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Journal article

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

Licence: CC-BY-NC-SA-4.0

5 claims from this source

clm-1bnnjwfn1mpresentoptogenetic circuit mappingproposed

SI (Substantia innominata) UBERON:0003017 functionally connects to Rat basal amygdaloid nucleus principal neurons nt-gv1k4bnh04 · Rat

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.

Fig. 4B–F

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

clm-4537srf1rjpresentoptogenetic circuit mappingproposed

SI (Substantia innominata) UBERON:0003017 functionally connects to Rat basal amygdaloid nucleus principal neurons nt-gv1k4bnh04 · Rat

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.

Fig. 5B–H; Fig. 6D

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

clm-8v9bryj9sspresentoptogenetic circuit mappingproposed

SI (Substantia innominata) UBERON:0003017 functionally connects to BLA (basal amygdaloid nucleus) UBERON:0002887 · Rat

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by physostigmine; optical inhibition of NBM terminals with halorhodopsin raised the paired-pulse ratio in ethanol-withdrawn rats.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.

Fig. 3B–G

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clm-daef3352trpresentanterograde tracerproposed

SI (Substantia innominata) UBERON:0003017 projects to BLA (basal amygdaloid nucleus) UBERON:0002887 · Rat

Four weeks after injecting an AAV carrying ChR2-eYFP under the hSyn promoter into the NBM, eYFP-labelled axon terminals were seen in the BLA, concentrated in the basolateral nucleus, while BLA cell bodies (DAPI) were unlabelled, showing the fibres originate in the NBM.

Fig. 2B,C; Results, optogenetics section

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clm-x24f5vkjttpresentelectrical stimulationproposed

st (stria terminalis) UBERON:0003029 functionally connects to Rat basal amygdaloid nucleus principal neurons nt-gv1k4bnh04 · Rat

Electrical stimulation of fibres within the stria terminalis evoked monosynaptic glutamatergic EPSCs in BLA pyramidal neurons, recorded with GABA-A and NMDA receptors blocked; polysynaptic responses were rare and excluded.

Materials and Methods, whole-cell patch-clamp; Fig. 3B,C

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