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Low-Intensity Repetitive Transcranial Magnetic Stimulation Improves Abnormal Visual Cortical Circuit Topography and Upregulates BDNF in Mice

Identifieur interne : 001D01 ( Ncbi/Checkpoint ); précédent : 001D00; suivant : 001D02

Low-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 [France] ; Jennifer Rodger

Source :

The Journal of Neuroscience [ 0270-6474 ] ; 2014.

RBID : PMC:4122806

Descripteurs français

KwdFr :
- ARN messager (métabolisme), Analyse de variance, Animaux, Biophysique, Cartographie cérébrale, Corps géniculés (anatomopathologie), Corps géniculés (malformations), Cortex visuel (malformations), Encéphalopathies (), Encéphalopathies (anatomopathologie), Encéphalopathies (génétique), Facteur neurotrophique dérivé du cerveau (génétique), Facteur neurotrophique dérivé du cerveau (métabolisme), Régulation positive (génétique), Régulation positive (physiologie), Souris, Souris de lignée C57BL, Souris transgéniques, Stimulation magnétique transcrânienne, Voies nerveuses (anatomopathologie), Voies nerveuses (malformations), Éphrine A2 (déficit), Éphrine A2 (génétique), Éphrine A5 (déficit), Éphrine A5 (génétique).
MESH :
- anatomopathologie : Corps géniculés, Encéphalopathies, Voies nerveuses.
- déficit : Éphrine A2, Éphrine A5.
- génétique : Encéphalopathies, Facteur neurotrophique dérivé du cerveau, Régulation positive, Éphrine A2, Éphrine A5.
- malformations : Corps géniculés, Cortex visuel, Voies nerveuses.
- métabolisme : ARN messager, Facteur neurotrophique dérivé du cerveau.
- physiologie : Régulation positive.
- Analyse de variance, Animaux, Biophysique, Cartographie cérébrale, Encéphalopathies, Souris, Souris de lignée C57BL, Souris transgéniques, Stimulation magnétique transcrânienne.

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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4122806

DOI: 10.1523/JNEUROSCI.0723-14.2014
PubMed: 25100609
PubMed Central: 4122806

Affiliations:

Links to Exploration step

PMC:4122806

Le document en format XML

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<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>
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<term>Ephrin-A2 (genetics)</term>
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<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>
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<term>Biophysique</term>
<term>Cartographie cérébrale</term>
<term>Corps géniculés (anatomopathologie)</term>
<term>Corps géniculés (malformations)</term>
<term>Cortex visuel (malformations)</term>
<term>Encéphalopathies ()</term>
<term>Encéphalopathies (anatomopathologie)</term>
<term>Encéphalopathies (génétique)</term>
<term>Facteur neurotrophique dérivé du cerveau (génétique)</term>
<term>Facteur neurotrophique dérivé du cerveau (métabolisme)</term>
<term>Régulation positive (génétique)</term>
<term>Régulation positive (physiologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Stimulation magnétique transcrânienne</term>
<term>Voies nerveuses (anatomopathologie)</term>
<term>Voies nerveuses (malformations)</term>
<term>Éphrine A2 (déficit)</term>
<term>Éphrine A2 (génétique)</term>
<term>Éphrine A5 (déficit)</term>
<term>Éphrine A5 (génétique)</term>
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<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Ephrin-A2</term>
<term>Ephrin-A5</term>
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<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="anatomopathologie" xml:lang="fr"><term>Corps géniculés</term>
<term>Encéphalopathies</term>
<term>Voies nerveuses</term>
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<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Éphrine A2</term>
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<term>Régulation positive</term>
<term>Éphrine A2</term>
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<term>Voies nerveuses</term>
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<term>Neural Pathways</term>
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<term>Cartographie cérébrale</term>
<term>Encéphalopathies</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en"><p>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, <italic>n</italic>
 = 22) and ephrin-A2A5<sup>−/−</sup>
 (<italic>n</italic>
 = 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<sup>−/−</sup>
 mice, indicating geniculocortical map refinement. In the corticotectal efferents, LI-rTMS improved topography of the most abnormal TZs in ephrin-A2A5<sup>−/−</sup>
 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<sup>−/−</sup>
 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.</p>
</div>
</front>
</TEI>
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<tree><noCountry><name sortKey="Harvey, Alan R" sort="Harvey, Alan R" uniqKey="Harvey A" first="Alan R." last="Harvey">Alan R. Harvey</name>
<name sortKey="Makowiecki, Kalina" sort="Makowiecki, Kalina" uniqKey="Makowiecki K" first="Kalina" last="Makowiecki">Kalina Makowiecki</name>
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<country name="France"><region name="Île-de-France"><name sortKey="Sherrard, Rachel M" sort="Sherrard, Rachel M" uniqKey="Sherrard R" first="Rachel M." last="Sherrard">Rachel M. Sherrard</name>
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Serveur d'exploration sur les relations entre la France et l'Australie

Low-Intensity Repetitive Transcranial Magnetic Stimulation Improves Abnormal Visual Cortical Circuit Topography and Upregulates BDNF in Mice

Low-Intensity Repetitive Transcranial Magnetic Stimulation Improves Abnormal Visual Cortical Circuit Topography and Upregulates BDNF in Mice

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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Pour générer des pages wiki

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