FIBROBLAST GROWTH FACTOR-2-LIKE IMMUNOREACTIVITY IN AUDITORY BRAIN-STEM NUCLEI OF THE DEVELOPING AND ADULT-RAT - CORRELATION WITH ONSET ANDLOSS OF HEARING

Citation
E. Riedel et al., FIBROBLAST GROWTH FACTOR-2-LIKE IMMUNOREACTIVITY IN AUDITORY BRAIN-STEM NUCLEI OF THE DEVELOPING AND ADULT-RAT - CORRELATION WITH ONSET ANDLOSS OF HEARING, Journal of comparative neurology, 354(3), 1995, pp. 353-360
Citations number
65
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
354
Issue
3
Year of publication
1995
Pages
353 - 360
Database
ISI
SICI code
0021-9967(1995)354:3<353:FGFIIA>2.0.ZU;2-N
Abstract
Fibroblast growth factor-2 (FGF-2; basic FGF) is widely distributed in the developing and adult brain and has numerous effects on cultured a nd lesioned neural cells. The physiological role of FGF-2 in the unles ioned nervous system, however, is still not understood. We have studie d 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 immunor eactivity (FGF-2-IR) occurred in neuronal cell bodies and/or nerve fib ers but was very rarely observed in glial cells. Several auditory brai nstem nuclei, including the superior paraolivary nucleus, the medial s uperior olive, the lateral and ventral trapezoid nuclei, and the centr al 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. Neuro ns in the medial geniculate body exhibited FGF-2-IR only transiently, from postnatal day (P) 5 until P16. Neurons in the medial nucleus of t he trapezoid body were immunoreactive from P8 onwards. FGF-2-IR in ant eroventral 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 c ommences was observed in the dorsal cortex of the inferior colliculus. Thus, regulation of neuronal FGF-2-IR in several, but not all, audito ry 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 medi al 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. (C) 1995 Wiley-Liss, Inc.