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Mice lacking brain-derived neurotrophic factor develop with sensory deficits
Abstract
During vertebrate development, neuronal survival depends on target-derived neurotrophic factors. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, can prevent the death of particular peripheral sensory neurons in vitro, and of central motor neurons as well as dopaminergic and cholinergic neurons of the basal forebrain during development. It also prevents the death of motor neurons and midbrain dopaminergic neurons induced by lesions. Here we show that mutant mice lacking BDNF have severe deficiencies in coordination and balance, associated with excessive degeneration in several sensory ganglia including the vestibular ganglion. The few remaining vestibular axons fail to contact the vestibular sensory epithelia, and terminate in the adjacent connective tissue. Survival of sympathetic, midbrain dopaminergic and motor neurons is not affected. These results indicate that BDNF is required for the survival and target innervation of particular neuronal populations.
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“In vivo evidences also support the critical role of BDNF in plasticity. In particular, mutation studies have demonstrated the role of this neurotrophin in structural and synaptic plasticity.”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Ernfors et al. 1994
In the citing paper
“Total BDNF deficiency is lethal and most of the mice lacking BDNF die during the second postnatal week (Ernfors et al. 1994).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Ernfors et al. 1994
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Metadata
- Authors
- Ernfors, P., Lee, K.-F., & Jaenisch, R.
- Affiliations
- Whitehead Institute for Biomedical Research (US)
- Venue
- Nature
- Published
- 1994-03
- Volume
- 368
- Issue
- 6467
- Pages
- 147-150
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2076894554
- Cited by
- 1,067
- References
- 22
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 10 · 2023: 19 · 2022: 14 · 2021: 22 · 2020: 33 · 2019: 20 · 2018: 27 · 2017: 15 · 2016: 20 · 2015: 26 · 2014: 28 · 2013: 25 · 2012: 40
- FWCI
- 25.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- brain-derived neurotrophic factor, BDNF knockout mice, sensory neuron survival, motor neuron survival, dopaminergic neurons, sympathetic neurons, neurotrophins
- MeSH terms
- Animals, Animals, Newborn, Cell Line, Embryo, Mammalian, Embryonic and Fetal Development, Ganglia, Ear, Inner, Mice, Inbred BALB C, Mice, Mutant Strains, Movement Disorders, Mutation, Nerve Tissue Proteins, Nervous System, Neurons, Afferent, Stem Cells, Cell Death, Peripheral Nervous System, Brain-Derived Neurotrophic Factor, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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