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Ephb2 Signaling Regulates Lesion-Induced Axon Sprouting but Not Critical Period Length in the Postnatal Auditory Brainstem

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Ephb2 Signaling Regulates Lesion-Induced Axon Sprouting but Not Critical Period Length in the Postnatal Auditory Brainstem UC Irvine UC Irvine Previously Published Works Title EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem Permalink https://escholarship.org/uc/item/8bq9r9wj Journal Neural Development, 8(1) ISSN 1749-8104 Authors Nakamura, Paul A Cramer, Karina S Publication Date 2013 DOI 10.1186/1749-8104-8-2 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Nakamura and Cramer Neural Development 2013, 8:2 http://www.neuraldevelopment.com/content/8/1/2 RESEARCH ARTICLE Open Access EphB2 signaling regulates lesion-induced axon sprouting but not critical period length in the postnatal auditory brainstem Paul A Nakamura and Karina S Cramer* Abstract Background: Studies 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. Results: We 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. Conclusions: Results 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. Keywords: MNTB, auditory, brainstem, axon guidance, deafferentation, regeneration Background differences, critical cues for sound source localization Development marks a period of remarkable plasticity [12-16]. In this study we used the VCN-MNTB pathway and circuit malleability. Neural circuitry is most suscep- as a model to study lesion-induced structural plasticity tible to changes in input during developmental critical during postnatal development. The projection from periods when connections display the most profound VCN to MNTB is well characterized and VCN calyceal functional and structural responses to changes in input terminations in the MNTB are easily identifiable and [1-8]. Axons of globular bushy cells in the ventral quantifiable because of their large size. Moreover, because cochlear nucleus (VCN) project contralaterally to the the VCN-MNTB pathway is normally strictly contralateral, medial nucleus of the trapezoid body (MNTB) in the lesion-induced aberrant ipsilateral projections are readily mammalian auditory brainstem. VCN axon terminals in observable [17-19]. the MNTB form large reticulated structures, known as During early postnatal development in rodents, the calyces of Held, which envelop MNTB principle neurons survival of VCN neurons is dependent on cochlear input. with multiple finger-like extensions [9-11]. This strictly Removal of the cochlea during the first postnatal week contralateral projection is an essential component of the results in substantial VCN cell death [20-22]. Following circuitry that computes interaural time and intensity early unilateral cochlea removal, axons from the intact VCN sprout novel projections directed at sites denervated by the lesion. Notably, under these conditions axons from * Correspondence: [email protected] Department of Neurobiology and Behavior and Center for the Neurobiology the intact VCN form calyces in both the ipsilateral and of Learning and Memory, University of California, Irvine, CA 92697, USA contralateral MNTB [23-25] and the emergence of the © 2013 Nakamura and Cramer; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Nakamura and Cramer Neural Development 2013, 8:2 Page 2 of 11 http://www.neuraldevelopment.com/content/8/1/2 ipsilateral projection coincides with maturation of the removal during the first few days of postnatal life normal contralateral projection [23,26,27]. In contrast, [19,25]. Here we sought to determine whether these cochlea removal after the first postnatal week does not molecules similarly affect the level of VCN-MNTB induce these novel projections, likely reflecting the structural plasticity at later ages following direct removal survival of VCN neurons after deafferentation at later of the cochlear nucleus. Additionally, we tested whether ages [17,21,22,28,29]. the function of these molecules affects the length of While this lesion-induced sprouting of VCN neurons the developmental critical period for lesion-induced is observed only when the cochlea is removed before P7, innervation of the ipsilateral MNTB. it can be elicited at later ages by direct removal of the In this study we show that mice, like gerbils, show VCN. Significant ipsilateral calyceal projections from the induced projections to the ipsilateral MNTB after cochlear intact VCN to the denervated MNTB were observed in nucleus lesions, but that the critical period for lesion- gerbils following unilateral cochlear nucleus lesions induced projections is more limited in mice than in gerbils. created at P10 to 15; these induced projections were We found that EphB2 mutant mice have more induced comparable to those seen with cochlea removal at P2 ipsilateral calyces in the MNTB than wild type mice [17]. Induced ipsilateral projections persisted with P25 after unilateral VCN removal at P7, which is similar to lesions, although the number of induced projections their effect after early cochlea removal. Lesions per- declined significantly compared to the earlier ages. These formed at later times showed that wild type mice and experiments suggest a limited developmental critical period mutants had similar critical period length, suggesting during which intact VCN axons are competent to that the extent of lesion-induced sprouting and the make new ipsilateral MNTB projections in response to length of the critical period for this reorganization are deafferentation of the MNTB. They further demonstrate regulated by independent factors. the formation of new VCN-MNTB projections after the normal contralateral projections are relatively mature. In Results gerbils, this critical period extends beyond that of deaffer- EphB2 expression at postnatal ages entation-induced cell death in the VCN [21,29] and beyond Before performing cochlear nucleus removal (CNR), we hearing onset. first tested EphB2 expression in the VCN-MNTB pathway Factors that regulate the extent of lesion-induced at later postnatal ages, as relative Eph protein expression sprouting in the VCN-MNTB pathway and its restriction patterns at the time of lesion formation have been shown to a limited postnatal period are incompletely under- to be correlated with lesion-induced reorganization [19,25]. stood. Candidate molecules include the Eph receptor At P7, EphB2 was expressed in the VCN (asterisk, tyrosine kinases and their ephrin ligands, which have Figure 1A) and MNTB (n = 4, Figure 1B), consistent significant roles in axon guidance and synapse formation with previously published results [19,38]. We confirmed [30,31]. The receptors represent the largest family of this pattern of expression using X-gal histochemistry on receptor tyrosine kinases and are divided into two EphB2lacZ/lacZ transgenic mice and found staining similar classes based on sequence homology. EphA receptors to the immunohistochemical results (n = 2); staining was bind to ephrin-A ligands, while EphB receptors bind to observed in the VCN (asterisk, Figure 1C) and in the ephrin-B ligands. While promiscuous binding is seen calyces of Held (Figure 1D). Interestingly, with this within classes, limited cross-talk between classes arises assay, in addition to calyceal expression we noted stain- from EphA4 binding to ephrin-B ligands [32] and EphB2 ing in axons near and in the MNTB (Figure 1D-E), but binding to ephrin-A5 [33]. Eph/ephrin interactions can no axonal expression at the midline (Figure 1E), where promote axon repulsion or attraction, depending on several VCN axons cross to the contralateral MNTB, nor in the factors including total concentration [34]. Significantly, VCN axons in the ventral acoustic stria near the VCN the ligands are associated with cell membranes through a (Figure 1F-G), where axons from the VCN on both sides glycosyl phosphatidyl inositol linkage (ephrin-A’s) or a do not cross each other. transmembrane domain (ephrin-B’s), so that interactions At P10 we found that EphB2 was expressed in the with Eph receptors generally require cell contact. Moreover, VCN (asterisk, Figure 2A) and calyces of Held (n = 4, these ligands permit reverse signaling, in which Eph recep-
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