Changes in glycine immunoreactivity in the rat superior olivary complex following deafness
The balance between inhibitory and excitatory amino acid neurotransmitters contributes to the control of normal functioning of the auditory brainstem. Changes in the level of neuronal activity within the auditory brainstem pathways influence the balance between inhibition and excitation. Activity‐de...
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Published in | Journal of comparative neurology (1911) Vol. 494; no. 1; pp. 179 - 189 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.01.2006
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Subjects | |
Online Access | Get full text |
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Summary: | The balance between inhibitory and excitatory amino acid neurotransmitters contributes to the control of normal functioning of the auditory brainstem. Changes in the level of neuronal activity within the auditory brainstem pathways influence the balance between inhibition and excitation. Activity‐dependent plasticity in the auditory pathways can be studied by creating a large decrease in activity through peripheral deafening. Deafness‐related decreases in GABA have previously been shown in the inferior colliculus. However, glycine is a more prevalent inhibitory transmitter in the mature superior olivary complex (SOC). The present study therefore examined if there were deafness‐related changes in glycine in the SOC using postembedding immunocytochemistry. Animals were bilaterally deafened by an intrascalar injection of neomycin. Five nuclei in the SOC, the lateral superior olive (LSO), superior paraolivary nucleus (SPoN), and the medial, lateral, and ventral nuclei of the trapezoid body (MNTB, LNTB, and VNTB) were examined 14 days following the deafening and compared to normal hearing age‐matched controls. The LSO and SPoN were divided into high and low frequency regions. The number of glycine immunoreactive puncta on the somata of principal cells showed significant decreases in all regions assessed, with changes ranging from 50% in the VNTB to 23% in the LSO. J. Comp. Neurol. 494:179–189, 2006. © 2005 Wiley‐Liss, Inc. |
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Bibliography: | ArticleID:CNE20795 istex:AF97CA88CBB26102D00B32466A518F88F429A63B ark:/67375/WNG-91Q2Q67W-N National Institutes of Health/National Institute on Deafness and Other Communication Disorders - No. DC00383; No. NIH-1F32GM013553; No. NIH-P30 DC05188 The first two authors contributed equally to the study. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.20795 |