Neuregulin-1 enhances depolarization-induced GABA release.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Woo, R-S; Li, X-M; Tao, Y; Carpenter-Hyland, E; Huang, YZ; Weber, J; Neiswender, H; Dong, X-P; Wu, J; Gassmann, M; Lai, C; Xiong, W-C; Gao, T-M; Mei, L

Published Date

  • May 24, 2007

Published In

Volume / Issue

  • 54 / 4

Start / End Page

  • 599 - 610

PubMed ID

  • 17521572

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/j.neuron.2007.04.009


  • eng

Conference Location

  • United States