4.5 Article

Upregulation of calretinin immunostaining in the ferret inferior colliculus after cochlear ablation

期刊

JOURNAL OF COMPARATIVE NEUROLOGY
卷 460, 期 4, 页码 585-596

出版社

WILEY
DOI: 10.1002/cne.10676

关键词

plasticity; hearing loss; calcium-binding proteins; axonal plexus; quantitative image analysis; immunohistochemistry

资金

  1. NIDCD NIH HHS [DC00813] Funding Source: Medline

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In many systems, including ascending auditory pathways, calcium-binding proteins are markers of specific neuronal circuits. Previous studies suggest that calretinin immunostaining may be a specific marker for circuits in the inferior colliculus (IC) that code timing information. We undertook experiments to determine the changes in calretinin immunostaining in the IC that take place in response to cochlear ablation. Cochlear ablation was performed unilaterally in ferrets just after hearing onset. Animals survived for 2-3 months after ablation and brains were then processed for calretinin immunocytochemistry. The mean optical density and stained area of the calretinin immunopositive plexus in the IC were determined for five coronal sections through the right and left IC. In controls (n = 3), measurements of these parameters in the central nucleus of the IC showed symmetry between the two sides. In experimental animals (n = 8) the calretinin immunopositive plexus contralateral to the cochlear ablation was denser and larger than that in either the ipsilateral IC or in the IC of control animals. The calretinin plexus in the ipsilateral IC was slightly less dense and smaller than in controls but the differences did not reach statistical significance. IC volume measurements and synaptophysin immunostaining analysis in the central nucleus of the IC revealed no statistical differences between ablated and control animals or between the two sides in ablated animals. The significant increase in both mean optical density and immunostained area of the calretinin plexus in the IC contralateral to the cochlear ablation may reflect an upregulation in calretinin expression in the nuclei that contribute to this plexus. (C) 2003 Wiley-Liss, Inc.

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