Inactivation of a CRF-dependent amygdalofugal pathway reverses addiction-like behaviors in alcohol-dependent rats

Rat central amygdala corticotropin-releasing hormone-expressing neurons nt-sexhekqxaa functionally connects to BST (Bed nuclei of the stria terminalis) UBERON:0001880 · Rat

In BNST slices from Crh-Cre rats with NpHR expressed in CeA CRF neurons, green-light inhibition of the CRF CeA-BNST terminals reduced action potential firing of BNST neurons (8 of 14 cells responded with reduced firing, 6 were non-responders; 6.5 s light: 0.37 to 0.22 Hz; 5 min light: 0.91 to 0.60 Hz). Pretreatment with the CRF1 receptor antagonist R121919 itself lowered BNST firing and occluded the light effect, indicating the terminal influence on BNST firing is driven by CRF acting on CRF1 receptors.

Fig. 5f–i; Supplementary Figure 8; Supplementary Figure 4C,D

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.

Rat central amygdala corticotropin-releasing hormone-expressing neurons nt-sexhekqxaa projects to BST (Bed nuclei of the stria terminalis) UBERON:0001880 · Rat

Cre-dependent AAV5-EF1a-DIO-NpHR-eYFP injected into the CeA of Crh-Cre rats produced eYFP-labelled CRF axon terminals in the ventral BNST, where optical fibers were placed; histology confirmed viral expression at the CeA injection site and in the BNST target.

Fig. 5b; Methods (Intracranial surgery, Histology)

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) is unsure. “The projection is implied by terminal photoinhibition, but the cited figure caption only mentions images of the injection and illumination sites, not explicit anterograde eYFP terminal labeling in BNST.”