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Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus
NEUROTROPHINS promote neuronal survival and differentiation, but the fact that their expression is modified by neuronal activity, suggests a role in regulating synapse development and plasticity 1–3 . In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its recep...
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Published in: | Nature (London) 1996-06, Vol.381 (6584), p.706-709 |
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creator | Figurov, Alexander Pozzo-Miller, Lucas D. Olafsson, Petur Wang, Ti Lu, Bai |
description | NEUROTROPHINS promote neuronal survival and differentiation, but the fact that their expression is modified by neuronal activity, suggests a role in regulating synapse development and plasticity
1–3
. In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB
4–7
increases in parallel with the ability to undergo long-term potentiation (LTP)
8–10
. Here we report a mechanism by which BDNF modulates hippocampal LTP. Exogenous BDNF promoted the induction of LTP by tetanic stimulation in young (postnatal day 12–13) hippocampal slices, which in the absence of BDNF show only short-term potentiation (STP). This effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation, rather than to a direct modulation of the LTP-triggering mechanism. A TrkB–IgG fusion protein, which scavenges endogenous BDNF
11
, reduced the synaptic responses to tetanus as well as the magnitude of LTP in adult hippocampus. Our results suggest that BDNF may regulate LTP in developing and adult hippocampus by enhancing synaptic responses to tetanic stimulation. |
doi_str_mv | 10.1038/381706a0 |
format | article |
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1–3
. In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB
4–7
increases in parallel with the ability to undergo long-term potentiation (LTP)
8–10
. Here we report a mechanism by which BDNF modulates hippocampal LTP. Exogenous BDNF promoted the induction of LTP by tetanic stimulation in young (postnatal day 12–13) hippocampal slices, which in the absence of BDNF show only short-term potentiation (STP). This effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation, rather than to a direct modulation of the LTP-triggering mechanism. A TrkB–IgG fusion protein, which scavenges endogenous BDNF
11
, reduced the synaptic responses to tetanus as well as the magnitude of LTP in adult hippocampus. Our results suggest that BDNF may regulate LTP in developing and adult hippocampus by enhancing synaptic responses to tetanic stimulation.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/381706a0</identifier><identifier>PMID: 8649517</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Biological and medical sciences ; Brain ; Brain-Derived Neurotrophic Factor ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Evoked Potentials ; Fundamental and applied biological sciences. Psychology ; Hippocampus - physiology ; Humanities and Social Sciences ; Humans ; Immunoglobulin G - immunology ; In Vitro Techniques ; letter ; Long-Term Potentiation - physiology ; Male ; Molecular biology ; multidisciplinary ; Nerve Growth Factors - antagonists & inhibitors ; Nerve Growth Factors - physiology ; Nerve Tissue Proteins - antagonists & inhibitors ; Nerve Tissue Proteins - physiology ; Neurons ; Plasticity ; Rats ; Rats, Sprague-Dawley ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Nerve Growth Factor - physiology ; Recombinant Proteins - pharmacology ; Science ; Science (multidisciplinary) ; Synapses - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Nature (London), 1996-06, Vol.381 (6584), p.706-709</ispartof><rights>Springer Nature Limited 1996</rights><rights>1996 INIST-CNRS</rights><rights>Copyright Macmillan Journals Ltd. Jun 20, 1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-418408eceb33ebf61b60b65cbaf5a13025d2ec3ed3123d5f5eecaca739c019d93</citedby><cites>FETCH-LOGICAL-c497t-418408eceb33ebf61b60b65cbaf5a13025d2ec3ed3123d5f5eecaca739c019d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3105038$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8649517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Figurov, Alexander</creatorcontrib><creatorcontrib>Pozzo-Miller, Lucas D.</creatorcontrib><creatorcontrib>Olafsson, Petur</creatorcontrib><creatorcontrib>Wang, Ti</creatorcontrib><creatorcontrib>Lu, Bai</creatorcontrib><title>Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>NEUROTROPHINS promote neuronal survival and differentiation, but the fact that their expression is modified by neuronal activity, suggests a role in regulating synapse development and plasticity
1–3
. In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB
4–7
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8–10
. Here we report a mechanism by which BDNF modulates hippocampal LTP. Exogenous BDNF promoted the induction of LTP by tetanic stimulation in young (postnatal day 12–13) hippocampal slices, which in the absence of BDNF show only short-term potentiation (STP). This effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation, rather than to a direct modulation of the LTP-triggering mechanism. A TrkB–IgG fusion protein, which scavenges endogenous BDNF
11
, reduced the synaptic responses to tetanus as well as the magnitude of LTP in adult hippocampus. Our results suggest that BDNF may regulate LTP in developing and adult hippocampus by enhancing synaptic responses to tetanic stimulation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain-Derived Neurotrophic Factor</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Evoked Potentials</subject><subject>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Nature (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Figurov, Alexander</au><au>Pozzo-Miller, Lucas D.</au><au>Olafsson, Petur</au><au>Wang, Ti</au><au>Lu, Bai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus</atitle><jtitle>Nature (London)</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>1996-06-20</date><risdate>1996</risdate><volume>381</volume><issue>6584</issue><spage>706</spage><epage>709</epage><pages>706-709</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><coden>NATUAS</coden><abstract>NEUROTROPHINS promote neuronal survival and differentiation, but the fact that their expression is modified by neuronal activity, suggests a role in regulating synapse development and plasticity
1–3
. In developing hippocampus, the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB
4–7
increases in parallel with the ability to undergo long-term potentiation (LTP)
8–10
. Here we report a mechanism by which BDNF modulates hippocampal LTP. Exogenous BDNF promoted the induction of LTP by tetanic stimulation in young (postnatal day 12–13) hippocampal slices, which in the absence of BDNF show only short-term potentiation (STP). This effect was due to an enhanced ability of hippocampal synapses to respond to tetanic stimulation, rather than to a direct modulation of the LTP-triggering mechanism. A TrkB–IgG fusion protein, which scavenges endogenous BDNF
11
, reduced the synaptic responses to tetanus as well as the magnitude of LTP in adult hippocampus. Our results suggest that BDNF may regulate LTP in developing and adult hippocampus by enhancing synaptic responses to tetanic stimulation.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>8649517</pmid><doi>10.1038/381706a0</doi><tpages>4</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Brain Brain-Derived Neurotrophic Factor Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Evoked Potentials Fundamental and applied biological sciences. Psychology Hippocampus - physiology Humanities and Social Sciences Humans Immunoglobulin G - immunology In Vitro Techniques letter Long-Term Potentiation - physiology Male Molecular biology multidisciplinary Nerve Growth Factors - antagonists & inhibitors Nerve Growth Factors - physiology Nerve Tissue Proteins - antagonists & inhibitors Nerve Tissue Proteins - physiology Neurons Plasticity Rats Rats, Sprague-Dawley Receptor, Ciliary Neurotrophic Factor Receptors, Nerve Growth Factor - physiology Recombinant Proteins - pharmacology Science Science (multidisciplinary) Synapses - physiology Vertebrates: nervous system and sense organs |
title | Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus |
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