ArticleCommunications biology2021
Dopaminergic co-transmission with sonic hedgehog inhibits abnormal involuntary movements in models of Parkinson's disease and L-Dopa induced dyskinesia.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- The Therapeutic Potential of Purmorphamine Across Disease Models.Journal of cellular and molecular medicine · 2026Review
- Review
- Sonic Hedgehog-Gli1 signaling promotes microglial activation via the IKKβ/NF-κB pathway.Acta pharmacologica Sinica · 2026Article
- The GPCR Smoothened on cholinergic interneurons modulates dopamine-associated acetylcholine dynamics, learning, and effort management.iScience · 2026Article
- Dopamine 2 receptor ablation from cholinergic neurons attenuates L-DOPA induced dyskinesias.Frontiers in aging neuroscience · 2026Article
- Sonic Hedgehog Mediates High Frequency-Dependent Deep Brain Stimulation for the Correction of Motor Deficits in a Parkinson's Disease Model.Neuroscience bulletin · 2024Article
- The primary cilium of cholinergic neurons may be a linchpin in the progression of Parkinson's Disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Application of Optogenetics in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2024Review
- Characterization of Sonic Hedgehog transcripts in the adult mouse brain: co-expression with neuronal and oligodendroglial markers.Brain structure & function · 2024Article
- Article
- Alterations in neurotransmitter co-release in Parkinson's disease.Experimental neurology · 2023Review
- Retrospective Multicenter Study on Outcome Measurement for Dyskinesia Improvement in Parkinson's Disease Patients with Pallidal and Subthalamic Nucleus Deep Brain Stimulation.Brain sciences · 2022Article
- Striatal synaptic adaptations in Parkinson's disease.Neurobiology of disease · 2022Review
- Intercellular Communication in the Central Nervous System as Deduced by Chemical Neuroanatomy and Quantitative Analysis of Images: Impact on Neuropharmacology.International journal of molecular sciences · 2022Review
- Developmental pathways linked to the vulnerability of adult midbrain dopaminergic neurons to neurodegeneration.Frontiers in molecular neuroscience · 2022Review
- Pathogenic LRRK2 control of primary cilia and Hedgehog signaling in neurons and astrocytes of mouse brain.eLife · 2021Article
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Authors and funding
10 authors.
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Abstract
L-Dopa induced dyskinesia (LID) is a debilitating side effect of dopamine replacement therapy for Parkinson's Disease. The mechanistic underpinnings of LID remain obscure. Here we report that diminished sonic hedgehog (Shh) signaling in the basal ganglia caused by the degeneration of midbrain dopamine neurons facilitates the formation and expression of LID. We find that the pharmacological activation of Smoothened, a downstream effector of Shh, attenuates LID in the neurotoxic 6-OHDA- and genetic aphakia mouse models of Parkinson's Disease. Employing conditional genetic loss-of-function approaches, we show that reducing Shh secretion from dopamine neurons or Smoothened activity in cholinergic interneurons promotes LID. Conversely, the selective expression of constitutively active Smoothened in cholinergic interneurons is sufficient to render the sensitized aphakia model of Parkinson's Disease resistant to LID. Furthermore, acute depletion of Shh from dopamine neurons through prolonged optogenetic stimulation in otherwise intact mice and in the absence of L-Dopa produces LID-like involuntary movements. These findings indicate that augmenting Shh signaling in the L-Dopa treated brain may be a promising therapeutic approach for mitigating the dyskinetic side effects of long-term treatment with L-Dopa.
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