The basolateral amygdala-anterior cingulate cortex circuit contributes to postherpetic neuralgia-anxiety comorbidity

BLA glutamatergic principal neurons nt-wprma5fcrr projects to ACA (Anterior cingulate area) MBA:31 · Mouse

After injecting a CaMKIIα-driven ChR2-mCherry virus into the BLA, labelled axons were found in large numbers in layers II/III of the anterior cingulate cortex; a separate chemogenetic virus injected in BLA likewise filled many mCherry-positive terminals in ACC.

Fig. 6A; Fig. S2E

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BLA glutamatergic principal neurons nt-wprma5fcrr functionally connects to ACA (Anterior cingulate area) MBA:31 · Mouse

Blue-light stimulation of ChR2-expressing BLA glutamatergic terminals evoked postsynaptic currents in layer II/III ACC pyramidal neurons that were abolished by the AMPA-receptor blocker CNQX; the responses were eliminated by TTX and restored by TTX plus 4-AP, indicating a direct monosynaptic excitatory input. In the pain/anxiety model these light-evoked currents were larger and the paired-pulse ratio was lower than in controls.

Fig. 6G-L; Fig. 8B-E

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BLA (Basolateral amygdalar nucleus) MBA:295 projects to ACA (Anterior cingulate area) MBA:31 · Mouse

A retrograde CaMKIIα virus placed in the ACC labelled cell bodies in the BLA, most of which were also immunopositive for glutamate; these ACC-projecting BLA cells made up most of the activity-labelled (c-fos positive) BLA population in the pain/anxiety model. The same retrograde strategy was used to target these neurons for recording and calcium imaging.

Fig. 6B-F; Fig. 9A-B

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