ArticleNature communications2024
Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Luteolin Potentially Alleviates Methamphetamine Withdrawal-Induced Negative Emotions and Cognitive Deficits Through the AKT/FOXO1/HO-1 Signaling Pathway in the Prefrontal Cortex and Caudate Putamen.International journal of molecular sciences · 2025Article
- Hormone-switching islet cells: parallels to transmitter-switching neurons.Frontiers in cell and developmental biology · 2025Article
- How the brain produces generalized fear.Clinical and translational medicine · 2025Article
- Drugs of abuse drive neurotransmitter plasticity that alters behavior: implications for mental health.Frontiers in behavioral neuroscience · 2025Review
- Role of Neural Circuits in Cognitive Impairment.Neurochemical research · 2024Review
- Embryonic exposure to environmental factors drives transmitter switching in the neonatal mouse cortex causing autistic-like adult behavior.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Abstract
Cognitive deficits are long-lasting consequences of drug use, yet the convergent mechanism by which classes of drugs with different pharmacological properties cause similar deficits is unclear. We find that both phencyclidine and methamphetamine, despite differing in their targets in the brain, cause the same glutamatergic neurons in the medial prefrontal cortex of male mice to gain a GABAergic phenotype and decrease expression of their glutamatergic phenotype. Suppressing drug-induced gain of GABA with RNA-interference prevents appearance of memory deficits. Stimulation of dopaminergic neurons in the ventral tegmental area is necessary and sufficient to produce this gain of GABA. Drug-induced prefrontal hyperactivity drives this change in transmitter identity. Returning prefrontal activity to baseline, chemogenetically or with clozapine, reverses the change in transmitter phenotype and rescues the associated memory deficits. This work reveals a shared and reversible mechanism that regulates the appearance of cognitive deficits upon exposure to different drugs.
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