ArticleMolecular psychiatry2022
Transcriptome profiling of the ventral pallidum reveals a role for pallido-thalamic neurons in cocaine reward.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Convergent neuroimmune signaling underlying rapid antidepressant response to ketamine and psychedelics.Molecular psychiatry · 2026Article
- Striatal transcriptomic alterations immediately after short-term abstinence from methamphetamine self-administration in rats.Molecular brain · 2025Article
- Remission from addiction: erasing the wrong circuits or making new ones?Nature reviews. Neuroscience · 2025Review
- Single-nucleus transcriptomics reveals time-dependent and cell-type-specific effects of psilocybin on gene expression.bioRxiv : the preprint server for biology · 2025Article
- Transcriptomic landscape of mammalian ventral pallidum at single-cell resolution.Science advances · 2024Article
- Parvalbumin expression does not account for discrete electrophysiological profiles of glutamatergic ventral pallidal subpopulations.Addiction neuroscience · 2024Article
- A large-scale c-Fos brain mapping study on extinction of cocaine-primed reinstatement.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Multimodal Interrogation of Ventral Pallidum Projections Reveals Projection-Specific Signatures and Effects on Cocaine Reward.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Dissecting 16p11.2 hemi-deletion to study sex-specific striatal phenotypes of neurodevelopmental disorders.Molecular psychiatry · 2024Article
- Ventral pallidum neurons projecting to the ventral tegmental area reinforce but do not invigorate reward-seeking behavior.Cell reports · 2024Article
- An approach for prioritizing candidate genes from RNA-seq using preclinical cocaine self-administration datasets as a test case.G3 (Bethesda, Md.) · 2023Article
- Inducible CRISPR Epigenome Systems Mimic Cocaine Induced Bidirectional Regulation of Nab2 and Egr3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Ventral pallidal regulation of motivated behaviors and reinforcement.Frontiers in neural circuits · 2023Review
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
Abstract
Psychostimulant exposure alters the activity of ventral pallidum (VP) projection neurons. However, the molecular underpinnings of these circuit dysfunctions are unclear. We used RNA-sequencing to reveal alterations in the transcriptional landscape of the VP that are induced by cocaine self-administration in mice. We then probed gene expression in select VP neuronal subpopulations to isolate a circuit associated with cocaine intake. Finally, we used both overexpression and CRISPR-mediated knockdown to test the role of a gene target on cocaine-mediated behaviors as well as dendritic spine density. Our results showed that a large proportion (55%) of genes associated with structural plasticity were changed 24 h following cocaine intake. Among them, the transcription factor Nr4a1 (Nuclear receptor subfamily 4, group A, member 1, or Nur77) showed high expression levels. We found that the VP to mediodorsal thalamus (VP → MDT) projection neurons specifically were recapitulating this increase in Nr4a1 expression. Overexpressing Nr4a1 in VP → MDT neurons enhanced drug-seeking and drug-induced reinstatement, while Nr4a1 knockdown prevented self-administration acquisition and subsequent cocaine-mediated behaviors. Moreover, we showed that Nr4a1 negatively regulated spine dynamics in this specific cell subpopulation. Together, our study identifies for the first time the transcriptional mechanisms occurring in VP in drug exposure. Our study provides further understanding on the role of Nr4a1 in cocaine-related behaviors and identifies the crucial role of the VP → MDT circuit in drug intake and relapse-like behaviors.
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