Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy

Xiaofei Zhang; Federica Bertaso; Jong W. Yoo; Karsten Baumgärtel; Sinead M. Clancy; Van Lee; Cynthia Cienfuegos; Carly Wilmot; Jacqueline Avis; Truc Hunyh; Catherine Daguia; Christian Schmedt; Jeffrey Noebels; Timothy Jegla

doi:10.1038/nn.2610

Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy

Xiaofei Zhang
, Federica Bertaso
, Jong W. Yoo
, Karsten Baumgärtel
, Sinead M. Clancy
, Van Lee
, Cynthia Cienfuegos
, Carly Wilmot
, Jacqueline Avis
, Truc Hunyh
, Catherine Daguia
, Christian Schmedt
, Jeffrey Noebels
, Timothy Jegla

Research output: Contribution to journal › Article › peer-review

63 Scopus citations

Abstract

We found the voltage-gated K⁺ channel Kv12.2 to be a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 substantially reduced the firing threshold of these neurons. Kv12.2^-/- (also known as Kcnh3^-/-) mice showed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol.

Original language	English (US)
Pages (from-to)	1056-1058
Number of pages	3
Journal	Nature Neuroscience
Volume	13
Issue number	9
DOIs	https://doi.org/10.1038/nn.2610
State	Published - Sep 2010

All Science Journal Classification (ASJC) codes

General Neuroscience

Access to Document

10.1038/nn.2610

Cite this

@article{6f09f4bd2ed744809cf7923d79b12e95,

title = "Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy",

abstract = "We found the voltage-gated K+ channel Kv12.2 to be a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 substantially reduced the firing threshold of these neurons. Kv12.2-/- (also known as Kcnh3-/-) mice showed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol.",

author = "Xiaofei Zhang and Federica Bertaso and Yoo, \{Jong W.\} and Karsten Baumg{\"a}rtel and Clancy, \{Sinead M.\} and Van Lee and Cynthia Cienfuegos and Carly Wilmot and Jacqueline Avis and Truc Hunyh and Catherine Daguia and Christian Schmedt and Jeffrey Noebels and Timothy Jegla",

note = "Funding Information: Institute of Neurological Disorders and Stroke grants awarded to T.J. and J.N., an American Heart Association fellowship supporting X.Z. and INSERM funds supporting F.B. Funding Information: Lentivirus vectors were kindly provided by A. Maximov. The project was funded by the Genomics Institute of the Novartis Research Foundation, US National",

year = "2010",

month = sep,

doi = "10.1038/nn.2610",

language = "English (US)",

volume = "13",

pages = "1056--1058",

journal = "Nature Neuroscience",

issn = "1097-6256",

publisher = "Nature Research",

number = "9",

}

TY - JOUR

T1 - Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy

AU - Zhang, Xiaofei

AU - Bertaso, Federica

AU - Yoo, Jong W.

AU - Baumgärtel, Karsten

AU - Clancy, Sinead M.

AU - Lee, Van

AU - Cienfuegos, Cynthia

AU - Wilmot, Carly

AU - Avis, Jacqueline

AU - Hunyh, Truc

AU - Daguia, Catherine

AU - Schmedt, Christian

AU - Noebels, Jeffrey

AU - Jegla, Timothy

N1 - Funding Information: Institute of Neurological Disorders and Stroke grants awarded to T.J. and J.N., an American Heart Association fellowship supporting X.Z. and INSERM funds supporting F.B. Funding Information: Lentivirus vectors were kindly provided by A. Maximov. The project was funded by the Genomics Institute of the Novartis Research Foundation, US National

PY - 2010/9

Y1 - 2010/9

N2 - We found the voltage-gated K+ channel Kv12.2 to be a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 substantially reduced the firing threshold of these neurons. Kv12.2-/- (also known as Kcnh3-/-) mice showed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol.

AB - We found the voltage-gated K+ channel Kv12.2 to be a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 substantially reduced the firing threshold of these neurons. Kv12.2-/- (also known as Kcnh3-/-) mice showed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol.

UR - https://www.scopus.com/pages/publications/77956187224

UR - https://www.scopus.com/pages/publications/77956187224#tab=citedBy

U2 - 10.1038/nn.2610

DO - 10.1038/nn.2610

M3 - Article

C2 - 20676103

AN - SCOPUS:77956187224

SN - 1097-6256

VL - 13

SP - 1056

EP - 1058

JO - Nature Neuroscience

JF - Nature Neuroscience

IS - 9

ER -

Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy

Abstract

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this