| First Author | Chen JY | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 10 | Pages | 107878 |
| PubMed ID | 37810240 | Mgi Jnum | J:350848 |
| Mgi Id | MGI:7540222 | Doi | 10.1016/j.isci.2023.107878 |
| Citation | Chen JY, et al. (2023) The PrL(Glu)-->avBNST(GABA) circuit rapidly modulates depression-like behaviors in male mice. iScience 26(10):107878 |
| abstractText | Depression is a global disease with a high prevalence. Here, we examine the role of the circuit from prelimbic mPFC (PrL) to the anterior ventral bed nucleus of the stria terminalis (avBNST) in depression-like mice through behavioral tests, immunofluorescence, chemogenetics, optogenetics, pharmacology, and fiber photometry. Mice exposed to chronic restraint stress with individual housing displayed depression-like behaviors. Optogenetic or chemogenetic activation of the avBNST-projecting glutamatergic neurons in the PrL had an antidepressant effect. Moreover, we found that alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptors (AMPARs) play a dominant role in this circuit. Systemic administration of ketamine profoundly alleviated depression-like behaviors in the mice and rapidly rescued the decreased activity in the PrL(Glu)-->avBNST(GABA) circuit. Furthermore, the fast-acting effect of ketamine on depressive behaviors was diminished when the circuit was inhibited. To summarize, activating the PrL(Glu)-->avBNST(GABA) circuit quickly ameliorated depression-like behaviors. Thus, we propose the PrL(Glu)-->avBNST(GABA) circuit as a target for fast regulation of depression. |
