Low-intensity repetitive transcranial magnetic stimulation improves abnormal visual cortical circuit topography and upregulates BDNF in mice.
Identifieur interne : 003567 ( PubMed/Corpus ); précédent : 003566; suivant : 003568Low-intensity repetitive transcranial magnetic stimulation improves abnormal visual cortical circuit topography and upregulates BDNF in mice.
Auteurs : Kalina Makowiecki ; Alan R. Harvey ; Rachel M. Sherrard ; Jennifer RodgerSource :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 1529-2401 ] ; 2014.
English descriptors
- KwdEn :
- Analysis of Variance, Animals, Biophysics, Brain Diseases (genetics), Brain Diseases (pathology), Brain Diseases (therapy), Brain Mapping, Brain-Derived Neurotrophic Factor (genetics), Brain-Derived Neurotrophic Factor (metabolism), Ephrin-A2 (deficiency), Ephrin-A2 (genetics), Ephrin-A5 (deficiency), Ephrin-A5 (genetics), Geniculate Bodies (abnormalities), Geniculate Bodies (pathology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Neural Pathways (abnormalities), Neural Pathways (pathology), RNA, Messenger (metabolism), Transcranial Magnetic Stimulation, Up-Regulation (genetics), Up-Regulation (physiology), Visual Cortex (abnormalities).
- MESH :
- chemical , deficiency : Ephrin-A2, Ephrin-A5.
- chemical , genetics : Brain-Derived Neurotrophic Factor, Ephrin-A2, Ephrin-A5.
- abnormalities : Geniculate Bodies, Neural Pathways, Visual Cortex.
- genetics : Brain Diseases, Up-Regulation.
- chemical , metabolism : Brain-Derived Neurotrophic Factor, RNA, Messenger.
- pathology : Brain Diseases, Geniculate Bodies, Neural Pathways.
- physiology : Up-Regulation.
- therapy : Brain Diseases.
- Analysis of Variance, Animals, Biophysics, Brain Mapping, Mice, Mice, Inbred C57BL, Mice, Transgenic, Transcranial Magnetic Stimulation.
Abstract
Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a treatment for neurological and psychiatric disorders. Although the induced field is focused on a target region during rTMS, adjacent areas also receive stimulation at a lower intensity and the contribution of this perifocal stimulation to network-wide effects is poorly defined. Here, we examined low-intensity rTMS (LI-rTMS)-induced changes on a model neural network using the visual systems of normal (C57Bl/6J wild-type, n = 22) and ephrin-A2A5(-/-) (n = 22) mice, the latter possessing visuotopic anomalies. Mice were treated with LI-rTMS or sham (handling control) daily for 14 d, then fluorojade and fluororuby were injected into visual cortex. The distribution of dorsal LGN (dLGN) neurons and corticotectal terminal zones (TZs) was mapped and disorder defined by comparing their actual location with that predicted by injection sites. In the afferent geniculocortical projection, LI-rTMS decreased the abnormally high dispersion of retrogradely labeled neurons in the dLGN of ephrin-A2A5(-/-) mice, indicating geniculocortical map refinement. In the corticotectal efferents, LI-rTMS improved topography of the most abnormal TZs in ephrin-A2A5(-/-) mice without altering topographically normal TZs. To investigate a possible molecular mechanism for LI-rTMS-induced structural plasticity, we measured brain derived neurotrophic factor (BDNF) in the visual cortex and superior colliculus after single and multiple stimulations. BDNF was upregulated after a single stimulation for all groups, but only sustained in the superior colliculus of ephrin-A2A5(-/-) mice. Our results show that LI-rTMS upregulates BDNF, promoting a plastic environment conducive to beneficial reorganization of abnormal cortical circuits, information that has important implications for clinical rTMS.
DOI: 10.1523/JNEUROSCI.0723-14.2014
PubMed: 25100609
Links to Exploration step
pubmed:25100609Le document en format XML
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Harvey</name><affiliation><nlm:affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, Western Australia 6009, and.</nlm:affiliation></affiliation></author><author><name sortKey="Sherrard, Rachel M" sort="Sherrard, Rachel M" uniqKey="Sherrard R" first="Rachel M" last="Sherrard">Rachel M. Sherrard</name><affiliation><nlm:affiliation>Sorbonne Universités, Pierre and Marie Curie University of Paris 06 and Centre National de la Recherche Scientifique, Institut de Biologie Paris Seine, UMR8256 Biological Adaptation and Ageing, F-75005 Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Rodger, Jennifer" sort="Rodger, Jennifer" uniqKey="Rodger J" first="Jennifer" last="Rodger">Jennifer Rodger</name><affiliation><nlm:affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and jennifer.rodger@uwa.edu.au.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25100609</idno><idno type="pmid">25100609</idno><idno type="doi">10.1523/JNEUROSCI.0723-14.2014</idno><idno type="wicri:Area/PubMed/Corpus">003567</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003567</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Low-intensity repetitive transcranial magnetic stimulation improves abnormal visual cortical circuit topography and upregulates BDNF in mice.</title><author><name sortKey="Makowiecki, Kalina" sort="Makowiecki, Kalina" uniqKey="Makowiecki K" first="Kalina" last="Makowiecki">Kalina Makowiecki</name><affiliation><nlm:affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and.</nlm:affiliation></affiliation></author><author><name sortKey="Harvey, Alan R" sort="Harvey, Alan R" uniqKey="Harvey A" first="Alan R" last="Harvey">Alan R. Harvey</name><affiliation><nlm:affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, Western Australia 6009, and.</nlm:affiliation></affiliation></author><author><name sortKey="Sherrard, Rachel M" sort="Sherrard, Rachel M" uniqKey="Sherrard R" first="Rachel M" last="Sherrard">Rachel M. Sherrard</name><affiliation><nlm:affiliation>Sorbonne Universités, Pierre and Marie Curie University of Paris 06 and Centre National de la Recherche Scientifique, Institut de Biologie Paris Seine, UMR8256 Biological Adaptation and Ageing, F-75005 Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Rodger, Jennifer" sort="Rodger, Jennifer" uniqKey="Rodger J" first="Jennifer" last="Rodger">Jennifer Rodger</name><affiliation><nlm:affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and jennifer.rodger@uwa.edu.au.</nlm:affiliation></affiliation></author></analytic><series><title level="j">The Journal of neuroscience : the official journal of the Society for Neuroscience</title><idno type="eISSN">1529-2401</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Biophysics</term><term>Brain Diseases (genetics)</term><term>Brain Diseases (pathology)</term><term>Brain Diseases (therapy)</term><term>Brain Mapping</term><term>Brain-Derived Neurotrophic Factor (genetics)</term><term>Brain-Derived Neurotrophic Factor (metabolism)</term><term>Ephrin-A2 (deficiency)</term><term>Ephrin-A2 (genetics)</term><term>Ephrin-A5 (deficiency)</term><term>Ephrin-A5 (genetics)</term><term>Geniculate Bodies (abnormalities)</term><term>Geniculate Bodies (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Neural Pathways (abnormalities)</term><term>Neural Pathways (pathology)</term><term>RNA, Messenger (metabolism)</term><term>Transcranial Magnetic Stimulation</term><term>Up-Regulation (genetics)</term><term>Up-Regulation (physiology)</term><term>Visual Cortex (abnormalities)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Ephrin-A2</term><term>Ephrin-A5</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Brain-Derived Neurotrophic Factor</term><term>Ephrin-A2</term><term>Ephrin-A5</term></keywords><keywords scheme="MESH" qualifier="abnormalities" xml:lang="en"><term>Geniculate Bodies</term><term>Neural Pathways</term><term>Visual Cortex</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Brain Diseases</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Brain-Derived Neurotrophic Factor</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Diseases</term><term>Geniculate Bodies</term><term>Neural Pathways</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Brain Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Biophysics</term><term>Brain Mapping</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Transcranial Magnetic Stimulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a treatment for neurological and psychiatric disorders. Although the induced field is focused on a target region during rTMS, adjacent areas also receive stimulation at a lower intensity and the contribution of this perifocal stimulation to network-wide effects is poorly defined. Here, we examined low-intensity rTMS (LI-rTMS)-induced changes on a model neural network using the visual systems of normal (C57Bl/6J wild-type, n = 22) and ephrin-A2A5(-/-) (n = 22) mice, the latter possessing visuotopic anomalies. Mice were treated with LI-rTMS or sham (handling control) daily for 14 d, then fluorojade and fluororuby were injected into visual cortex. The distribution of dorsal LGN (dLGN) neurons and corticotectal terminal zones (TZs) was mapped and disorder defined by comparing their actual location with that predicted by injection sites. In the afferent geniculocortical projection, LI-rTMS decreased the abnormally high dispersion of retrogradely labeled neurons in the dLGN of ephrin-A2A5(-/-) mice, indicating geniculocortical map refinement. In the corticotectal efferents, LI-rTMS improved topography of the most abnormal TZs in ephrin-A2A5(-/-) mice without altering topographically normal TZs. To investigate a possible molecular mechanism for LI-rTMS-induced structural plasticity, we measured brain derived neurotrophic factor (BDNF) in the visual cortex and superior colliculus after single and multiple stimulations. BDNF was upregulated after a single stimulation for all groups, but only sustained in the superior colliculus of ephrin-A2A5(-/-) mice. Our results show that LI-rTMS upregulates BDNF, promoting a plastic environment conducive to beneficial reorganization of abnormal cortical circuits, information that has important implications for clinical rTMS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25100609</PMID><DateCreated><Year>2014</Year><Month>08</Month><Day>07</Day></DateCreated><DateCompleted><Year>2014</Year><Month>10</Month><Day>03</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1529-2401</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>32</Issue><PubDate><Year>2014</Year><Month>Aug</Month><Day>06</Day></PubDate></JournalIssue><Title>The Journal of neuroscience : the official journal of the Society for Neuroscience</Title><ISOAbbreviation>J. Neurosci.</ISOAbbreviation></Journal><ArticleTitle>Low-intensity repetitive transcranial magnetic stimulation improves abnormal visual cortical circuit topography and upregulates BDNF in mice.</ArticleTitle><Pagination><MedlinePgn>10780-92</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1523/JNEUROSCI.0723-14.2014</ELocationID><Abstract><AbstractText>Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a treatment for neurological and psychiatric disorders. Although the induced field is focused on a target region during rTMS, adjacent areas also receive stimulation at a lower intensity and the contribution of this perifocal stimulation to network-wide effects is poorly defined. Here, we examined low-intensity rTMS (LI-rTMS)-induced changes on a model neural network using the visual systems of normal (C57Bl/6J wild-type, n = 22) and ephrin-A2A5(-/-) (n = 22) mice, the latter possessing visuotopic anomalies. Mice were treated with LI-rTMS or sham (handling control) daily for 14 d, then fluorojade and fluororuby were injected into visual cortex. The distribution of dorsal LGN (dLGN) neurons and corticotectal terminal zones (TZs) was mapped and disorder defined by comparing their actual location with that predicted by injection sites. In the afferent geniculocortical projection, LI-rTMS decreased the abnormally high dispersion of retrogradely labeled neurons in the dLGN of ephrin-A2A5(-/-) mice, indicating geniculocortical map refinement. In the corticotectal efferents, LI-rTMS improved topography of the most abnormal TZs in ephrin-A2A5(-/-) mice without altering topographically normal TZs. To investigate a possible molecular mechanism for LI-rTMS-induced structural plasticity, we measured brain derived neurotrophic factor (BDNF) in the visual cortex and superior colliculus after single and multiple stimulations. BDNF was upregulated after a single stimulation for all groups, but only sustained in the superior colliculus of ephrin-A2A5(-/-) mice. Our results show that LI-rTMS upregulates BDNF, promoting a plastic environment conducive to beneficial reorganization of abnormal cortical circuits, information that has important implications for clinical rTMS.</AbstractText><CopyrightInformation>Copyright © 2014 the authors 0270-6474/14/3410780-13$15.00/0.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Makowiecki</LastName><ForeName>Kalina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Harvey</LastName><ForeName>Alan R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, Western Australia 6009, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sherrard</LastName><ForeName>Rachel M</ForeName><Initials>RM</Initials><AffiliationInfo><Affiliation>Sorbonne Universités, Pierre and Marie Curie University of Paris 06 and Centre National de la Recherche Scientifique, Institut de Biologie Paris Seine, UMR8256 Biological Adaptation and Ageing, F-75005 Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rodger</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Experimental and Regenerative Neuroscience, School of Animal Biology, and jennifer.rodger@uwa.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Neurosci</MedlineTA><NlmUniqueID>8102140</NlmUniqueID><ISSNLinking>0270-6474</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019208">Brain-Derived Neurotrophic Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036383">Ephrin-A2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036386">Ephrin-A5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Electroencephalogr Clin Neurophysiol. 1992 Jun;85(3):215-9</RefSource><PMID Version="1">1376680</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Brain Res. 2005 May;163(1):1-12</RefSource><PMID 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