Neuro-glial neurotrophic interaction in the S-100 beta retarded mutant mouse (Polydactyly Nagoya). I. Immunocytochemical and neurochemical studies.
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. In order to clarify the effects of the retarded production of S-100 beta on the development of monoaminergic neuronal systems and supporting glial cells, immunocytochemical studies of tyrosine hydroxylase (TH), serotonin (5-HT), S-100 beta and glial fibrillary acidic protein (GFAP). In addition, high-performance liquid-chromatography (HPLC) measurements of serotonin and 5-hydroxyindoleacetic acid (5-HIAA) of homozygote (Pdn/Pdn) mouse were examined, and the results were compared with those of other genotypes; heterozygote (Pdn/+) and wild type (+/+) mice. In all types of mice, S-100 beta positive cells and serotonergic fibers were widely distributed throughout the brains and serotonergic cell bodies were located in the brainstem. However, the hippocampus and caudo-dorsal cortex of Pdn/Pdn mouse were markedly reduced in S-100 beta positive cells and in serotonergic fibers. Furthermore, abnormal distribution of GFAP positive cells and fibers were observed in the neocortex and hippocampus of Pdn/Pdn brain. No differences were seen in the distribution of TH neurons or fibers distribution. In the HPLC study, the content of 5-HT and 5-HIAA of the hippocampus and cortex of Pdn/Pdn mouse was lower than those of Pdn/+ and +/+ mice. The present results suggest that the developmental defect of serotonergic fibers in the Pdn mutant mouse is correlate to the deficiency of S-100 beta in the astrocyte of this mutant.[1]References
- Neuro-glial neurotrophic interaction in the S-100 beta retarded mutant mouse (Polydactyly Nagoya). I. Immunocytochemical and neurochemical studies. Ueda, S., Gu, X.F., Whitaker-Azmitia, P.M., Naruse, I., Azmitia, E.C. Brain Res. (1994) [Pubmed]
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