ArticleFrontiers in cellular neuroscience2013
A role for the canonical nuclear factor-κB pathway in coupling neurotrophin-induced differential survival of developing spiral ganglion neurons.
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Protective effect of adenovirus-mediated erythropoietin expression on the spiral ganglion neurons in the rat inner ear.International journal of molecular medicine · 2018Article
- High mobility group box 1 (HMGB1): dual functions in the cochlear auditory neurons in response to stress?Histochemistry and cell biology · 2017Article
- Morphometrical Analysis of Developing Cochlear Ganglion Neurons: A Light Microscopic Fetal Study.Journal of clinical and diagnostic research : JCDR · 2015Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
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Abstract
Neurotrophins are key players of neural development by controlling cell death programs. However, the signaling pathways that mediate their selective responses in different populations of neurons remain unclear. In the mammalian cochlea, sensory neurons differentiate perinatally into type I and II populations both expressing TrkB and TrkC, which bind respectively brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3). How these two neuronal populations respond differentially to these two neurotrophins remains unknown. Here, we report in rat the segregation of the nuclear factor-κB (NFκB) subunit p65 specifically within the type II population postnatally. Using dissociated cultures of embryonic and postnatal spiral ganglion neurons, we observed a specific requirement of NFκB for BDNF but not NT3-dependent neuronal survival during a particular postnatal time window that corresponds to a period of neuronal cell death and hair cell innervation refinement in the developing cochlea. Consistently, postnatal p65 knockout mice showed a specific decreased number in type II spiral ganglion neurons. Taken together, these results identify NFκB as a type II neuron-specific factor that participates in the selective survival effects of BDNF and NT3 signaling on developing spiral ganglion neurons.
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