Neuro-glial neurotrophic interaction in the S-100 beta retarded mutant mouse (Polydactyly Nagoya). II. Co-cultures study.
The homozygote of a mouse strain with genetic polydactyly (Polydactyly Nagoya, Pdn) shows several brain abnormalities, and significant decrease of S-100 beta in the brain [17]. An accompanying paper [18] demonstrates that the hippocampus and caudo-dorsal cortex of homozygote (Pdn/Pdn) mouse were markedly reduced in S-100 beta positive astrocytes and serotonergic fibers, and the content of 5-HT and 5-HIAA of hippocampus and cortex of Pdn/Pdn mouse was lower than those of heterozygote (Pdn/+) or wild type (+/+) mice. To further clarify the effects of target tissues from different type brains on the development of serotonergic neurons, raphe neurons from Pdn/Pdn or +/+ newborn mice were co-cultured with hippocampus or cortex of +/+ or Pdn/Pdn newborn mice. The growth of the serotonergic neurons in the mesencephalic raphe tissue dissociated cultures was estimated by measuring the specific uptake of [3H]5-HT. The development of both genotypes (Pdn/Pdn and +/+) of serotonergic neurons was enhanced by co-cultures with target tissues (hippocampus 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 serotonergic 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 model to study neural-glial neurotrophic interactions.
Ueda
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S
Department of Biology, New York University, NY 10003.
Hou
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XP
Whitaker-Azmitia
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Azmitia
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EC
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008818:Mice, Neurologic Mutants; D009457:Neuroglia / Q000378:metabolism*; D017689:Polydactyly / Q000235:genetics* / Q000473:pathology; D011903:Raphe Nuclei / Q000378:metabolism / Q000473:pathology; D009418:S100 Proteins / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics; D012701:Serotonin / Q000502:physiology
D009418:S100 Proteins; D012701:Serotonin