Format

Send to

Choose Destination
Transl Psychiatry. 2018 Jan 31;8(1):33. doi: 10.1038/s41398-017-0074-6.

Extended amygdala connectivity changes during sustained shock anticipation.

Author information

1
Section on the Neurobiology of Fear and Anxiety, National Institute of Mental Health, Bethesda, MD, USA. sam.torrisi@nih.gov.
2
Section on the Neurobiology of Fear and Anxiety, National Institute of Mental Health, Bethesda, MD, USA.
3
Section on Functional Imaging Methods, Laboratory of Brain and Cognition, NIMH, Bethesda, MD, USA.

Abstract

The bed nucleus of the stria terminalis (BNST) and central amygdala (CeA) of the extended amygdala are small, anatomically interconnected brain regions. They are thought to mediate responses to sustained, unpredictable threat stimuli and phasic, predictable threat stimuli, respectively. They perform these operations largely through their interconnected networks. In two previous studies, we mapped and contrasted the resting functional connectivity networks of the BNST and CeA at 7 Tesla with high resolution. This follow-up study investigates the changes in functional connectivity of these structures during sustained anticipation of electric shock. Results show that the BNST and CeA become less strongly coupled with the ventromedial prefrontal cortex (vmPFC), cingulate, and nucleus accumbens in shock threat relative to a safety condition. In addition, the CeA becomes more strongly coupled with the thalamus under threat. An exploratory, whole-brain connectivity analysis reveals that, although the BNST/CeA exhibits generally decreased connectivity, many other cortical regions demonstrate greater coupling under threat than safety. Understanding the differential network structures of these two regions and how they contribute to processing under threat will help elucidate the building blocks of the anxious state.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT00047853 NCT00001360.

PMID:
29382815
PMCID:
PMC5802685
DOI:
10.1038/s41398-017-0074-6
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center