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Role of BDNF in the development of an OFC-amygdala circuit regulating sociability in mouse and human.

Abstract：

:Social deficits are common in many psychiatric disorders. However, due to inadequate tools for manipulating circuit activity in humans and unspecific paradigms for modeling social behaviors in rodents, our understanding of the molecular and circuit mechanisms mediating social behaviors remains relatively limited. Using human functional neuroimaging and rodent fiber photometry, we identified a mOFC-BLA projection that modulates social approach behavior and influences susceptibility to social anxiety. In humans and knock-in mice with a loss of function BDNF SNP (Val66Met), the functionality of this circuit was altered, resulting in social behavioral changes in human and mice. We further showed that the development of this circuit is disrupted in BDNF Met carriers due to insufficient BDNF bioavailability, specifically during a peri-adolescent timeframe. These findings define one mechanism by which social anxiety may stem from altered maturation of orbitofronto-amygdala projections and identify a developmental window in which BDNF-based interventions may have therapeutic potential.

journal_name

Mol Psychiatry

journal_title

Molecular psychiatry

authors

Li A,Jing D,Dellarco DV,Hall BS,Yang R,Heilberg RT,Huang C,Liston C,Casey BJ,Lee FS

doi

10.1038/s41380-019-0422-4

subject

Has Abstract

pub_date

2019-04-16 00:00:00

eissn

1359-4184

issn

1476-5578

pii

10.1038/s41380-019-0422-4

pub_type

杂志文章

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