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FGF‐9 is an autocrine/paracrine neurotrophic substance for spinal motoneurons
Author(s) -
Kanda Takashi,
Iwasaki Takayuki,
Nakamura Satoshi,
Ueki Akira,
Kurokawa Tsutomu,
Ikeda Kazuhiko,
Mizusawa Hidehiro
Publication year - 1999
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(99)00026-x
Subject(s) - autocrine signalling , paracrine signalling , neurotrophic factors , motor neuron , neurotrophin , ciliary neurotrophic factor , neuroscience , fibroblast growth factor , spinal cord , biology , medicine , cell culture , receptor , genetics
Motoneurons need muscle‐derived neurotrophic substances for their survival during the initial phase of their development, but after maturation they lose this requirement and can survive after axotomy. This suggests that some neurotrophic substances other than target‐derived ones control the survival of motoneurons in adults. Because spinal motoneurons express fibroblast growth factor‐9 (FGF‐9) messenger RNA, we hypothesized that FGF‐9 might be an autocrine or paracrine survival factor for motoneurons. FGF‐9 promoted the survival of motoneurons and upregulated the choline acetyltransferase (ChAT) activity in the dissociated cultures of ventral half of rat E13 spinal cord. Externally added FGF‐9 was more effective in low density cultures, and polyclonal blocking antibody against FGF‐9 significantly lowered the ChAT activity. Our results support an autocrine or paracrine role for FGF‐9 in mediating the survival of spinal motoneurons. Non‐target‐derived neurotrophic substances for motoneurons including FGF‐9 should be important in the pathogenesis of motor neuron disorders in the adults, especially amyotrophic lateral sclerosis.