Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin
Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were prefere...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Chia-Ming Lee [verfasserIn] |
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| Format: |
Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Rechteinformationen: |
Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences |
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| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - Washington, DC : NAS, 1877, 112(2015), 32, Seite E4475-E4484 |
|---|---|
| Übergeordnetes Werk: |
volume:112 ; year:2015 ; number:32 ; pages:E4475-E4484 |
| Links: |
Volltext |
|---|
| DOI / URN: |
10.1073/pnas.1511830112 |
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OLC197028160X |
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| 520 | |a Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. | ||
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| 650 | 4 | |a Brain-Derived Neurotrophic Factor - metabolism | |
| 650 | 4 | |a Calcium - metabolism | |
| 650 | 4 | |a Receptors, Glutamate - metabolism | |
| 650 | 4 | |a Intracellular Space - metabolism | |
| 650 | 4 | |a Synaptotagmins - metabolism | |
| 650 | 4 | |a Green Fluorescent Proteins - metabolism | |
| 650 | 4 | |a Axons - metabolism | |
| 650 | 4 | |a Hippocampus - cytology | |
| 650 | 4 | |a Adaptor Proteins, Vesicular Transport - metabolism | |
| 650 | 4 | |a Nerve Tissue Proteins - metabolism | |
| 650 | 4 | |a Quantum Dots - metabolism | |
| 650 | 4 | |a Brain-derived neurotrophic factor | |
| 650 | 4 | |a Observations | |
| 650 | 4 | |a Endocytosis | |
| 650 | 4 | |a Health aspects | |
| 650 | 4 | |a Neural transmission | |
| 650 | 4 | |a Membranes | |
| 650 | 4 | |a Molecules | |
| 650 | 4 | |a Quantum dots | |
| 650 | 4 | |a Neurons | |
| 650 | 4 | |a complexin | |
| 650 | 4 | |a secretion | |
| 650 | 4 | |a BDNF | |
| 650 | 4 | |a PNAS Plus | |
| 650 | 4 | |a synaptotagmin | |
| 650 | 4 | |a endocytosis | |
| 650 | 4 | |a Biological Sciences | |
| 700 | 0 | |a Yu-Hui Wong |4 oth | |
| 700 | 0 | |a Wenjun Xie |4 oth | |
| 700 | 0 | |a Mu-ming Poo |4 oth | |
| 700 | 0 | |a Bianxiao Cui |4 oth | |
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10.1073/pnas.1511830112 doi PQ20160211 (DE-627)OLC197028160X (DE-599)GBVOLC197028160X (PRQ)g2379-3ef815e12ff1d2d1b980168141c54bbf4b7a5670bd59e4a3a309abc11c18f4090 (KEY)0583363920150000112003204475activitydependentbdnfreleaseviaendocyticpathwaysis DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Chia-Ming Lee verfasserin aut Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Brain-Derived Neurotrophic Factor - metabolism Calcium - metabolism Receptors, Glutamate - metabolism Intracellular Space - metabolism Synaptotagmins - metabolism Green Fluorescent Proteins - metabolism Axons - metabolism Hippocampus - cytology Adaptor Proteins, Vesicular Transport - metabolism Nerve Tissue Proteins - metabolism Quantum Dots - metabolism Brain-derived neurotrophic factor Observations Endocytosis Health aspects Neural transmission Membranes Molecules Quantum dots Neurons complexin secretion BDNF PNAS Plus synaptotagmin endocytosis Biological Sciences Yu-Hui Wong oth Wenjun Xie oth Mu-ming Poo oth Bianxiao Cui oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 32, Seite E4475-E4484 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:32 pages:E4475-E4484 http://dx.doi.org/10.1073/pnas.1511830112 Volltext http://www.pnas.org/content/112/32/E4475.abstract http://www.ncbi.nlm.nih.gov/pubmed/26216953 http://search.proquest.com/docview/1704124106 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4538679&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 32 E4475-E4484 |
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10.1073/pnas.1511830112 doi PQ20160211 (DE-627)OLC197028160X (DE-599)GBVOLC197028160X (PRQ)g2379-3ef815e12ff1d2d1b980168141c54bbf4b7a5670bd59e4a3a309abc11c18f4090 (KEY)0583363920150000112003204475activitydependentbdnfreleaseviaendocyticpathwaysis DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Chia-Ming Lee verfasserin aut Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Brain-Derived Neurotrophic Factor - metabolism Calcium - metabolism Receptors, Glutamate - metabolism Intracellular Space - metabolism Synaptotagmins - metabolism Green Fluorescent Proteins - metabolism Axons - metabolism Hippocampus - cytology Adaptor Proteins, Vesicular Transport - metabolism Nerve Tissue Proteins - metabolism Quantum Dots - metabolism Brain-derived neurotrophic factor Observations Endocytosis Health aspects Neural transmission Membranes Molecules Quantum dots Neurons complexin secretion BDNF PNAS Plus synaptotagmin endocytosis Biological Sciences Yu-Hui Wong oth Wenjun Xie oth Mu-ming Poo oth Bianxiao Cui oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 32, Seite E4475-E4484 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:32 pages:E4475-E4484 http://dx.doi.org/10.1073/pnas.1511830112 Volltext http://www.pnas.org/content/112/32/E4475.abstract http://www.ncbi.nlm.nih.gov/pubmed/26216953 http://search.proquest.com/docview/1704124106 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4538679&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 32 E4475-E4484 |
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10.1073/pnas.1511830112 doi PQ20160211 (DE-627)OLC197028160X (DE-599)GBVOLC197028160X (PRQ)g2379-3ef815e12ff1d2d1b980168141c54bbf4b7a5670bd59e4a3a309abc11c18f4090 (KEY)0583363920150000112003204475activitydependentbdnfreleaseviaendocyticpathwaysis DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Chia-Ming Lee verfasserin aut Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Brain-Derived Neurotrophic Factor - metabolism Calcium - metabolism Receptors, Glutamate - metabolism Intracellular Space - metabolism Synaptotagmins - metabolism Green Fluorescent Proteins - metabolism Axons - metabolism Hippocampus - cytology Adaptor Proteins, Vesicular Transport - metabolism Nerve Tissue Proteins - metabolism Quantum Dots - metabolism Brain-derived neurotrophic factor Observations Endocytosis Health aspects Neural transmission Membranes Molecules Quantum dots Neurons complexin secretion BDNF PNAS Plus synaptotagmin endocytosis Biological Sciences Yu-Hui Wong oth Wenjun Xie oth Mu-ming Poo oth Bianxiao Cui oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 32, Seite E4475-E4484 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:32 pages:E4475-E4484 http://dx.doi.org/10.1073/pnas.1511830112 Volltext http://www.pnas.org/content/112/32/E4475.abstract http://www.ncbi.nlm.nih.gov/pubmed/26216953 http://search.proquest.com/docview/1704124106 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4538679&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 32 E4475-E4484 |
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10.1073/pnas.1511830112 doi PQ20160211 (DE-627)OLC197028160X (DE-599)GBVOLC197028160X (PRQ)g2379-3ef815e12ff1d2d1b980168141c54bbf4b7a5670bd59e4a3a309abc11c18f4090 (KEY)0583363920150000112003204475activitydependentbdnfreleaseviaendocyticpathwaysis DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Chia-Ming Lee verfasserin aut Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Brain-Derived Neurotrophic Factor - metabolism Calcium - metabolism Receptors, Glutamate - metabolism Intracellular Space - metabolism Synaptotagmins - metabolism Green Fluorescent Proteins - metabolism Axons - metabolism Hippocampus - cytology Adaptor Proteins, Vesicular Transport - metabolism Nerve Tissue Proteins - metabolism Quantum Dots - metabolism Brain-derived neurotrophic factor Observations Endocytosis Health aspects Neural transmission Membranes Molecules Quantum dots Neurons complexin secretion BDNF PNAS Plus synaptotagmin endocytosis Biological Sciences Yu-Hui Wong oth Wenjun Xie oth Mu-ming Poo oth Bianxiao Cui oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 32, Seite E4475-E4484 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:32 pages:E4475-E4484 http://dx.doi.org/10.1073/pnas.1511830112 Volltext http://www.pnas.org/content/112/32/E4475.abstract http://www.ncbi.nlm.nih.gov/pubmed/26216953 http://search.proquest.com/docview/1704124106 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4538679&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 32 E4475-E4484 |
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10.1073/pnas.1511830112 doi PQ20160211 (DE-627)OLC197028160X (DE-599)GBVOLC197028160X (PRQ)g2379-3ef815e12ff1d2d1b980168141c54bbf4b7a5670bd59e4a3a309abc11c18f4090 (KEY)0583363920150000112003204475activitydependentbdnfreleaseviaendocyticpathwaysis DE-627 ger DE-627 rakwb eng 500 DNB 570 AVZ LING fid BIODIV fid Chia-Ming Lee verfasserin aut Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. Nutzungsrecht: © COPYRIGHT 2015 National Academy of Sciences Brain-Derived Neurotrophic Factor - metabolism Calcium - metabolism Receptors, Glutamate - metabolism Intracellular Space - metabolism Synaptotagmins - metabolism Green Fluorescent Proteins - metabolism Axons - metabolism Hippocampus - cytology Adaptor Proteins, Vesicular Transport - metabolism Nerve Tissue Proteins - metabolism Quantum Dots - metabolism Brain-derived neurotrophic factor Observations Endocytosis Health aspects Neural transmission Membranes Molecules Quantum dots Neurons complexin secretion BDNF PNAS Plus synaptotagmin endocytosis Biological Sciences Yu-Hui Wong oth Wenjun Xie oth Mu-ming Poo oth Bianxiao Cui oth Enthalten in Proceedings of the National Academy of Sciences of the United States of America Washington, DC : NAS, 1877 112(2015), 32, Seite E4475-E4484 (DE-627)129505269 (DE-600)209104-5 (DE-576)014909189 0027-8424 nnns volume:112 year:2015 number:32 pages:E4475-E4484 http://dx.doi.org/10.1073/pnas.1511830112 Volltext http://www.pnas.org/content/112/32/E4475.abstract http://www.ncbi.nlm.nih.gov/pubmed/26216953 http://search.proquest.com/docview/1704124106 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4538679&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-MAT SSG-OPC-FOR GBV_ILN_40 GBV_ILN_59 AR 112 2015 32 E4475-E4484 |
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Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin |
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Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. |
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Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. |
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Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation. |
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Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. 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