Influence of neonatal cochlear removal on the development of mouse cochlear nucleus: I. Number, size, and density of its neurons

TLDR

The study aimed to determine how removal of the right cochlea in 6‑day‑old mice affects cochlear nucleus development. Cochleae were aspirated from 6‑day‑old mice, confirmed destroyed at 45 days, and the cochlear nuclei of deafferented and control animals were morphometrically analyzed. Deafferentation before hearing onset caused widespread reductions in cochlear nucleus size and neuronal number—down to 46 % of normal size and 34 % of normal neurons—along with layer‑specific decreases in volume, neuron count, and size, supporting a critical developmental period for presynaptic integrity.

Abstract

Abstract Right cochleae were aspirated from 6‐day‐old mice to determine the influence of cochlear integrity on the development of cochlear nucleus (CN). At 45 days of age, cochlear destruction was confirmed histologically, and the CN of unilaterally deafferented and control animals were analyzed morphometrically. The molecular, fusiform, and polymorphic layers of deafferented dorsal CN were reduced in volume, and the polymorphic layer neurons were fewer, smaller, and less dense. The octopus and multipolar cell regions in deafferented ventral CN (VCN) were smaller, and their neurons were fewer, smaller, and more densely packed. The VCN globular and small spherical cell regions were also smaller with fewer, denser, but normal‐sized neurons. There were fewer VCN large spherical cells, but no change was measured in their size. The granule cell regions throughout CN were also reduced in volume. Overall, CN was reduced to 46% of its normal size and 34% of its normal neuronal numbers. These results in the mouse show that deafferentation before the onset of hearing causes more severe CN changes than those reported after adult deafferentation in other mammals and support the theory of a critical period in development when presynaptic integrity is much more important for neuronal maturation than it is for maintenance after the neuron is mature. This suggests that any congenital pathology that compromises the sensorineural structures of the cochlea may cause severe structural and functional abnormalities in the maturing central auditory nuclei.