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Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB

Neurons in the superior olivary complex (SOC) integrate excitatory and inhibitory inputs to localize sounds in space. The majority of these inhibitory inputs have been thought to arise within the SOC from the medial nucleus of the trapezoid body (MNTB). However, recent work demonstrates that glycine...

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Autores principales: Altieri, Stefanie C., Zhao, Tianna, Jalabi, Walid, Maricich, Stephen M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162373/
https://www.ncbi.nlm.nih.gov/pubmed/25309335
http://dx.doi.org/10.3389/fncir.2014.00109
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author Altieri, Stefanie C.
Zhao, Tianna
Jalabi, Walid
Maricich, Stephen M.
author_facet Altieri, Stefanie C.
Zhao, Tianna
Jalabi, Walid
Maricich, Stephen M.
author_sort Altieri, Stefanie C.
collection PubMed
description Neurons in the superior olivary complex (SOC) integrate excitatory and inhibitory inputs to localize sounds in space. The majority of these inhibitory inputs have been thought to arise within the SOC from the medial nucleus of the trapezoid body (MNTB). However, recent work demonstrates that glycinergic innervation of the SOC persists in Egr2; En1(CKO) mice that lack MNTB neurons, suggesting that there are other sources of this innervation (Jalabi et al., 2013). To study the development of MNTB- and non-MNTB-derived glycinergic SOC innervation, we compared immunostaining patterns of glycine transporter 2 (GlyT2) at several postnatal ages in control and Egr2; En1(CKO) mice. GlyT2 immunostaining was present at birth (P0) in controls and reached adult levels by P7 in the superior paraolivary nucleus (SPN) and by P12 in the lateral superior olive (LSO). In Egr2; En1(CKO) mice, glycinergic innervation of the LSO developed at a similar rate but was delayed by one week in the SPN. Conversely, consistent reductions in the number of GlyT2(+) boutons located on LSO somata were seen at all ages in Egr2; En1(CKO) mice, while these numbers reached control levels in the SPN by adulthood. Dendritic localization of GlyT2+ boutons was unaltered in both the LSO and SPN of adult Egr2; En1(CKO) mice. On the postsynaptic side, adult Egr2; En1(CKO) mice had reduced glycine receptor α1 (GlyRα1) expression in the LSO but normal levels in the SPN. GlyRα2 was not expressed by LSO or SPN neurons in either genotype. These findings contribute important information for understanding the development of MNTB- and non-MNTB-derived glycinergic pathways to the mouse SOC.
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spelling pubmed-41623732014-10-10 Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB Altieri, Stefanie C. Zhao, Tianna Jalabi, Walid Maricich, Stephen M. Front Neural Circuits Neuroscience Neurons in the superior olivary complex (SOC) integrate excitatory and inhibitory inputs to localize sounds in space. The majority of these inhibitory inputs have been thought to arise within the SOC from the medial nucleus of the trapezoid body (MNTB). However, recent work demonstrates that glycinergic innervation of the SOC persists in Egr2; En1(CKO) mice that lack MNTB neurons, suggesting that there are other sources of this innervation (Jalabi et al., 2013). To study the development of MNTB- and non-MNTB-derived glycinergic SOC innervation, we compared immunostaining patterns of glycine transporter 2 (GlyT2) at several postnatal ages in control and Egr2; En1(CKO) mice. GlyT2 immunostaining was present at birth (P0) in controls and reached adult levels by P7 in the superior paraolivary nucleus (SPN) and by P12 in the lateral superior olive (LSO). In Egr2; En1(CKO) mice, glycinergic innervation of the LSO developed at a similar rate but was delayed by one week in the SPN. Conversely, consistent reductions in the number of GlyT2(+) boutons located on LSO somata were seen at all ages in Egr2; En1(CKO) mice, while these numbers reached control levels in the SPN by adulthood. Dendritic localization of GlyT2+ boutons was unaltered in both the LSO and SPN of adult Egr2; En1(CKO) mice. On the postsynaptic side, adult Egr2; En1(CKO) mice had reduced glycine receptor α1 (GlyRα1) expression in the LSO but normal levels in the SPN. GlyRα2 was not expressed by LSO or SPN neurons in either genotype. These findings contribute important information for understanding the development of MNTB- and non-MNTB-derived glycinergic pathways to the mouse SOC. Frontiers Media S.A. 2014-09-12 /pmc/articles/PMC4162373/ /pubmed/25309335 http://dx.doi.org/10.3389/fncir.2014.00109 Text en Copyright © 2014 Altieri, Zhao, Jalabi and Maricich. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Altieri, Stefanie C.
Zhao, Tianna
Jalabi, Walid
Maricich, Stephen M.
Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title_full Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title_fullStr Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title_full_unstemmed Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title_short Development of glycinergic innervation to the murine LSO and SPN in the presence and absence of the MNTB
title_sort development of glycinergic innervation to the murine lso and spn in the presence and absence of the mntb
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162373/
https://www.ncbi.nlm.nih.gov/pubmed/25309335
http://dx.doi.org/10.3389/fncir.2014.00109
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