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SI (Substantia innominata) functionally connects to BLA (basal amygdaloid nucleus)

Species: Rat
Result: present
Method: optogenetic circuit mapping
Sign: modulatory
Evidence: Optical activation of ChR2- or ChrimsonR-expressing NBM terminals just before electrical stimulation of stria terminalis fibres lowered the paired-pulse ratio of glutamatergic EPSCs in BLA pyramidal neurons of air-exposed rats, an effect reversed by the nicotinic antagonist mecamylamine and mimicked by physostigmine; optical inhibition of NBM terminals with halorhodopsin raised the paired-pulse ratio in ethanol-withdrawn rats. This shows NBM terminals modulate glutamate release in the BLA through presynaptic nicotinic receptors.
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. 3B–G
Licence: CC-BY-NC-SA-4.0
Named in the paper: “NBM” and “BLA (stria terminalis glutamatergic synapses in the basolateral nucleus)”
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
“Opto activation/inhibition of NBM terminals altered stria terminalis PPR in a mecamylamine-sensitive way, supporting modulatory NBM action in BLA.”
Status: proposed
Drafted and checked by AI models; it stays proposed until people have audited a sample of such claims.