clm-4537srf1rj

SI (Substantia innominata) functionally connects to Rat basal amygdaloid nucleus principal neurons

Species: Rat
Result: present
Method: optogenetic circuit mapping
Sign: excitatory
Evidence: Blue-light activation of ChR2-expressing NBM terminals evoked short-latency EPSCs in BLA pyramidal neurons that were abolished by TTX and restored by 4-AP, indicating a monosynaptic connection; the EPSC was eliminated by DNQX plus mecamylamine, showing both glutamatergic and nicotinic components. Optical silencing of NBM terminals with halorhodopsin reduced the elevated firing of BLA pyramidal neurons after chronic ethanol withdrawal.
Measurements: conduction delay: 4 ms (SEM 0.3), n = 22
conduction delay: 4.3 ms (SEM 0.3), n = 20
Source: Chronic Intermittent Ethanol Exposure Dysregulates Nucleus Basalis Magnocellularis Afferents in the Basolateral Amygdala
eneuro, 2022
DOI 10.1523/eneuro.0164-22.2022 · PubMed 36280288 · PMC9668348, Fig. 5B–H; Fig. 6D
Licence: CC-BY-NC-SA-4.0
Named in the paper: “NBM” and “BLA pyramidal (principal) neurons”
Made by: an AI model reading the paper (claude-opus-5, extract@0.3.0), 2026-10-10
Checked by: a second AI model (claude-opus-5) agrees, 2026-10-10
“Optically evoked monosynaptic EPSCs (latencies 4.0±0.3, n=22; 4.3±0.3, n=20) with glutamatergic/nicotinic components and halorhodopsin firing results match the Results text.”
Status: proposed
Drafted and checked by AI models; it stays proposed until people have audited a sample of such claims.