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Fibroblast growth factor‐2‐like immunoreactivity in auditory brainstem nuclei of the developing and adult rat: Correlation with onset and loss of hearing
Author(s) -
Riedel Bettina,
Friauf Eckhard,
Grothe Claudia,
Unsicker Klaus
Publication year - 1995
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903540305
Subject(s) - inferior colliculus , lateral lemniscus , superior olivary complex , biology , trapezoid body , medial geniculate body , brainstem , cochlear nucleus , auditory cortex , neuroscience , dorsal cochlear nucleus , nucleus , anatomy , auditory system
Fibroblast growth factor‐2 (FGF‐2; basic FGF) is widely distributed in the developing and adult brain and has numerous effects on cultured and lesioned neural cells. The physiological role of FGF‐2 in the unlesioned nervous system, however, is still not understood. We have studied the distribution of FGF‐2 in the developing, adult, and functionally impaired central auditory system of the rat using specific antibodies and peroxidase‐antiperoxidase immunocytochemistry. FGF‐2‐like immunoreactivity (FGF‐2‐IR) occurred in neuronal cell bodies and/or nerve fibers but was very rarely observed in glial cells. Several auditory brainstem nuclei, including the superior paraolivary nucleus, the medial superior olive, the lateral and ventral trapezoid nuclei, and the central nucleus, as well as the external cortex of the inferior colliculus, were entirely devoid of FGF‐2‐IR. In the dorsal cochlear nucleus, the lateral superior olive, and the nuclei of the lateral lemniscus, FGF‐2‐IR was not detectable in nerve cell bodies prior to adult age. Neurons in the medial geniculate body exhibited FGF‐2‐IR only transiently, from postnatal day (P) 5 until P16. Neurons in the medial nucleus of the trapezoid body were immunoreactive from P8 onwards. FGF‐2‐IR in anteroventral and posteroventral cochlear neurons disappeared at P14, i. e., at the onset of hearing, but immunoreactivity returned after P21. A transient expression of FGF‐2 around the time when hearing function commences was observed in the dorsal cortex of the inferior colliculus. Thus, regulation of neuronal FGF‐2‐IR in several, but not all, auditory, nuclei is related to the onset of hearing, in that IR disappears at that time or transiently appears. This suggests a causal link between the onset of hearing and FGF‐2 expression. In support of this notion, ototoxic treatment with gentamycin abolished FGF‐2‐IR in the P16 medial geniculate body but not in other auditory brainstem centers. Thus, FGF‐2 may be considered a regulator or indicator of the acquisition of functional activity and responsiveness to sensory stimuli in several areas of the auditory system. © 1995 Wiley‐Liss, Inc.