ArticleNature communications2020
Orbitofrontal-striatal potentiation underlies cocaine-induced hyperactivity.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Anterior Cingulate Cortex Contributes to the Hyperlocomotion under Nitrogen Narcosis.Neuroscience bulletin · 2025Article
- A disinhibitory microcircuit of the orbitofrontal cortex mediates cocaine preference in mice.Molecular psychiatry · 2024Article
- Optogenetic inhibition of light-captured alcohol-taking striatal engrams facilitates extinction and suppresses reinstatement.Alcohol, clinical & experimental research · 2024Article
- Updating the striatal-pallidal wiring diagram.Nature neuroscience · 2024Review
- Cell-type specific synaptic plasticity in dorsal striatum is associated with punishment-resistance compulsive-like cocaine self-administration in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- The roles of rat medial prefrontal and orbitofrontal cortices in relapse to cocaine-seeking: A comparison across methods for identifying neurocircuits.Addiction neuroscience · 2022Article
- Reelin deficiency exacerbates cocaine-induced hyperlocomotion by enhancing neuronal activity in the dorsomedial striatum.Genes, brain, and behavior · 2022Article
- An Shen Ding Zhi Ling Ameliorates the Symptoms of Attention Deficit Hyperactivity Disorder via Modulating Brain-Derived Neurotrophic Factor-Related Signaling Pathways.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol.Biological psychiatry · 2021Review
- Optogenetic induction of orbitostriatal long-term potentiation in the dorsomedial striatum elicits a persistent reduction of alcohol-seeking behavior in rats.Neuropharmacology · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Psychomotor stimulants increase dopamine levels in the striatum and promote locomotion; however, their effects on striatal pathway function in vivo remain unclear. One model that has been proposed to account for these motor effects suggests that stimulants drive hyperactivity via activation and inhibition of direct and indirect pathway striatal neurons, respectively. Although this hypothesis is consistent with the cellular actions of dopamine receptors and received support from optogenetic and chemogenetic studies, it has been rarely tested with in vivo recordings. Here, we test this model and observe that cocaine increases the activity of both pathways in the striatum of awake mice. These changes are linked to a dopamine-dependent cocaine-induced strengthening of upstream orbitofrontal cortex (OFC) inputs to the dorsomedial striatum (DMS) in vivo. Finally, depressing OFC-DMS pathway with a high frequency stimulation protocol in awake mice over-powers the cocaine-induced potentiation of OFC-DMS pathway and attenuates the expression of locomotor sensitization, directly linking OFC-DMS potentiation to cocaine-induced hyperactivity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.