N-cofilin can compensate for the loss of ADF in excitatory synapses.
Actin plays important roles in a number of synaptic processes, including synaptic vesicle organization and exocytosis, mobility of postsynaptic receptors, and synaptic plasticity. However, little is known about the mechanisms that control actin at synapses. Actin dynamics crucially depend on LIM kin...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3203908?pdf=render |
| _version_ | 1818236038251806720 |
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| author | Andreas Görlich Michael Wolf Anika-Maria Zimmermann Christine B Gurniak Mumna Al Banchaabouchi Marco Sassoè-Pognetto Walter Witke Eckhard Friauf Marco B Rust |
| author_facet | Andreas Görlich Michael Wolf Anika-Maria Zimmermann Christine B Gurniak Mumna Al Banchaabouchi Marco Sassoè-Pognetto Walter Witke Eckhard Friauf Marco B Rust |
| author_sort | Andreas Görlich |
| collection | DOAJ |
| description | Actin plays important roles in a number of synaptic processes, including synaptic vesicle organization and exocytosis, mobility of postsynaptic receptors, and synaptic plasticity. However, little is known about the mechanisms that control actin at synapses. Actin dynamics crucially depend on LIM kinase 1 (LIMK1) that controls the activity of the actin depolymerizing proteins of the ADF/cofilin family. While analyses of mouse mutants revealed the importance of LIMK1 for both pre- and postsynaptic mechanisms, the ADF/cofilin family member n-cofilin appears to be relevant merely for postsynaptic plasticity, and not for presynaptic physiology. By means of immunogold electron microscopy and immunocytochemistry, we here demonstrate the presence of ADF (actin depolymerizing factor), a close homolog of n-cofilin, in excitatory synapses, where it is particularly enriched in presynaptic terminals. Surprisingly, genetic ablation of ADF in mice had no adverse effects on synapse structure or density as assessed by electron microscopy and by the morphological analysis of Golgi-stained hippocampal pyramidal cells. Moreover, a series of electrophysiological recordings in acute hippocampal slices revealed that presynaptic recruitment and exocytosis of synaptic vesicles as well as postsynaptic plasticity were unchanged in ADF mutant mice. The lack of synaptic defects may be explained by the elevated n-cofilin levels observed in synaptic structures of ADF mutants. Indeed, synaptic actin regulation was impaired in compound mutants lacking both ADF and n-cofilin, but not in ADF single mutants. From our results we conclude that n-cofilin can compensate for the loss of ADF in excitatory synapses. Further, our data suggest that ADF and n-cofilin cooperate in controlling synaptic actin content. |
| first_indexed | 2024-12-12T12:03:30Z |
| format | Article |
| id | doaj.art-1ce53aeb0ed04f3c9881bd234b7fe7dc |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-12T12:03:30Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-1ce53aeb0ed04f3c9881bd234b7fe7dc2022-12-22T00:25:03ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-01610e2678910.1371/journal.pone.0026789N-cofilin can compensate for the loss of ADF in excitatory synapses.Andreas GörlichMichael WolfAnika-Maria ZimmermannChristine B GurniakMumna Al BanchaabouchiMarco Sassoè-PognettoWalter WitkeEckhard FriaufMarco B RustActin plays important roles in a number of synaptic processes, including synaptic vesicle organization and exocytosis, mobility of postsynaptic receptors, and synaptic plasticity. However, little is known about the mechanisms that control actin at synapses. Actin dynamics crucially depend on LIM kinase 1 (LIMK1) that controls the activity of the actin depolymerizing proteins of the ADF/cofilin family. While analyses of mouse mutants revealed the importance of LIMK1 for both pre- and postsynaptic mechanisms, the ADF/cofilin family member n-cofilin appears to be relevant merely for postsynaptic plasticity, and not for presynaptic physiology. By means of immunogold electron microscopy and immunocytochemistry, we here demonstrate the presence of ADF (actin depolymerizing factor), a close homolog of n-cofilin, in excitatory synapses, where it is particularly enriched in presynaptic terminals. Surprisingly, genetic ablation of ADF in mice had no adverse effects on synapse structure or density as assessed by electron microscopy and by the morphological analysis of Golgi-stained hippocampal pyramidal cells. Moreover, a series of electrophysiological recordings in acute hippocampal slices revealed that presynaptic recruitment and exocytosis of synaptic vesicles as well as postsynaptic plasticity were unchanged in ADF mutant mice. The lack of synaptic defects may be explained by the elevated n-cofilin levels observed in synaptic structures of ADF mutants. Indeed, synaptic actin regulation was impaired in compound mutants lacking both ADF and n-cofilin, but not in ADF single mutants. From our results we conclude that n-cofilin can compensate for the loss of ADF in excitatory synapses. Further, our data suggest that ADF and n-cofilin cooperate in controlling synaptic actin content.http://europepmc.org/articles/PMC3203908?pdf=render |
| spellingShingle | Andreas Görlich Michael Wolf Anika-Maria Zimmermann Christine B Gurniak Mumna Al Banchaabouchi Marco Sassoè-Pognetto Walter Witke Eckhard Friauf Marco B Rust N-cofilin can compensate for the loss of ADF in excitatory synapses. PLoS ONE |
| title | N-cofilin can compensate for the loss of ADF in excitatory synapses. |
| title_full | N-cofilin can compensate for the loss of ADF in excitatory synapses. |
| title_fullStr | N-cofilin can compensate for the loss of ADF in excitatory synapses. |
| title_full_unstemmed | N-cofilin can compensate for the loss of ADF in excitatory synapses. |
| title_short | N-cofilin can compensate for the loss of ADF in excitatory synapses. |
| title_sort | n cofilin can compensate for the loss of adf in excitatory synapses |
| url | http://europepmc.org/articles/PMC3203908?pdf=render |
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