• Lin-Lin Bi, Xiang-Dong Sun, Jie Zhang, Yi-Sheng Lu, Yi-Hua Chen, Jue Wang, Fei Geng, Fang Liu, Meng Zhang, Ji-Hong Liu, Xiao-Wen Li, Lin Mei, and Tian-Ming Gao.
• 1] State Key Laboratory of Organ Failure Research, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China [2] Key Laboratory of Psychiatric Disorders of Guangdong Province, Southern Medical University, Guangzhou, China [3] Institute for Brain Research, Huazhong University of Science and Technology, Wuhan, China.
• Neuropsychopharmacology. 2015 Mar 1;40(4):974-86.

AbstractAnxiety disorder is related to the pathophysiology of psychiatric diseases, including major depression, substance abuse, and schizophrenia. The amygdala is important for manifestation and modulation of anxiety. However, relatively little is known regarding the mechanisms that control the amygdala inhibitory activity that is involved in anxiety. We found that almost all ErbB4, which is the only autonomous receptor of neuregulin 1 (NRG1) in the basolateral amygdala (BLA), was expressed in GABAergic neurons. Endogenous NRG1-ErbB4 signaling pathway in the BLA could modulate anxiety-like behaviors and GABA release, whereas it had no effect on glutamatergic transmission. The administration of NRG1 into the BLA of high-anxiety mice alleviated their anxiety and enhanced GABAergic neurotransmission. Moreover, exogenous NRG1 also produced an anxiolytic effect in the stressed mice. Together, these observations indicated that NRG1-ErbB4 signaling is critical to maintaining GABAergic activity in the amygdala and thus to modulating anxiety-like behaviors. Because NRG1 and ErbB4 are susceptibility genes of schizophrenia, our findings might also help to explain the potential mechanism of emotional abnormality in schizophrenia.

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