Histology and in situ hybridization histochemistry of the intracellular signal transduction system in neurological mutant animals.

观察神经突变小鼠的形态学异常，如神经元变性，层压破坏，神经元过程异常，突触或神经元回路形成异常。我们还研究了神经元蛋白和基因的定位，以了解这些物质在神经元中的功能意义。用组织学方法观察了dreher突变小鼠的新皮层和编织小鼠的海马。发现多种异常，如异位浦肯野细胞聚集。形态异常并不局限于小脑，而是在中枢神经系统的各个部位发现。这些报告将为今后免疫组织化学和原位杂交组织化学的研究提供必要的依据。我们采用原位杂交组织化学方法，在正常小鼠浦肯野细胞、staggerer （sg/sg）和reeler （rl/rl）突变小鼠浦肯野细胞中寻找2Abeta、2B、2Cbeta型蛋白磷酸酶mrna的表达。mrna的表达在正常和散列浦肯野细胞中是相当的，但在散列浦肯野细胞中显著降低。我们将这一发现解释为：(a)交错突变基因可能直接影响sg/sg Punkinje细胞中蛋白质磷酸化-去磷酸化周期的磷酸酶成分；或者(b) mRNA表达减少可能是继发性现象，是由于缺乏突触输入导致浦肯野细胞功能异常所致。

Neurological mutant mice were investigated to observe morphological abnormalities, such as, degeneration of neurons, disruptions of laminations, abnormal neuronal processes, and abnormal synapse or neuronal circuit formation. We also investigated the localization of neuronal protein and genes, to understand the functional significance of these substances in neurons.Neocortex of dreher mutant mice and hippocampus of weaver mice were observed by histological methods. Various abnormalities were found, such as, aggregation of ectopic Pukinje cells. Morphological abnormalities were not confined to cerebellum, but they were found in various locations in central nervous systems. These reports will be necessary for future study by immunohistopchemistry and in situ hybridization histochemistry.We used in situ hybridization histochemistry to search for the expression of mRNAs of protein phosphatases type 2Abeta, 2B,2Cbeta, in Purkinje cells of normal mice, and staggerer (sg/sg) and reeler (rl/rl) mutant mice, two strains with known Purkinje cell disorders. The expression of the mRNAs was comparable in the normal and reeler Purkinje cells, but considerably reduced in the staggerer Purkinje cells. We interpret this finding as indicating : (a) the staggerer mutant gene may directly affect the phosphatase component of the protein phosphorylation-dephosphorylation cycle in the sg/sg Punkinje cells ; or (b) the reduced mRNA expression may be a secondary phenomenon, resulting from abnormal Purkinje cell function due to the lack of synaptic input.