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