Generation of motor function and its relation with neuronal chemical substances.

我们用免疫组织化学方法研究了一些钙调素依赖性蛋白激酶(CaM-Ks)在脑和脊髓中的分布，它们被认为是调节细胞内第二信使Ca^&lt；2+和gt；最近两年，我们对CaM-KKβ(CaM-KKβ)和CaM-KPase(CaM-KPase)进行了研究，并发表了两篇论文。CaM-KKβ分布在除苍白球、内侧丘核和黑质网状部以外的大多数神经元的胞浆和胞核中。但在巨细胞网状核、前庭外侧核或三叉神经中脑核内的一些大型神经元的细胞核未见标记。CaM-KKβ不同于另一种CaM-KK(CaM-KKα)，后者主要定位于细胞核，CaM-K Pase仅定位于细胞质。在嗅球、齿状回和小脑皮质的颗粒细胞、嗅结节和Ammon‘s角的锥体神经元、纹状体的投射神经元、黑质致密部的神经元或浦肯野细胞中未见阳性反应。另一方面，海马结构和纹状体的内源性神经元被大量标记。后者还用胆碱乙酰转移酶(ChAT)标记。电子显微镜观察显示，许多区域的突触后密度呈CaM-K-Pase免疫阳性。由于CaM-K Pase使已知与突触LTP有关的CaM-K II去磷酸化，因此CaM-K Pase可能调节这一突触功能。

We have examined immnunohistochemically the distribution of some Ca^<2+>/calmodulin dependent protein kinases (CaM-Ks) in the brain and spinal cord, which are known to regulate intracellular second messenger, Ca^<2+>. Last two years, we studied CaM-kinase kinase β (CaM-KKβ) and CaM-kinase phosphatase (CaM-K Pase), and published two papers.CaM-KKβ was distributed in the cytoplasm and nucleus of most neurons except in the globus pallidus, entopeduncular nuclcus and reticular part of the substantia nigra. However, cellular nuclei of some large neurons such as in the gigantocellular reticular nucleus, lateral vestibular nucleus or mesencephalic trigeminal nucleus were not labeled. CaM-KK β was different from another CaM-KK (CaM-KKα) in that the latter was located mostly in the cellular nuclei.CaM-K Pase was located only in the cytoplasm. This was not found in the granule cells in the olfactory bulb, dentate gyrus and cerebellar cortex, pyramidal neurons in the olfactory tubercle and Ammon's horn, projection neurons in the striatum, neurons in the substantia nigra pars compacta or Purkinje cells. On the other hand, intrinsic neurons in the hippocampal formation and striatum were heavily labeled. The latter were also labeled with choline acetyl transferase (ChAT). Electron microscopic observations revealed that the postsynaptic density of many regions was immunopositive for CaM-K Pase. Because CaM-K Pase dephosphorylates CaM-K II that has been known to have relation with LTP at synaptic sites, CaM-K Pase might regulate this synaptic function.