EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem

Karina S Cramer,Paul A Nakamura

doi:10.1186/1749-8104-8-2

Karina S Cramer, Paul A Nakamura

Open Access

https://doi.org/10.1186/1749-8104-8-2

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Journal: Neural Development	Publication Date: Jan 1, 2013
Citations: 58	License type: cc-by

Affiliation: University of California, Irvine

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.

Highlights

Studies of developmental plasticity may provide insight into plasticity during adulthood, when neural circuitry is less responsive to losses or changes in input
EphB2 expression at postnatal ages Before performing cochlear nucleus removal (CNR), we first tested EphB2 expression in the ventral cochlear nucleus (VCN)-medial nucleus of the trapezoid body (MNTB) pathway at later postnatal ages, as relative Eph protein expression patterns at the time of lesion formation have been shown to be correlated with lesion-induced reorganization [19,25]
With this assay, in addition to calyceal expression we noted staining in axons near and in the MNTB (Figure 1D-E), but no axonal expression at the midline (Figure 1E), where VCN axons cross to the contralateral MNTB, nor in the VCN axons in the ventral acoustic stria near the VCN (Figure 1F-G), where axons from the VCN on both sides do not cross each other

Summary

Introduction

Studies of developmental plasticity may provide insight into plasticity during adulthood, when neural circuitry is less responsive to losses or changes in input. Axons of globular bushy cells in the ventral cochlear nucleus (VCN) project contralaterally to the medial nucleus of the trapezoid body (MNTB) in the mammalian auditory brainstem. VCN axon terminals in the MNTB form large reticulated structures, known as calyces of Held, which envelop MNTB principle neurons with multiple finger-like extensions [9,10,11]. This strictly contralateral projection is an essential component of the circuitry that computes interaural time and intensity differences, critical cues for sound source localization [12,13,14,15,16]. Because the VCN-MNTB pathway is normally strictly contralateral, lesion-induced aberrant ipsilateral projections are readily observable [17,18,19]

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