Affordable Access

deepdyve-link
Publisher Website

The distribution of calbindin-D28k, parvalbumin, and calretinin immunoreactivity in the inferior colliculus of circling mouse.

Authors
  • Lee, Jin-Koo1
  • Kim, Myeung Ju2
  • 1 Department of Pharmacology, Dankook University College of Medicine, Cheonan, Korea. , (North Korea)
  • 2 Department of Anatomy, Dankook University College of Medicine, Cheonan, Korea. , (North Korea)
Type
Published Article
Journal
Anatomy & cell biology
Publication Date
Sep 01, 2017
Volume
50
Issue
3
Pages
230–238
Identifiers
DOI: 10.5115/acb.2017.50.3.230
PMID: 29043102
Source
Medline
Keywords
License
Unknown

Abstract

The circling mice with tmie gene mutation are known as an animal deafness model, which showed hyperactive circling movement. Recently, the reinvestigation of circling mouse was performed to check the inner ear pathology as a main lesion of early hearing loss. In this trial, the inner ear organs were not so damaged to cause the hearing deficit of circling (cir/cir) mouse at 18 postnatal day (P18) though auditory brainstem response data indicated hearing loss of cir/cir mice at P18. Thus, another mechanism may be correlated with the early hearing loss of cir/cir mice at P18. Hearing loss in the early life can disrupt the ascending and descending information to inferior colliculus (IC) as integration site. There were many reports that hearing loss could result in the changes in Ca2+ concentration by either cochlear ablation or genetic defect. However, little was known to be reported about the correlation between the pathology of IC and Ca2+ changes in circling mice. Therefore, the present study investigated the distribution of calcium-binding proteins (CaBPs), calbindin-D28k, parvalbumin, and calretinin immunoreactivity (IR) in the IC to compare among wild-type (+/+), heterozygous (+/cir), and homozygous (cir/cir) mice by immunohistochemistry. The decreases of CaBPs IR in cir/cir were statistically significant in the neurons as well as neuropil of IC. Thus, this study proposed overall distributional alteration of CaBPs IR in the IC caused by early hearing defect and might be helpful to elucidate the pathology of central auditory disorder related with Ca2+ metabolism.

Report this publication

Statistics

Seen <100 times