Plasticity of the auditory brainstem: Cochleotomy-induced changes of calbindin-D28k expression in the rat

Citation
Cr. Forster et Rb. Illing, Plasticity of the auditory brainstem: Cochleotomy-induced changes of calbindin-D28k expression in the rat, J COMP NEUR, 416(2), 2000, pp. 173-187
Citations number
54
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF COMPARATIVE NEUROLOGY
ISSN journal
00219967 → ACNP
Volume
416
Issue
2
Year of publication
2000
Pages
173 - 187
Database
ISI
SICI code
0021-9967(20000110)416:2<173:POTABC>2.0.ZU;2-3
Abstract
Calbindin is a calcium binding protein that is characteristically expressed in several auditory brainstem nuclei during ontogeny and is thought to ser ve as a buffer, protecting cells against toxic levels of calcium. Upon matu ration, calbindin is drastically reduced or entirely lost in many auditory nuclei. We made cochleotomies in mature rats to study effects of deafening and deafferentation on the expression of calbindin in the auditory brainste m. Following unilateral cochleotomy, we observed a substantial increase in the number of calbindin-immunoreactive fibers and boutons in the ventral su bdivisions of the ipsilateral cochlear nucleus. At the same time, calbindin -positive astrocytes emerged in the dorsal and ventral cochlear nucleus. Be yond the immediately affected ipsilateral cochlear nucleus, we found calbin din-positive neurons in the lateral superior olive and in the central infer ior colliculus, both contralateral to the operation. The loss of one cochle a reduces auditory input and puts the flow of neuronal activity originating in the two ears out of balance. Our findings indicate that the need for th e neuronal networks in the auditory brainstem to adjust to this drastically changed pattern of sensory signals invokes the expression of calbindin in glial cells as well as in directly and indirectly affected neuronal cell po pulations. J. Comp. Neurol. 416:173-187, 2000. (C) 2000 Wiley-Liss, Inc.