Journal
NEUROSCIENCE
Volume 321, Issue -, Pages 197-209Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2015.07.041
Keywords
optogenetics; prelimbic; infralimbic; fear; stress; anxiety disorders
Categories
Funding
- National Research Service Award Institutional Research Training Grant [5T32GM007484-38]
- NARSAD Young Investigator Award (Brain and Behavior Research Foundation)
- NIMH Research Supplement to Promote Diversity in Health-Related Sciences
- Integrative Neuronal Systems Fellowship
- James R. Killian Fellowship
- JPB Foundation
- PIIF
- PNDRF
- JFDP
- Whitehall Foundation
- Klingenstein Foundation
- NARSAD Young Investigator Award
- Alfred P. Sloan Foundation
- New York Stem Cell Foundation
- Whitehead Career Development Chair
- NIH [R01-MH102441-01]
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The basolateral amygdala (BLA) and the medial prefrontal cortex (mPFC) modulate anxiety and social behaviors. It remains to be elucidated, however, whether direct projections from the BLA to the mPFC play a functional role in these behaviors. We used optogenetic approaches in behaving mice to either activate or inhibit BLA inputs to the mPFC during behavioral assays that assess anxiety-like behavior and social interaction. Channelrhodopsin-2 (ChR2)mediated activation of BLA inputs to the mPFC produced anxiogenic effects in the elevated plus maze and open field test, whereas halorhodopsin (NpHR)-mediated inhibition produced anxiolytic effects. Furthermore, activation of the BLA-mPFC pathway reduced social interaction in the resident-intruder test, whereas inhibition facilitated social interaction. These results establish a causal relationship between activity in the BLA-mPFC pathway and the bidirectional modulation of anxiety-related and social behaviors. This article is part of a Special Issue entitled: Neuropsychiatric Disease. (C) 2015 The Authors. Published by Elsevier Ltd. on behalf of IBRO.
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