Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling
NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity. Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes. Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma membrane. In NMD...
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| Veröffentlicht in: | Nature communications 2020-06, Vol.11 (1), p.2979-2979, Article 2979 |
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| description | NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity. Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes. Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma membrane. In NMDAR-LTD, however, they are diverted to late endosomes for degradation. The mechanism for this switch is largely unclear. Additionally, the inducibility of NMDAR-LTD is greatly reduced in adulthood. The underlying mechanism and physiological significance of this phenomenon are elusive. Here, we report that autophagy inhibition is essential for the induction and developmental dampening of NMDAR-LTD. Autophagy is inhibited during NMDAR-LTD to decrease endocytic recycling. Autophagy inhibition is both necessary and sufficient for LTD induction. In adulthood, autophagy is up-regulated to make LTD induction harder, thereby preventing the adverse effect of excessive LTD on memory consolidation. These findings reveal the unrecognized functions of autophagy in synaptic plasticity, endocytic recycling, and memory.
NMDA receptor-dependent long-term depression (NMDAR-LTD) is a form of synaptic plasticity mediated by reduced recycling of AMPA receptors to the plasma membrane. Here the authors show that autophagy is a regulator of this endocytic recycling and autophagy upregulation dampens NMDAR-LTD in adulthood. |
| doi_str_mv | 10.1038/s41467-020-16794-5 |
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NMDA receptor-dependent long-term depression (NMDAR-LTD) is a form of synaptic plasticity mediated by reduced recycling of AMPA receptors to the plasma membrane. Here the authors show that autophagy is a regulator of this endocytic recycling and autophagy upregulation dampens NMDAR-LTD in adulthood.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-020-16794-5</identifier><identifier>PMID: 32532981</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 14/19 ; 631/378/2591 ; 631/80/313/1461 ; 631/80/39/2346 ; 64/60 ; 9/30 ; 9/74 ; Animals ; Autophagy ; Autophagy - genetics ; Autophagy - physiology ; Cells, Cultured ; Endocytosis - physiology ; Endosomes ; Glutamic acid receptors ; Glutamic acid receptors (ionotropic) ; Hippocampus - cytology ; Hippocampus - metabolism ; Hippocampus - physiology ; Humanities and Social Sciences ; Long-term depression ; Long-Term Synaptic Depression - physiology ; Male ; Membranes ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; multidisciplinary ; N-Methyl-D-aspartic acid receptors ; Neuronal Plasticity - physiology ; Neurons - metabolism ; Neurons - physiology ; Phagocytosis ; Plasticity ; Receptors ; Receptors, N-Methyl-D-Aspartate - metabolism ; Science ; Science (multidisciplinary) ; Synapses - physiology ; Synaptic plasticity ; Tissue Culture Techniques ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors</subject><ispartof>Nature communications, 2020-06, Vol.11 (1), p.2979-2979, Article 2979</ispartof><rights>This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020</rights><rights>This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c606t-aa52aac261e60d198d8f513396526ace43652d4edf5f1430690a346d1ff208bf3</citedby><cites>FETCH-LOGICAL-c606t-aa52aac261e60d198d8f513396526ace43652d4edf5f1430690a346d1ff208bf3</cites><orcidid>0000-0001-5609-4040 ; 0000-0003-0384-7306 ; 0000-0002-2978-2531 ; 0000-0003-0048-4554 ; 0000-0003-4774-1167</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293213/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293213/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32532981$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shen, Hongmei</creatorcontrib><creatorcontrib>Zhu, Huiwen</creatorcontrib><creatorcontrib>Panja, Debabrata</creatorcontrib><creatorcontrib>Gu, Qinhua</creatorcontrib><creatorcontrib>Li, Zheng</creatorcontrib><title>Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity. Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes. Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma membrane. In NMDAR-LTD, however, they are diverted to late endosomes for degradation. The mechanism for this switch is largely unclear. Additionally, the inducibility of NMDAR-LTD is greatly reduced in adulthood. The underlying mechanism and physiological significance of this phenomenon are elusive. Here, we report that autophagy inhibition is essential for the induction and developmental dampening of NMDAR-LTD. Autophagy is inhibited during NMDAR-LTD to decrease endocytic recycling. Autophagy inhibition is both necessary and sufficient for LTD induction. In adulthood, autophagy is up-regulated to make LTD induction harder, thereby preventing the adverse effect of excessive LTD on memory consolidation. These findings reveal the unrecognized functions of autophagy in synaptic plasticity, endocytic recycling, and memory.
NMDA receptor-dependent long-term depression (NMDAR-LTD) is a form of synaptic plasticity mediated by reduced recycling of AMPA receptors to the plasma membrane. Here the authors show that autophagy is a regulator of this endocytic recycling and autophagy upregulation dampens NMDAR-LTD in adulthood.</description><subject>13/51</subject><subject>14/19</subject><subject>631/378/2591</subject><subject>631/80/313/1461</subject><subject>631/80/39/2346</subject><subject>64/60</subject><subject>9/30</subject><subject>9/74</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy - genetics</subject><subject>Autophagy - physiology</subject><subject>Cells, Cultured</subject><subject>Endocytosis - physiology</subject><subject>Endosomes</subject><subject>Glutamic acid receptors</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - physiology</subject><subject>Humanities and Social Sciences</subject><subject>Long-term depression</subject><subject>Long-Term Synaptic Depression - physiology</subject><subject>Male</subject><subject>Membranes</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>multidisciplinary</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Neuronal Plasticity - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Hongmei</au><au>Zhu, Huiwen</au><au>Panja, Debabrata</au><au>Gu, Qinhua</au><au>Li, Zheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2020-06-12</date><risdate>2020</risdate><volume>11</volume><issue>1</issue><spage>2979</spage><epage>2979</epage><pages>2979-2979</pages><artnum>2979</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity. Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes. Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma membrane. In NMDAR-LTD, however, they are diverted to late endosomes for degradation. The mechanism for this switch is largely unclear. Additionally, the inducibility of NMDAR-LTD is greatly reduced in adulthood. The underlying mechanism and physiological significance of this phenomenon are elusive. Here, we report that autophagy inhibition is essential for the induction and developmental dampening of NMDAR-LTD. Autophagy is inhibited during NMDAR-LTD to decrease endocytic recycling. Autophagy inhibition is both necessary and sufficient for LTD induction. In adulthood, autophagy is up-regulated to make LTD induction harder, thereby preventing the adverse effect of excessive LTD on memory consolidation. These findings reveal the unrecognized functions of autophagy in synaptic plasticity, endocytic recycling, and memory.
NMDA receptor-dependent long-term depression (NMDAR-LTD) is a form of synaptic plasticity mediated by reduced recycling of AMPA receptors to the plasma membrane. Here the authors show that autophagy is a regulator of this endocytic recycling and autophagy upregulation dampens NMDAR-LTD in adulthood.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32532981</pmid><doi>10.1038/s41467-020-16794-5</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-5609-4040</orcidid><orcidid>https://orcid.org/0000-0003-0384-7306</orcidid><orcidid>https://orcid.org/0000-0002-2978-2531</orcidid><orcidid>https://orcid.org/0000-0003-0048-4554</orcidid><orcidid>https://orcid.org/0000-0003-4774-1167</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 14/19 631/378/2591 631/80/313/1461 631/80/39/2346 64/60 9/30 9/74 Animals Autophagy Autophagy - genetics Autophagy - physiology Cells, Cultured Endocytosis - physiology Endosomes Glutamic acid receptors Glutamic acid receptors (ionotropic) Hippocampus - cytology Hippocampus - metabolism Hippocampus - physiology Humanities and Social Sciences Long-term depression Long-Term Synaptic Depression - physiology Male Membranes Mice, Inbred C57BL Mice, Knockout Mice, Transgenic multidisciplinary N-Methyl-D-aspartic acid receptors Neuronal Plasticity - physiology Neurons - metabolism Neurons - physiology Phagocytosis Plasticity Receptors Receptors, N-Methyl-D-Aspartate - metabolism Science Science (multidisciplinary) Synapses - physiology Synaptic plasticity Tissue Culture Techniques α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors |
| title | Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling |
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