Neuregulin 1-ErbB4 signaling in the bed nucleus of the stria terminalis regulates anxiety-like behavior

Geng, Fei; Zhang, Jie; Wu, Jianlin; Zou, Wen-Jun; Liang, Zhi-Ping; Bi, Lin-Lin; Liu, Jihong; Kong, Ying; Huang, Chu-Qiang; Li, Xiaowen; Yang, Jian‐Ming; Gao, Tianming

doi:10.1016/j.neuroscience.2016.05.018

Cited by 18 publications

(15 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, this effect requires ErbB4 because it is diminished by pharmacological inhibition of the kinase activity of ErbB4 or genetic deletion of the ErbB4 gene in null or interneuron-specific mutant mice (17,18,21,24). Third, treating brain slices with an NRG1-neutralizing peptide decreases mIPSCs and eIPSCs (17,18,20,21,23,24,61). Fourth, NRG1 neutralization and/or ErbB4 mutation impair behaviors in various paradigms involving prefrontal cortex, the hippocampus, and the amygdala (3,15,(18)(19)(20)(21)(22)(23)(24), where ErbB4 is enriched.…”

Section: Discussionmentioning

confidence: 99%

Genetic recovery of ErbB4 in adulthood partially restores brain functions in null mice

Wang

Liu

Chen

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Neurotrophic factor NRG1 and its receptor ErbB4 play a role in GABAergic circuit assembly during development. ErbB4 null mice possess fewer interneurons, have decreased GABA release, and show impaired behavior in various paradigms. In addition, NRG1 and ErbB4 have also been implicated in regulating GABAergic transmission and plasticity in matured brains. However, current ErbB4 mutant strains are unable to determine whether phenotypes in adult mutant mice result from abnormal neural development. This important question, a glaring gap in understanding NRG1–ErbB4 function, was addressed by using two strains of mice with temporal control of ErbB4 deletion and expression, respectively. We found that ErbB4 deletion in adult mice impaired behavior and GABA release but had no effect on neuron numbers and morphology. On the other hand, some deficits due to the ErbB4 null mutation during development were alleviated by restoring ErbB4 expression at the adult stage. Together, our results indicate a critical role of NRG1–ErbB4 signaling in GABAergic transmission and behavior in adulthood and suggest that restoring NRG1–ErbB4 signaling at the postdevelopmental stage might benefit relevant brain disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

Genetic recovery of ErbB4 in adulthood partially restores brain functions in null mice

Wang

Liu

Chen

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…To further investigate whether Co-derived cells contributed to specific circuits, we focused on their contribution to the BNST, which organization and function has been recently investigated (Asok, Schulkin, & Rosen, 2016;Choi et al, 2007;Daldrup, Lesting, Meuth, Seidenbecher, & Pape, 2016;Dong, Petrovich, & Swanson, 2001;Geng et al, 2016;Hott et al, 2016;Kim et al, 2013). The BNST is a complex structure which comprise a large number of subdivisions that are difficult to identify on anatomical criterions (Bayer, 1987;Ju & Han, 1989).…”

Section: Co-derived Neurons Contribute To Nuclei That Mediate Anxiementioning

confidence: 99%

“…Indeed, even though the internal capsule is only present in mammals, cells with a molecular identity similar to Co cells have been also identified in avian and reptile embryos (Bielle, Marcos‐Mondejar, Keita, et al, ; Bielle, Marcos‐Mondéjar, Leyva‐Díaz, et al, 2011; Bupesh, Abellán, & Medina, ). Moreover, gene expression studies suggest contribution of LGE derivatives to the central and extended amygdala, evolutionarily conserved superstructures located in the subpallium that contain neurons of different developmental origin and are involved in fear and anxiety control (Hott et al, ; Ranjan et al, ) and anxiety (Geng et al, ; Morano, Bailey, Cahill, & Dumont, ; Ventura‐Silva et al, ). These observations raised the intriguing possibility that guidepost might be an acquired function for Co cells, which would have a distinct, evolutionary conserved role.…”

Section: Introductionmentioning

confidence: 99%

Tangential migration of corridor guidepost neurons contributes to anxiety circuits

Tinterri

Deck

Keita

et al. 2017

J of Comparative Neurology

View full text Add to dashboard Cite

In mammals, thalamic axons are guided internally toward their neocortical target by corridor (Co) neurons that act as axonal guideposts. The existence of Co-like neurons in non-mammalian species, in which thalamic axons do not grow internally, raised the possibility that Co cells might have an ancestral role. Here, we investigated the contribution of corridor (Co) cells to mature brain circuits using a combination of genetic fate-mapping and assays in mice. We unexpectedly found that Co neurons contribute to striatal-like projection neurons in the central extended amygdala. In particular, Co-like neurons participate in specific nuclei of the bed nucleus of the stria terminalis, which plays essential roles in anxiety circuits. Our study shows that Co neurons possess an evolutionary conserved role in anxiety circuits independently from an acquired guidepost function. It furthermore highlights that neurons can have multiple sequential functions during brain wiring and supports a general role of tangential migration in the building of subpallial circuits.

show abstract

“…Bicuculline (BMI) was purchased from Tocris. NRG1, PD158780 (PD), and AG1478 were used [18,19]. The concentration of dimethyl sulfoxide was < 0.001.…”

Section: Experimental Animalsmentioning

confidence: 99%

ErbB4 Receptors in the Medial Habenula Regulate Contextual Fear Memory

et al. 2018

Self Cite

View full text Add to dashboard Cite

The Medial Habenular (MHb) and the Lateral Habenular nuclei are 2 main parts of the habenular complex (Hb). Recent studies showed that MHb plays an important role in memory, and in the expression of ErbB4. However, the expression of MHb ErbB4 receptor and its role in fear memory is not well understood. In this study, western blotting and quantitative real-time polymerase chain reaction were used to assess the protein and mRNA levels of ErbB4 in the process of contextual fear conditioning. A pharmacological approach was used to block and stimulate the ErbB4 receptor. Contextual fear conditioning tests induced a significant increase on the expression of ErbB4 at various times in the Hb and the MHb. Moreover, the blockade and stimulation of MHb ErbB4 receptors did not affect the fear formation but impaired and improved the contextual-dependent fear expression. Furthermore, in vitro electrophysiological recordings showed that the blockade of the MHb ErbB4 receptor reduced the presynaptic gamma-amino butyric acid release. ErbB4 is a susceptible gene for schizophrenia and the above findings may provide new insights into the mechanisms of fear-related responses.

show abstract

Neuregulin 1-ErbB4 signaling in the bed nucleus of the stria terminalis regulates anxiety-like behavior

Cited by 18 publications

References 34 publications

Genetic recovery of ErbB4 in adulthood partially restores brain functions in null mice

Genetic recovery of ErbB4 in adulthood partially restores brain functions in null mice

Tangential migration of corridor guidepost neurons contributes to anxiety circuits

ErbB4 Receptors in the Medial Habenula Regulate Contextual Fear Memory

Contact Info

Product

Resources

About