AI Article Synopsis
- Cholinergic interneurons (ChINs) in the nucleus accumbens play a crucial role in extinguishing associations between drugs and their contexts, particularly for cocaine in male mice.
- High levels of natural acetylcholine signaling are linked to more effective extinction of drug-context associations, while the plastic changes in medium spiny neurons (MSNs) are observed through the weakening of glutamatergic synapses.
- The ability to manipulate ChIN activity further influences both the speed of extinction and the synaptic changes in MSNs, suggesting that variations in acetylcholine levels might explain differences in how individuals experience extinction.
Article Abstract
Cholinergic interneurons (ChINs) in the nucleus accumbens (NAc) have been implicated in the extinction of drug associations, as well as related plasticity in medium spiny neurons (MSNs). However, since most previous work relied on artificial manipulations, whether endogenous acetylcholine signaling relates to drug associations is unclear. Moreover, despite great interest in the opposing effects of dopamine on MSN subtypes, whether ChIN-mediated effects vary by MSN subtype is also unclear. Here, we find that high endogenous acetylcholine event frequency correlates with greater extinction of cocaine-context associations across male mice. Additionally, extinction is associated with a weakening of glutamatergic synapses across MSN subtypes. Manipulating ChIN activity bidirectionally controls both the rate of extinction and the associated plasticity at MSNs. Our findings indicate that NAc ChINs mediate drug-context extinction by reducing glutamatergic synaptic strength across MSN subtypes, and that natural variation in acetylcholine signaling may contribute to individual differences in extinction.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9196889 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2022.110874 | DOI Listing |
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