ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2006
Neurotrophin-3 ameliorates sensory-motor deficits in Er81-deficient mice.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed, 10 citations in OpenAlex.
- The Role of Pea3 Transcription Factor Subfamily in the Nervous System.Molecular neurobiology · 2025Review
- Molecular mechanisms underlying monosynaptic sensory-motor circuit development in the spinal cord.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Review
- Etv1 inactivation reveals proprioceptor subclasses that reflect the level of NT3 expression in muscle targets.Neuron · 2013Article
- Mechanisms regulating the specificity and strength of muscle afferent inputs in the spinal cord.Annals of the New York Academy of Sciences · 2010Article
- Permanent reorganization of Ia afferent synapses on motoneurons after peripheral nerve injuries.Annals of the New York Academy of Sciences · 2010Article
- Prenatal exposure to elevated NT3 disrupts synaptic selectivity in the spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Two factors, the ETS transcription factor ER81 and skeletal muscle-derived neurotrophin-3 (NT3), are essential for the formation of muscle spindles and the function of spindle afferent-motoneuron synapses in the spinal cord. Spindles either degenerate completely or are abnormal, and spindle afferents fail to project to spinal motoneurons in Er81 null mice; however, the interactions between ER81 and NT3 during the processes of afferent neuron and muscle spindle development are poorly understood. To examine if overexpression of NT3 in muscle rescues spindles and afferent-motoneuron connectivity in the absence of ER81, we generated myoNT3;Er81(-/-) double-mutant mice that selectively overexpress NT3 in muscle in the absence of ER81. Spindle reflex arcs in myoNT3;Er81(-/-) mutants differed greatly from Er81 null mice. Muscle spindle densities were greater and more afferents projected into the ventral spinal cord in myoNT3;Er81(-/-) mice. Spindles of myoNT3;Er81(-/-) muscles responded normally to repetitive muscle taps, and the monosynaptic inputs from Ia afferents to motoneurons, grossly reduced in Er81(-/-) mutants, were restored to wild-type levels in myoNT3;Er81(-/-) mice. Thus, an excess of muscle-derived NT3 reverses deficits in spindle numbers and afferent function induced by the absence of ER81. We conclude that muscle-derived NT3 can modulate spindle density and afferent-motoneuron connectivity independently of ER81.
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