Rat central amygdala corticotropin-releasing hormone-expressing neurons functionally connects to CEA (central amygdaloid nucleus)

CNO activation of hM3Dq in CeL CRF neurons also induced Fos in a subset of CeM neurons, an effect strongly attenuated by systemic CRF1 receptor blockade with R121919 while activation of the CRF neurons themselves was unaffected.

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) disagrees. “The CeM Fos result came from chemogenetic (hM3Dq/CNO) activation, not optogenetic circuit mapping.”

Optogenetic stimulation of CeL CRF terminals evoked picrotoxin-sensitive IPSCs in only 8 of 71 non-CRF CeM neurons, which were scattered across the CeM rather than clustered; IPSC amplitudes were comparable to those in CeL cells.

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

Blue-light stimulation of ChR2-expressing CeL CRF neurons evoked IPSCs in 8 of 18 recorded non-CRF CeL neurons; the evoked IPSCs were nearly abolished by picrotoxin, indicating GABAergic local inhibition.

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

Chemogenetic activation of CeL CRF neurons with hM3Dq plus CNO induced Fos in non-CRF CeL neurons (absent with hM4Di or mCherry controls), and this Fos induction was reduced by about two-thirds by the CRF1 receptor antagonist R121919, indicating peptidergic excitation via local CRF release.

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) disagrees. “The CRF1-dependent Fos induction in CeL non-CRF neurons was obtained chemogenetically, not by optogenetic circuit mapping.”