROL-
dc.subject.keywordPlusAKAP150-ANCHORED PKA-
dc.subject.keywordPlusAREA CA1-
dc.subject.keywordPlusPOTENTIATION-
dc.subject.keywordPlusLOCALIZATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordAuthorTranslin-
dc.subject.keywordAuthorTrax-
dc.subject.keywordAuthorLong-term potentiation-
dc.subject.keywordAuthorLong-term depression-
dc.subject.keywordAuthorLocal protein synthesis-
dc.subject.keywordAuthorHippocampal synaptic plasticity-
dc.subject.keywordAuthorFMRP-
dc.subject.keywordAuthorRNA-binding protein-
dc.subject.keywordAuthormicroRNA-
dc.subject.keywordAuthorPKA-
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Research Area Computational decoding, Electrophysiology, Neuroscience

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