ArticleNeural development2013
EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem.
Article in Neural development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Temporal patterns of gene expression during calyx of held development.Developmental neurobiology · 2016Article
- The extracellular matrix molecule brevican is an integral component of the machinery mediating fast synaptic transmission at the calyx of Held.The Journal of physiology · 2015Article
- Distribution of glial cells in the auditory brainstem: normal development and effects of unilateral lesion.Neuroscience · 2014Article
- Loss of EphB6 protein expression in human colorectal cancer correlates with poor prognosis.Journal of molecular histology · 2014Article
- Axon guidance in the auditory system: multiple functions of Eph receptors.Neuroscience · 2014Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
backgroundStudies of developmental plasticity may provide insight into plasticity during adulthood, when neural circuitry is less responsive to losses or changes in input. In the mammalian auditory brainstem, globular bushy cell axons of the ventral cochlear nucleus (VCN) innervate the contralateral medial nucleus of the trapezoid body (MNTB) principal neurons. VCN axonal terminations in MNTB, known as calyces of Held, are very large and specialized for high-fidelity transmission of auditory information. Following unilateral deafferentation during postnatal development, VCN axons from the intact side form connections with novel targets, including the ipsilateral MNTB. EphB signaling has been shown to play a role in this process during the first postnatal week, but mechanisms involved in this reorganization during later developmental periods remain unknown.
resultsWe found that EphB2 signaling reduces the number of induced ipsilateral projections to the MNTB after unilateral VCN removal at postnatal day seven (P7), but not after removal of the VCN on one side at P10, after the closure of the critical period for lesion-induced innervation of the ipsilateral MNTB.
conclusionsResults from this study indicate that molecular mechanisms involved in the development of circuitry may also play a part in rewiring after deafferentation during development, but do not appear to regulate the length of critical periods for plasticity.
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