Neuregulin-1 Enhances Depolarization-Induced GABA Release

Ran Sook Woo; Xiao Ming Li; Yanmei Tao; Ezekiel Carpenter-Hyland; Yang Z. Huang; Janet Weber; Hannah Neiswender; Xian Ping Dong; Jiong Wu; Martin Gassmann; Cary Lai; Wen Cheng Xiong; Tian Ming Gao; Lin Mei

doi:10.1016/j.neuron.2007.04.009

Neuregulin-1 Enhances Depolarization-Induced GABA Release

Ran Sook Woo, Xiao Ming Li, Yanmei Tao, Ezekiel Carpenter-Hyland, Yang Z. Huang, Janet Weber, Hannah Neiswender, Xian Ping Dong, Jiong Wu, Martin Gassmann, Cary Lai, Wen Cheng Xiong, Tian Ming Gao, Lin Mei

Graduate Studies

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

263 Scopus citations

Abstract

Neuregulin-1 (NRG1), a regulator of neural development, has been shown to regulate neurotransmission at excitatory synapses. Although ErbB4, a key NRG1 receptor, is expressed in glutamic acid decarboxylase (GAD)-positive neurons, little is known about its role in GABAergic transmission. We show that ErbB4 is localized at GABAergic terminals of the prefrontal cortex. Our data indicate a role of NRG1, both endogenous and exogenous, in regulation of GABAergic transmission. This effect was blocked by inhibition or mutation of ErbB4, suggesting the involvement of ErbB4. Together, these results indicate that NRG1 regulates GABAergic transmission via presynaptic ErbB4 receptors, identifying a novel function of NRG1. Because both NRG1 and ErbB4 have emerged as susceptibility genes of schizophrenia, these observations may suggest a mechanism for abnormal GABAergic neurotransmission in this disorder.

Original language	English (US)
Pages (from-to)	599-610
Number of pages	12
Journal	Neuron
Volume	54
Issue number	4
DOIs	https://doi.org/10.1016/j.neuron.2007.04.009
State	Published - May 24 2007

Keywords

HUMDISEASE
MOLNEURO
SYSNEURO

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neuron.2007.04.009

Cite this

@article{8111111b6ad349d3a6eba4325a220260,

title = "Neuregulin-1 Enhances Depolarization-Induced GABA Release",

abstract = "Neuregulin-1 (NRG1), a regulator of neural development, has been shown to regulate neurotransmission at excitatory synapses. Although ErbB4, a key NRG1 receptor, is expressed in glutamic acid decarboxylase (GAD)-positive neurons, little is known about its role in GABAergic transmission. We show that ErbB4 is localized at GABAergic terminals of the prefrontal cortex. Our data indicate a role of NRG1, both endogenous and exogenous, in regulation of GABAergic transmission. This effect was blocked by inhibition or mutation of ErbB4, suggesting the involvement of ErbB4. Together, these results indicate that NRG1 regulates GABAergic transmission via presynaptic ErbB4 receptors, identifying a novel function of NRG1. Because both NRG1 and ErbB4 have emerged as susceptibility genes of schizophrenia, these observations may suggest a mechanism for abnormal GABAergic neurotransmission in this disorder.",

keywords = "HUMDISEASE, MOLNEURO, SYSNEURO",

author = "Woo, {Ran Sook} and Li, {Xiao Ming} and Yanmei Tao and Ezekiel Carpenter-Hyland and Huang, {Yang Z.} and Janet Weber and Hannah Neiswender and Dong, {Xian Ping} and Jiong Wu and Martin Gassmann and Cary Lai and Xiong, {Wen Cheng} and Gao, {Tian Ming} and Lin Mei",

note = "Funding Information: We thank Ren-ping Zhou for providing the pC4 vector, M. Slikowski for NRG1, and Xiangdong Zhu for TAT protein constructs. This work was supported in part by grants from NIH (L.M. and W.C.X.), MDA (L.M.), and NSFC (#30330240 and U0632007, T.M.G.). T.M.G. and L.M. are Chang Jiang Scholars. R.S.W. was supported in part by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, KRF-2004-214-H00004). ",

year = "2007",

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doi = "10.1016/j.neuron.2007.04.009",

language = "English (US)",

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journal = "Neuron",

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T1 - Neuregulin-1 Enhances Depolarization-Induced GABA Release

AU - Woo, Ran Sook

AU - Li, Xiao Ming

AU - Tao, Yanmei

AU - Carpenter-Hyland, Ezekiel

AU - Huang, Yang Z.

AU - Weber, Janet

AU - Neiswender, Hannah

AU - Dong, Xian Ping

AU - Wu, Jiong

AU - Gassmann, Martin

AU - Lai, Cary

AU - Xiong, Wen Cheng

AU - Gao, Tian Ming

AU - Mei, Lin

N1 - Funding Information: We thank Ren-ping Zhou for providing the pC4 vector, M. Slikowski for NRG1, and Xiangdong Zhu for TAT protein constructs. This work was supported in part by grants from NIH (L.M. and W.C.X.), MDA (L.M.), and NSFC (#30330240 and U0632007, T.M.G.). T.M.G. and L.M. are Chang Jiang Scholars. R.S.W. was supported in part by the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, KRF-2004-214-H00004).

PY - 2007/5/24

Y1 - 2007/5/24

N2 - Neuregulin-1 (NRG1), a regulator of neural development, has been shown to regulate neurotransmission at excitatory synapses. Although ErbB4, a key NRG1 receptor, is expressed in glutamic acid decarboxylase (GAD)-positive neurons, little is known about its role in GABAergic transmission. We show that ErbB4 is localized at GABAergic terminals of the prefrontal cortex. Our data indicate a role of NRG1, both endogenous and exogenous, in regulation of GABAergic transmission. This effect was blocked by inhibition or mutation of ErbB4, suggesting the involvement of ErbB4. Together, these results indicate that NRG1 regulates GABAergic transmission via presynaptic ErbB4 receptors, identifying a novel function of NRG1. Because both NRG1 and ErbB4 have emerged as susceptibility genes of schizophrenia, these observations may suggest a mechanism for abnormal GABAergic neurotransmission in this disorder.

AB - Neuregulin-1 (NRG1), a regulator of neural development, has been shown to regulate neurotransmission at excitatory synapses. Although ErbB4, a key NRG1 receptor, is expressed in glutamic acid decarboxylase (GAD)-positive neurons, little is known about its role in GABAergic transmission. We show that ErbB4 is localized at GABAergic terminals of the prefrontal cortex. Our data indicate a role of NRG1, both endogenous and exogenous, in regulation of GABAergic transmission. This effect was blocked by inhibition or mutation of ErbB4, suggesting the involvement of ErbB4. Together, these results indicate that NRG1 regulates GABAergic transmission via presynaptic ErbB4 receptors, identifying a novel function of NRG1. Because both NRG1 and ErbB4 have emerged as susceptibility genes of schizophrenia, these observations may suggest a mechanism for abnormal GABAergic neurotransmission in this disorder.

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KW - MOLNEURO

KW - SYSNEURO

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JO - Neuron

JF - Neuron

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ER -

Neuregulin-1 Enhances Depolarization-Induced GABA Release

Abstract

Keywords

ASJC Scopus subject areas

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