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

Blue-light stimulation of ChR2-expressing NBM terminals in the BLA produced large GABAergic IPSCs in pyramidal neurons; these were blocked by TTX and recovered with 4-AP and had short, exposure-independent latencies, consistent with a direct monosynaptic GABAergic input from the NBM. Chronic intermittent ethanol and withdrawal reduced IPSC amplitude.

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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.

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