NPAS4 supports cocaine-conditioned cues in rodents by controlling the cell type-specific activation balance in the nucleus accumbens.
Brandon W HughesJessica L HuebschmanEvgeny TsvetkovBenjamin M SiemsenKirsten K SnyderRose Marie AkikiDaniel J WoodRachel D PenrodMichael D ScofieldStefano BertoMakoto TaniguchiChristopher W CowanPublished in: Nature communications (2024)
Powerful associations that link drugs of abuse with cues in the drug-paired environment often serve as prepotent relapse triggers. Drug-associated contexts and cues activate ensembles of nucleus accumbens (NAc) neurons, including D1-class medium spiny neurons (MSNs) that typically promote, and D2-class MSNs that typically oppose, drug seeking. We found that in mice, cocaine conditioning upregulated transiently the activity-regulated transcription factor, Neuronal PAS Domain Protein 4 (NPAS4), in a small subset of NAc neurons. The NPAS4+ NAc ensemble was required for cocaine conditioned place preference. We also observed that NPAS4 functions within NAc D2-, but not D1-, MSNs to support cocaine-context associations and cue-induced cocaine, but not sucrose, seeking. Together, our data show that the NPAS4+ ensemble of NAc neurons is essential for cocaine-context associations in mice, and that NPAS4 itself functions in NAc D2-MSNs to support cocaine-context associations by suppressing drug-induced counteradaptations that oppose relapse-related behaviour.
Keyphrases
- transcription factor
- drug induced
- liver injury
- dna binding
- spinal cord
- prefrontal cortex
- adverse drug
- mental health
- genome wide analysis
- emergency department
- spinal cord injury
- metabolic syndrome
- electronic health record
- endothelial cells
- oxidative stress
- skeletal muscle
- diabetic rats
- small molecule
- machine learning
- neural network