ArticleCell reports2017
Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRα1 or RET Impairs Normal Cerebellar Motor Learning.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases.Experimental neurobiology · 2025Review
- GDNF receptor GFRα1 is necessary for the maintenance of dopaminergic neurons in the adult substantia nigra.PloS one · 2025Article
- Revisiting the development of cerebellar inhibitory interneurons in the light of single-cell genetic analyses.Histochemistry and cell biology · 2024Review
- Increased understanding of complex neuronal circuits in the cerebellar cortex.Frontiers in cellular neuroscience · 2024Review
- The activation of mGluR4 rescues parallel fiber synaptic transmission and LTP, motor learning and social behavior in a mouse model of Fragile X Syndrome.Molecular autism · 2023Article
- Neonatal subarachnoid hemorrhage disrupts multiple aspects of cerebellar development.Frontiers in molecular neuroscience · 2023Article
- Long-term depression-inductive stimulation causes long-term potentiation in mouse Purkinje cells with a mutant thyroid hormone receptor.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GDNF Increases Inhibitory Synaptic Drive on Principal Neurons in the Hippocampus via Activation of the Ret Pathway.International journal of molecular sciences · 2022Article
- Dendritic Inhibition by Shh Signaling-Dependent Stellate Cell Pool Is Critical for Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Morphological pseudotime ordering and fate mapping reveal diversification of cerebellar inhibitory interneurons.Nature communications · 2022Article
- Adult medial habenula neurons require GDNF receptor GFRα1 for synaptic stability and function.PLoS biology · 2021Article
- Transcriptome programs involved in the development and structure of the cerebellum.Cellular and molecular life sciences : CMLS · 2021Review
- The γ-Protocadherins Regulate the Survival of GABAergic Interneurons during Developmental Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Molecular layer interneurons shape the spike activity of cerebellar Purkinje cells.Scientific reports · 2019Article
- Neonatal brain injury causes cerebellar learning deficits and Purkinje cell dysfunction.Nature communications · 2018Article
- HITS-CLIP in various brain areas reveals new targets and new modalities of RNA binding by fragile X mental retardation protein.Nucleic acids research · 2018Article
- Cell-autonomous role of GFRα1 in the development of olfactory bulb GABAergic interneurons.Biology open · 2018Article
- Loss-of-function mutation of c-Ret causes cerebellar hypoplasia in mice with Hirschsprung disease and Down's syndrome.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of neurotrophic factors as endogenous survival proteins for brain neurons remains contentious. In the cerebellum, the signals controlling survival of molecular layer interneurons (MLIs) are unknown, and direct evidence for the requirement of a full complement of MLIs for normal cerebellar function and motor learning has been lacking. Here, we show that Purkinje cells (PCs), the target of MLIs, express the neurotrophic factor GDNF during MLI development and survival of MLIs depends on GDNF receptors GFRα1 and RET. Conditional mutant mice lacking either receptor lose a quarter of their MLIs, resulting in compromised synaptic inhibition of PCs, increased PC firing frequency, and abnormal acquisition of eyeblink conditioning and vestibulo-ocular reflex performance, but not overall motor activity or coordination. These results identify an endogenous survival mechanism for MLIs and reveal the unexpected vulnerability and selective requirement of MLIs in the control of cerebellar-dependent motor learning.
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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.