S. Ueda et al., NEURO-GLIAL NEUROTROPHIC INTERACTION IN THE S-100-BETA RETARDED MUTANT MOUSE (POLYDACTYLY-NAGOYA) .2. COCULTURES STUDY, Brain research, 633(1-2), 1994, pp. 284-288
The homozygote of a mouse strain with genetic polydactyly (Polydactyly
Nagoya, Pdn) shows several brain abnormalities, and significant decre
ase of S-100 beta in the brain [17]. An accompanying paper [18] demons
trates that the hippocampus and caudo-dorsal cortex of homozygote (Pdn
/Pdn) mouse were markedly reduced in S-100 beta positive astrocytes an
d serotonergic fibers, and the content of 5-HT and 5-HIAA of hippocamp
us and cortex of Pdn/Pdn mouse was lower than those of heterozygote (P
dn/+) or wild type (+/+) mice. To further clarify the effects of targe
t tissues from different type brains on the development of serotonergi
c neurons, raphe neurons from Pdn/Pdn or +/+ newborn mice were co-cult
ured with hippocampus or cortex of +/+ or Pdn/Pdn newborn mice. The gr
owth of the serotonergic neurons in the mesencephalic raphe tissue dis
sociated cultures was estimated by measuring the specific uptake of [H
-3]5-HT. The development of both genotypes (Pdn/Pdn and +/+) of seroto
nergic neurons was enhanced by co-cultures with target tissues (hippoc
ampus and cortex) of +/+ brain. This effect was not observed in the co
-cultures with Pdn/Pdn brain as a source of target tissue. The present
results support the idea that the developmental defect of serotonergi
c fibers in the Pdn mutant mouse is caused by the deficiency of S-100
beta in the astrocyte of this mutant, and suggest that S-100 beta is a
serotonergic growth factor. This mutant mouse is a useful in vivo mod
el to study neural-glial neurotrophic interactions.