ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Spinal glutamatergic neurons defined by EphA4 signaling are essential components of normal locomotor circuits.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Comment on Schwarz et al. "EFNB3 Frameshift Variant in Weimaraner Dogs with a Condition Resembling a Congenital Mirror Movement Disorder".Movement disorders : official journal of the Movement Disorder Society · 2025Article
- EPHA4 signaling dysregulation links abnormal locomotion and the development of idiopathic scoliosis.eLife · 2025Article
- Investigation of central pattern generators in the spinal cord of chicken embryos.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2024Article
- Ventricular Netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice.Cell death & disease · 2024Article
- Unraveling the Potential of EphA4: A Breakthrough Target and Beacon of Hope for Neurological Diseases.Cellular and molecular neurobiology · 2023Review
- An extended Hilbert transform method for reconstructing the phase from an oscillatory signal.Scientific reports · 2023Article
- PTPRD and DCC Are Novel BACE1 Substrates Differentially Expressed in Alzheimer's Disease: A Data Mining and Bioinformatics Study.International journal of molecular sciences · 2022Article
- Role of DSCAM in the Development of Neural Control of Movement and Locomotion.International journal of molecular sciences · 2021Review
- Review
- Natural loss of function of ephrin-B3 shapes spinal flight circuitry in birds.Science advances · 2021Article
- EphA4 Is Required for Neural Circuits Controlling Skilled Reaching.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Regeneration ThroughFrontiers in cellular neuroscience · 2020Review
- Roles of axon guidance molecules in neuronal wiring in the developing spinal cord.Nature reviews. Neuroscience · 2019Review
- Abnormal Pyramidal Decussation and Bilateral Projection of the Corticospinal Tract Axons in Mice Lacking the Heparan Sulfate Endosulfatases, Sulf1 and Sulf2.Frontiers in molecular neuroscience · 2019Article
- Pituitary Adenylate Cyclase-Activating Polypeptide-27 (PACAP-27) in the Thalamic Paraventricular Nucleus Is Stimulated by Ethanol Drinking.Alcoholism, clinical and experimental research · 2018Article
- Age- and speed-dependent modulation of gaits in DSCAMJournal of neurophysiology · 2018Article
- Diversity of molecularly defined spinal interneurons engaged in mammalian locomotor pattern generation.Journal of neurophysiology · 2017Review
- Offspring genes indirectly influence sibling and maternal behavioural strategies over resource share.Proceedings. Biological sciences · 2017Article
- Spinal RacGAP α-Chimaerin Is Required to Establish the Midline Barrier for Proper Corticospinal Axon Guidance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Non cell-autonomous role of DCC in the guidance of the corticospinal tract at the midline.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EphA4 signaling is essential for the spatiotemporal organization of neuronal circuit formation. In mice, deletion of this signaling pathway causes aberrant midline crossing of axons from both brain and spinal neurons and the complete knock-outs (KOs) exhibit a pronounced change in motor behavior, where alternating gaits are replaced by a rabbit-like hopping gait. The neuronal mechanism that is responsible for the gait switch in these KO mice is not known. Here, using intersectional genetics, we demonstrate that a spinal cord-specific deletion of EphA4 signaling is sufficient to generate the overground hopping gait. In contrast, selective deletion of EphA4 signaling in forebrain neurons, including the corticospinal tract neurons, did not result in a change in locomotor pattern. The gait switch was attributed to the loss of EphA4 signaling in excitatory Vglut2+ neurons, which is accompanied by an increased midline crossing of Vglut2+ neurons in the ventral spinal cord. Our findings functionally define spinal EphA4 signaling in excitatory Vglut2+ neurons as required for proper organization of the spinal locomotor circuitry, and place these cells as essential components of the mammalian locomotor network.
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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.