Literature DB >> 11223463

Immunohistochemical localization of Ca(2+)/calmodulin-dependent protein kinase kinase beta in the rat central nervous system.

Y Nakamura1, S Okuno, T Kitani, K Otake, F Sato, H Fujisawa.   

Abstract

We examined regional and intracellular distribution of Ca(2+)/calmodulin-dependent protein kinase kinase beta (CaM-KK beta), which activated Ca(2+)/calmodulin-dependent protein kinase I and IV (CaM-K I and IV) immunohistochemically in the central nervous system of the rat by light and electron microscopy. Although most neurons in the brain and spinal cord exhibited the immunoreactivity, no labeled neurons were observed in the globus pallidus or entopeduncular nucleus, and only a small number of neurons showed weak immunoreactivity in the substantia nigra pars reticulata. In general, the immunoreactivity was observed both in the cytoplasm and cellular nucleus, although the immunoreactivity was not found in the cellular nucleus in some large neurons such as in the mesencephalic trigeminal nucleus, lateral vestibular nucleus or gigant cellular reticular formation. As to motoneurons of the cranial nerve nuclei and the anterior horn of the spinal cord, they revealed the immunoreactivity both in the cytoplasm and nucleus. The reaction product appeared as fine granules in the cytoplasm and nucleus under light microscopy. Electron microscopic observations confirmed that the reaction product was localized mainly on the Golgi apparatus or on the nuclear chromatin. Immunolabeling for antibody against CaM-KK beta was discussed with the distribution of CaM-K I, IV and another CaM-KK, CaM-KK alpha, in the central nervous system.

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Year:  2001        PMID: 11223463     DOI: 10.1016/s0168-0102(00)00209-1

Source DB:  PubMed          Journal:  Neurosci Res        ISSN: 0168-0102            Impact factor:   3.304


  8 in total

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Review 2.  Calmodulin-kinases: modulators of neuronal development and plasticity.

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4.  Ca2+/calmodulin kinase kinase alpha is dispensable for brain development but is required for distinct memories in male, though not in female, mice.

Authors:  Keiko Mizuno; Laurence Ris; Amelia Sánchez-Capelo; Emile Godaux; K Peter Giese
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5.  Neuronal Inactivity Co-opts LTP Machinery to Drive Potassium Channel Splicing and Homeostatic Spike Widening.

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Journal:  Cell       Date:  2020-06-02       Impact factor: 66.850

6.  Enhanced expression of WD repeat-containing protein 35 via CaMKK/AMPK activation in bupivacaine-treated Neuro2a cells.

Authors:  Lei Huang; Fumio Kondo; Masahiko Gosho; Guo-Gang Feng; Misako Harato; Zhong-yuan Xia; Naohisa Ishikawa; Yoshihiro Fujiwara; Shoshiro Okada
Journal:  PLoS One       Date:  2014-05-23       Impact factor: 3.240

7.  Haloperidol inactivates AMPK and reduces tau phosphorylation in a tau mouse model of Alzheimer's disease.

Authors:  Jeremy Koppel; Heidy Jimenez; Leslie Adrien; Blaine S Greenwald; Philippe Marambaud; Ezra Cinamon; Peter Davies
Journal:  Alzheimers Dement (N Y)       Date:  2016-06-21

Review 8.  Molecular Mechanisms Underlying Ca2+/Calmodulin-Dependent Protein Kinase Kinase Signal Transduction.

Authors:  Hiroshi Tokumitsu; Hiroyuki Sakagami
Journal:  Int J Mol Sci       Date:  2022-09-20       Impact factor: 6.208

  8 in total

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