Neurexin-Neuroligin Transsynaptic Interaction Mediates Learning-Related Synaptic Remodeling and Long-Term Facilitation in Aplysia
Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2011-05, Vol.70 (3), p.468-481 |
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| creator | Choi, Yun-Beom Li, Hsiu-Ling Kassabov, Stefan R. Jin, Iksung Puthanveettil, Sathyanarayanan V. Karl, Kevin A. Lu, Yang Kim, Joung-Hun Bailey, Craig H. Kandel, Eric R. |
| description | Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in
Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
► Neurexin in the presynaptic neuron mediates LTF and presynaptic structural changes ► Neuroligin in the postsynaptic neuron mediates LTF and presynaptic structural changes ► Neurexin and neuroligin are also important for persistence of long-term facilitation ► Neuroligin autism-linked mutant blocks intermediate-term and long-term facilitation |
| doi_str_mv | 10.1016/j.neuron.2011.03.020 |
| format | Article |
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Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
► Neurexin in the presynaptic neuron mediates LTF and presynaptic structural changes ► Neuroligin in the postsynaptic neuron mediates LTF and presynaptic structural changes ► Neurexin and neuroligin are also important for persistence of long-term facilitation ► Neuroligin autism-linked mutant blocks intermediate-term and long-term facilitation</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2011.03.020</identifier><identifier>PMID: 21555073</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Analysis of Variance ; Animals ; Aplysia ; Arginine - genetics ; Autism ; Behavior ; Cell Adhesion Molecules, Neuronal - genetics ; Cell Adhesion Molecules, Neuronal - metabolism ; Cells, Cultured ; Central Nervous System - cytology ; Cloning, Molecular - methods ; Cysteine - genetics ; Excitatory Postsynaptic Potentials - drug effects ; Excitatory Postsynaptic Potentials - physiology ; Gene expression ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Green Fluorescent Proteins - genetics ; Humans ; Long-Term Potentiation - drug effects ; Long-Term Potentiation - physiology ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Microinjections - methods ; Molecular Sequence Data ; Motor Neurons - drug effects ; Motor Neurons - physiology ; Mutation - genetics ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Nervous system ; Neurons ; Oligodeoxyribonucleotides, Antisense - pharmacology ; Protein Binding - physiology ; Proteins ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Sensory Receptor Cells - drug effects ; Sensory Receptor Cells - physiology ; Serotonin - pharmacology ; Studies ; Synapses - metabolism ; Synapses - physiology</subject><ispartof>Neuron (Cambridge, Mass.), 2011-05, Vol.70 (3), p.468-481</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited May 12, 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-eaf478688500454fbe485600feceb0634395880a9966e93ca15a5fe90cc8ef853</citedby><cites>FETCH-LOGICAL-c533t-eaf478688500454fbe485600feceb0634395880a9966e93ca15a5fe90cc8ef853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S089662731100290X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21555073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Choi, Yun-Beom</creatorcontrib><creatorcontrib>Li, Hsiu-Ling</creatorcontrib><creatorcontrib>Kassabov, Stefan R.</creatorcontrib><creatorcontrib>Jin, Iksung</creatorcontrib><creatorcontrib>Puthanveettil, Sathyanarayanan V.</creatorcontrib><creatorcontrib>Karl, Kevin A.</creatorcontrib><creatorcontrib>Lu, Yang</creatorcontrib><creatorcontrib>Kim, Joung-Hun</creatorcontrib><creatorcontrib>Bailey, Craig H.</creatorcontrib><creatorcontrib>Kandel, Eric R.</creatorcontrib><title>Neurexin-Neuroligin Transsynaptic Interaction Mediates Learning-Related Synaptic Remodeling and Long-Term Facilitation in Aplysia</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in
Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
► Neurexin in the presynaptic neuron mediates LTF and presynaptic structural changes ► Neuroligin in the postsynaptic neuron mediates LTF and presynaptic structural changes ► Neurexin and neuroligin are also important for persistence of long-term facilitation ► Neuroligin autism-linked mutant blocks intermediate-term and long-term facilitation</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Aplysia</subject><subject>Arginine - genetics</subject><subject>Autism</subject><subject>Behavior</subject><subject>Cell Adhesion Molecules, Neuronal - genetics</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cells, Cultured</subject><subject>Central Nervous System - cytology</subject><subject>Cloning, Molecular - methods</subject><subject>Cysteine - genetics</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Humans</subject><subject>Long-Term Potentiation - drug effects</subject><subject>Long-Term Potentiation - physiology</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Microinjections - methods</subject><subject>Molecular Sequence Data</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - physiology</subject><subject>Mutation - genetics</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Nervous system</subject><subject>Neurons</subject><subject>Oligodeoxyribonucleotides, Antisense - pharmacology</subject><subject>Protein Binding - physiology</subject><subject>Proteins</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Sensory Receptor Cells - drug effects</subject><subject>Sensory Receptor Cells - physiology</subject><subject>Serotonin - pharmacology</subject><subject>Studies</subject><subject>Synapses - metabolism</subject><subject>Synapses - physiology</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1v1DAQhi0EokvhHyAUiQOnhHH8EfuCVFUUKi0gleVseZ1J5VViL3aC2GP_eb1sy4EDJ1v2M--M5iHkNYWGApXvd03AJcXQtEBpA6yBFp6QFQXd1Zxq_ZSsQGlZy7ZjZ-RFzjsAyoWmz8lZS4UQ0LEVuftaQvC3D_XxEkd_60O1STbkfAh2P3tXXYcZk3Wzj6H6gr23M-ZqjTYFH27rGxzLQ199f8RvcIo9juWvsqGv1rFAG0xTdWWdH_1s_wSVLhf78ZC9fUmeDXbM-OrhPCc_rj5uLj_X62-fri8v1rUTjM012oF3SiolALjgwxa5EhJgQIdbkIwzLZQCq7WUqJmzVFgxoAbnFA5KsHPy7pS7T_Hngnk2k88Ox9EGjEs2qmsp63gnC_n2H3IXlxTKcIZKqYBrJXmh-IlyKeaccDD75CebDoaCORoyO3MyZI6GDDBTDJWyNw_hy3bC_m_Ro5ICfDgBWJbxy2My2XkMrmw-oZtNH_3_O9wDDcildg</recordid><startdate>20110512</startdate><enddate>20110512</enddate><creator>Choi, Yun-Beom</creator><creator>Li, Hsiu-Ling</creator><creator>Kassabov, Stefan R.</creator><creator>Jin, Iksung</creator><creator>Puthanveettil, Sathyanarayanan V.</creator><creator>Karl, Kevin A.</creator><creator>Lu, Yang</creator><creator>Kim, Joung-Hun</creator><creator>Bailey, Craig H.</creator><creator>Kandel, Eric R.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20110512</creationdate><title>Neurexin-Neuroligin Transsynaptic Interaction Mediates Learning-Related Synaptic Remodeling and Long-Term Facilitation in Aplysia</title><author>Choi, Yun-Beom ; Li, Hsiu-Ling ; Kassabov, Stefan R. ; Jin, Iksung ; Puthanveettil, Sathyanarayanan V. ; Karl, Kevin A. ; Lu, Yang ; Kim, Joung-Hun ; Bailey, Craig H. ; Kandel, Eric R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-eaf478688500454fbe485600feceb0634395880a9966e93ca15a5fe90cc8ef853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Aplysia</topic><topic>Arginine - genetics</topic><topic>Autism</topic><topic>Behavior</topic><topic>Cell Adhesion Molecules, Neuronal - genetics</topic><topic>Cell Adhesion Molecules, Neuronal - metabolism</topic><topic>Cells, Cultured</topic><topic>Central Nervous System - cytology</topic><topic>Cloning, Molecular - methods</topic><topic>Cysteine - genetics</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - genetics</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>Humans</topic><topic>Long-Term Potentiation - drug effects</topic><topic>Long-Term Potentiation - physiology</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Microinjections - methods</topic><topic>Molecular Sequence Data</topic><topic>Motor Neurons - drug effects</topic><topic>Motor Neurons - physiology</topic><topic>Mutation - genetics</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Oligodeoxyribonucleotides, Antisense - pharmacology</topic><topic>Protein Binding - physiology</topic><topic>Proteins</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Sensory Receptor Cells - drug effects</topic><topic>Sensory Receptor Cells - physiology</topic><topic>Serotonin - pharmacology</topic><topic>Studies</topic><topic>Synapses - metabolism</topic><topic>Synapses - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Yun-Beom</creatorcontrib><creatorcontrib>Li, Hsiu-Ling</creatorcontrib><creatorcontrib>Kassabov, Stefan R.</creatorcontrib><creatorcontrib>Jin, Iksung</creatorcontrib><creatorcontrib>Puthanveettil, Sathyanarayanan V.</creatorcontrib><creatorcontrib>Karl, Kevin A.</creatorcontrib><creatorcontrib>Lu, Yang</creatorcontrib><creatorcontrib>Kim, Joung-Hun</creatorcontrib><creatorcontrib>Bailey, Craig H.</creatorcontrib><creatorcontrib>Kandel, Eric R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Yun-Beom</au><au>Li, Hsiu-Ling</au><au>Kassabov, Stefan R.</au><au>Jin, Iksung</au><au>Puthanveettil, Sathyanarayanan V.</au><au>Karl, Kevin A.</au><au>Lu, Yang</au><au>Kim, Joung-Hun</au><au>Bailey, Craig H.</au><au>Kandel, Eric R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neurexin-Neuroligin Transsynaptic Interaction Mediates Learning-Related Synaptic Remodeling and Long-Term Facilitation in Aplysia</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2011-05-12</date><risdate>2011</risdate><volume>70</volume><issue>3</issue><spage>468</spage><epage>481</epage><pages>468-481</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in
Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
► Neurexin in the presynaptic neuron mediates LTF and presynaptic structural changes ► Neuroligin in the postsynaptic neuron mediates LTF and presynaptic structural changes ► Neurexin and neuroligin are also important for persistence of long-term facilitation ► Neuroligin autism-linked mutant blocks intermediate-term and long-term facilitation</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21555073</pmid><doi>10.1016/j.neuron.2011.03.020</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis of Variance Animals Aplysia Arginine - genetics Autism Behavior Cell Adhesion Molecules, Neuronal - genetics Cell Adhesion Molecules, Neuronal - metabolism Cells, Cultured Central Nervous System - cytology Cloning, Molecular - methods Cysteine - genetics Excitatory Postsynaptic Potentials - drug effects Excitatory Postsynaptic Potentials - physiology Gene expression Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Green Fluorescent Proteins - genetics Humans Long-Term Potentiation - drug effects Long-Term Potentiation - physiology Membrane Proteins - genetics Membrane Proteins - metabolism Microinjections - methods Molecular Sequence Data Motor Neurons - drug effects Motor Neurons - physiology Mutation - genetics Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Nervous system Neurons Oligodeoxyribonucleotides, Antisense - pharmacology Protein Binding - physiology Proteins Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism Sensory Receptor Cells - drug effects Sensory Receptor Cells - physiology Serotonin - pharmacology Studies Synapses - metabolism Synapses - physiology |
| title | Neurexin-Neuroligin Transsynaptic Interaction Mediates Learning-Related Synaptic Remodeling and Long-Term Facilitation in Aplysia |
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