ArticlePLoS biology2019
NF1-cAMP signaling dissociates cell type-specific contributions of striatal medium spiny neurons to reward valuation and motor control.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 20 citations in OpenAlex.
- Nucleus accumbens neuron subtype translatome signatures in socially stressed females.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Advancing neurofibromatosis research: a comparative review of animal models and their utility in dissecting the tumor microenvironment.Laboratory animal research · 2026Review
- Genetic and non-genetic factors influencing phenotypic variability in neurofibromatosis type 1.Orphanet journal of rare diseases · 2026Review
- Bmal1 Modulates Striatal cAMP Signaling and Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Fluorescent sensors for intracellular signaling in the brain: imaging neurons, glia, and vascular cells.Neurophotonics · 2025Article
- The G protein modifier KCTD5 tunes the decoding of neuromodulatory signals necessary for motor function in striatal neurons.PLoS biology · 2025Article
- Comprehensive medicinal chemistry survey highlights a portfolio of lead molecules for Alzheimer's disease therapy.Frontiers in chemistry · 2025Review
- KCTD1 regulation of Adenylyl cyclase type 5 adjusts striatal cAMP signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- NF1Clinical and translational science · 2024Article
- Targeting cAMP in D1-MSNs in the nucleus accumbens, a new rapid antidepressant strategy.Acta pharmaceutica Sinica. B · 2024Article
- Customizable Open-Source Rotating Rod (Rotarod) Enables Robust Low-Cost Assessment of Motor Performance in Mice.eNeuro · 2023Article
- A Targeted, Low-Throughput Compound Screen in aeNeuro · 2023Article
- The therapeutic potential of neurofibromin signaling pathways and binding partners.Communications biology · 2023Review
- Adaptive behaviors of Drosophila larvae on slippery surfaces.Journal of biological physics · 2023Article
- Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.Disease models & mechanisms · 2022Review
- The role of orphan receptor GPR139 in neuropsychiatric behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Assessing Psychiatric Comorbidity and Pharmacologic Treatment Patterns Among Patients With Neurofibromatosis Type 1.Cureus · 2021Article
- Review
- Developmental loss of neurofibromin across distributed neuronal circuits drives excessive grooming in Drosophila.PLoS genetics · 2020Article
- Understanding divergent domestication traits from the whole-genome sequencing of swamp- and river-buffalo populations.National science review · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The striatum plays a fundamental role in motor learning and reward-related behaviors that are synergistically shaped by populations of D1 dopamine receptor (D1R)- and D2 dopamine receptor (D2R)-expressing medium spiny neurons (MSNs). How various neurotransmitter inputs converging on common intracellular pathways are parsed out to regulate distinct behavioral outcomes in a neuron-specific manner is poorly understood. Here, we reveal that distinct contributions of D1R-MSNs and D2R-MSNs towards reward and motor behaviors are delineated by the multifaceted signaling protein neurofibromin 1 (NF1). Using genetic mouse models, we show that NF1 in D1R-MSN modulates opioid reward, whereas loss of NF1 in D2R-MSNs delays motor learning by impeding the formation and consolidation of repetitive motor sequences. We found that motor learning deficits upon NF1 loss were associated with the disruption in dopamine signaling to cAMP in D2R-MSN. Restoration of cAMP levels pharmacologically or chemogenetically rescued the motor learning deficits seen upon NF1 loss in D2R-MSN. Our findings illustrate that multiplex signaling capabilities of MSNs are deployed at the level of intracellular pathways to achieve cell-specific control over behavioral outcomes.
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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.