Presbyacusis and calcium-binding protein immunoreactivity in the cochlear nucleus of BALB/c mice.
The BALB/c mouse is an established model for the early development of sensorineural hearing loss, and is homozygous for the Ahl allele (age-related hearing loss). The present study was designed to determine how auditory peripheral pathology influences calcium-binding protein immunoreactivity in the cochlear nucleus in aged BALB/c mice. To address this issue the loss of hair cells, spiral ganglion neurons (SGN), and neurons in the dorsal (DCN) and posteroventral (PVCN) cochlear nucleus of BALB/c mice at 1 and 24 months of age were quantified using CAST stereological methods. These values were then compared to the percent increase in immunopositive calcium-binding proteins in the cochlear nucleus. By 24 months of age there was a near complete loss of all outer hair cells (OHC). The inner hair cell (IHC) loss was near complete in the more apical and basal regions, while in the mid-regions approximately 50% were missing. The SGN in the apical and middle turns show a 20% loss (re: 1 month) and the basal turn up to 80% loss. A statistically significant decrease in the density of DCN and PVCN neurons (25%) was found at 24 months of age compared to the one month old animals. The percentage of parvalbumin and calretinin positive neurons in the DCN and the PVCN in relation to the density of Nissl stained neurons showed significant increases at 24 months compared to the 1 month old animals. We also determine the relationship between peripheral pathology and the percent increase in calcium-binding protein immunoreactivity. In the DCN, the percent increase of calretinin and parvalbumin was correlated to the loss of SGN, IHCs and OHCs. In the PVCN, parvalbumin was correlated to SGN, IHC, and OHC loss. The percent increase in calbindin immunoreactivity was not correlated to any peripheral pathology. The data here suggest a percent increase in calcium-binding protein immunoreactivity in the cochlea nucleus in the 24 month old mice may reflect an endogenous protective strategy that is designed to counteract calcium overload that is prominent during aging and degeneration. These results will be valuable for understanding the relationship among the peripheral and central auditory system in a model demonstrating a rapidly progressive presbyacusis.
Idrizbegovic
Esma
E
Department of Audiology Karolinska University Hospital, Stockholm, Sweden
Salman
Hazim
H
Niu
Xianzhi
X
Canlon
Barbara
B
D000375:Aging / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000032:analysis / Q000276:immunology / Q000378:metabolism*; D003056:Cochlear Nerve / Q000378:metabolism; D017626:Cochlear Nucleus / Q000166:cytology / Q000378:metabolism*; D005260:Female; D006198:Hair Cells, Auditory / Q000378:metabolism / Q000502:physiology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000166:cytology; D010320:Parvalbumins / Q000276:immunology / Q000378:metabolism; D011304:Presbycusis / Q000378:metabolism*; D064030:S100 Calcium Binding Protein G / Q000276:immunology / Q000378:metabolism; D013136:Spiral Ganglion / Q000166:cytology / Q000378:metabolism
C576511:Calb2 protein, mouse; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G