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

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268 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	599-610
Número de páginas	12
Publicación	Neuron
Volumen	54
N.º	4
DOI	https://doi.org/10.1016/j.neuron.2007.04.009
Estado	Published - may. 24 2007
Publicado de forma externa	Sí

Nota bibliográfica

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).

ASJC Scopus Subject Areas

General Neuroscience

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10.1016/j.neuron.2007.04.009

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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.",

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AU - Li, Xiao Ming

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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

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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.

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Neuregulin-1 Enhances Depolarization-Induced GABA Release

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Nota bibliográfica

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