Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons
- Autores
- Heidenreich, Matthias; Tzingounis, Anastassios V.; Kharkovets, Tatjana; Spitzmaul, Guillermo Federico; Nicoll, Roger A.; Jentsch, Thomas J.
- Año de publicación
- 2009
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which contribute to the medium afterhyperpolarization current (ImAHP) and slow afterhyperpolarization current (IsAHP) in hippocampal neurons. KCNQ5 is not yet linked to any human disease but is broadly expressed in the brain similar to KCNQ2 and KCNQ3. To investigate the role of KCNQ5 in the brain we generated a KCNQ5 dominantnegative (Kcnq5dn/dn) mouse. Histological analysis did not reveal structural brain abnormalities. Western blots of total brain proteins revealed that there is no detectable influence of the mutated KCNQ5 protein on overall KCNQ2, KCNQ3 and KCNQ5 levels. In addition, the subcellular localization of KCNQ2 and KCNQ3 is not altered in Kcnq5dn/dn mice. Using electrophysiological analysis we could show that KCNQ5 contributes to the ImAHP and IsAHP in a subset of hippocampal neurons where KCNQ5 is highly expressed. Therefore, our study is a direct demonstration that in addition to KCNQ2 and KCNQ3, KCNQ5 channels contribute to the ImAHP and IsAHP.
Fil: Heidenreich, Matthias. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania
Fil: Tzingounis, Anastassios V.. University of California; Estados Unidos
Fil: Kharkovets, Tatjana. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania
Fil: Spitzmaul, Guillermo Federico. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania
Fil: Nicoll, Roger A.. University of California; Estados Unidos
Fil: Jentsch, Thomas J.. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania
Berlin Brain Days 2009
Berlin
Alemania
Berlin School of Mind and Brain
Humboldt-Universität zu Berlin - Materia
-
KCNQ5
HIPPOCAMPUS
AFTERHYPERPOLARIZATION - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/242325
Ver los metadatos del registro completo
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Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neuronsHeidenreich, MatthiasTzingounis, Anastassios V.Kharkovets, TatjanaSpitzmaul, Guillermo FedericoNicoll, Roger A.Jentsch, Thomas J.KCNQ5HIPPOCAMPUSAFTERHYPERPOLARIZATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which contribute to the medium afterhyperpolarization current (ImAHP) and slow afterhyperpolarization current (IsAHP) in hippocampal neurons. KCNQ5 is not yet linked to any human disease but is broadly expressed in the brain similar to KCNQ2 and KCNQ3. To investigate the role of KCNQ5 in the brain we generated a KCNQ5 dominantnegative (Kcnq5dn/dn) mouse. Histological analysis did not reveal structural brain abnormalities. Western blots of total brain proteins revealed that there is no detectable influence of the mutated KCNQ5 protein on overall KCNQ2, KCNQ3 and KCNQ5 levels. In addition, the subcellular localization of KCNQ2 and KCNQ3 is not altered in Kcnq5dn/dn mice. Using electrophysiological analysis we could show that KCNQ5 contributes to the ImAHP and IsAHP in a subset of hippocampal neurons where KCNQ5 is highly expressed. Therefore, our study is a direct demonstration that in addition to KCNQ2 and KCNQ3, KCNQ5 channels contribute to the ImAHP and IsAHP.Fil: Heidenreich, Matthias. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; AlemaniaFil: Tzingounis, Anastassios V.. University of California; Estados UnidosFil: Kharkovets, Tatjana. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; AlemaniaFil: Spitzmaul, Guillermo Federico. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; AlemaniaFil: Nicoll, Roger A.. University of California; Estados UnidosFil: Jentsch, Thomas J.. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; AlemaniaBerlin Brain Days 2009BerlinAlemaniaBerlin School of Mind and BrainHumboldt-Universität zu BerlinMax Delbrück Centrum für Molekulare Medizin2009info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectSimposioJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/242325Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons; Berlin Brain Days 2009; Berlin; Alemania; 2009; 67-67CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mind-and-brain.de/news/detail/berlin-brain-daysNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-11-05T10:12:21Zoai:ri.conicet.gov.ar:11336/242325instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-11-05 10:12:21.348CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| title |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| spellingShingle |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons Heidenreich, Matthias KCNQ5 HIPPOCAMPUS AFTERHYPERPOLARIZATION |
| title_short |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| title_full |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| title_fullStr |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| title_full_unstemmed |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| title_sort |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons |
| dc.creator.none.fl_str_mv |
Heidenreich, Matthias Tzingounis, Anastassios V. Kharkovets, Tatjana Spitzmaul, Guillermo Federico Nicoll, Roger A. Jentsch, Thomas J. |
| author |
Heidenreich, Matthias |
| author_facet |
Heidenreich, Matthias Tzingounis, Anastassios V. Kharkovets, Tatjana Spitzmaul, Guillermo Federico Nicoll, Roger A. Jentsch, Thomas J. |
| author_role |
author |
| author2 |
Tzingounis, Anastassios V. Kharkovets, Tatjana Spitzmaul, Guillermo Federico Nicoll, Roger A. Jentsch, Thomas J. |
| author2_role |
author author author author author |
| dc.subject.none.fl_str_mv |
KCNQ5 HIPPOCAMPUS AFTERHYPERPOLARIZATION |
| topic |
KCNQ5 HIPPOCAMPUS AFTERHYPERPOLARIZATION |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which contribute to the medium afterhyperpolarization current (ImAHP) and slow afterhyperpolarization current (IsAHP) in hippocampal neurons. KCNQ5 is not yet linked to any human disease but is broadly expressed in the brain similar to KCNQ2 and KCNQ3. To investigate the role of KCNQ5 in the brain we generated a KCNQ5 dominantnegative (Kcnq5dn/dn) mouse. Histological analysis did not reveal structural brain abnormalities. Western blots of total brain proteins revealed that there is no detectable influence of the mutated KCNQ5 protein on overall KCNQ2, KCNQ3 and KCNQ5 levels. In addition, the subcellular localization of KCNQ2 and KCNQ3 is not altered in Kcnq5dn/dn mice. Using electrophysiological analysis we could show that KCNQ5 contributes to the ImAHP and IsAHP in a subset of hippocampal neurons where KCNQ5 is highly expressed. Therefore, our study is a direct demonstration that in addition to KCNQ2 and KCNQ3, KCNQ5 channels contribute to the ImAHP and IsAHP. Fil: Heidenreich, Matthias. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania Fil: Tzingounis, Anastassios V.. University of California; Estados Unidos Fil: Kharkovets, Tatjana. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania Fil: Spitzmaul, Guillermo Federico. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania Fil: Nicoll, Roger A.. University of California; Estados Unidos Fil: Jentsch, Thomas J.. Max Delbruk Center For Molecular Medicine; Alemania. Humboldt-Universität zu Berlin; Alemania Berlin Brain Days 2009 Berlin Alemania Berlin School of Mind and Brain Humboldt-Universität zu Berlin |
| description |
Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which contribute to the medium afterhyperpolarization current (ImAHP) and slow afterhyperpolarization current (IsAHP) in hippocampal neurons. KCNQ5 is not yet linked to any human disease but is broadly expressed in the brain similar to KCNQ2 and KCNQ3. To investigate the role of KCNQ5 in the brain we generated a KCNQ5 dominantnegative (Kcnq5dn/dn) mouse. Histological analysis did not reveal structural brain abnormalities. Western blots of total brain proteins revealed that there is no detectable influence of the mutated KCNQ5 protein on overall KCNQ2, KCNQ3 and KCNQ5 levels. In addition, the subcellular localization of KCNQ2 and KCNQ3 is not altered in Kcnq5dn/dn mice. Using electrophysiological analysis we could show that KCNQ5 contributes to the ImAHP and IsAHP in a subset of hippocampal neurons where KCNQ5 is highly expressed. Therefore, our study is a direct demonstration that in addition to KCNQ2 and KCNQ3, KCNQ5 channels contribute to the ImAHP and IsAHP. |
| publishDate |
2009 |
| dc.date.none.fl_str_mv |
2009 |
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info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/conferenceObject Simposio Journal http://purl.org/coar/resource_type/c_5794 info:ar-repo/semantics/documentoDeConferencia |
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publishedVersion |
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conferenceObject |
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http://hdl.handle.net/11336/242325 Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons; Berlin Brain Days 2009; Berlin; Alemania; 2009; 67-67 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/242325 |
| identifier_str_mv |
Contribution of KCNQ5 to the medium and slow afterhyperpolarization currents in hippocampal neurons; Berlin Brain Days 2009; Berlin; Alemania; 2009; 67-67 CONICET Digital CONICET |
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eng |
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eng |
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Nacional |
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Max Delbrück Centrum für Molekulare Medizin |
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Max Delbrück Centrum für Molekulare Medizin |
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