TY - JOUR
T1 - Interaction between Cav2.1α1 and CaMKII in Cav2.1α1 mutant mice, rolling nagoya
AU - Takahashi, Eiki
AU - Niimi, Kimie
AU - Itakura, Chitoshi
N1 - Funding Information:
All animal procedures were approved by the Animal Experiments Committee of RIKEN. All animals were treated in accordance with the Institutional Guidelines for Experiments using Animals. The Rolling Nagoya strain was provided by the RIKEN BRC with the support of the National BioResource Project from the Ministry of Education, Culture, Sports, Science, and Technology, Japan. Male wild-type (+/+) and homozygous (rol/rol) F1 progeny derived from a cross between heterozygous (rol/+) mice and were genotyped by PCR using tail DNA as previous report (Takahashi and Niimi 2009). The mice were given free access to water and food pellets (CRF-1, Oriental Yeast Co., Ltd., Tokyo, Japan) and were kept under a 12/12-h light/dark cycle (lights on from 08:00 to 20:00) at 23±1°C and 55±5% humidity. Two-month-old (5-to 8-week-old) mice (+/+, rol/rol; n=10, 10) were used in this study.
PY - 2010/6
Y1 - 2010/6
N2 - It has been reported earlier that interactions between Ca v2.1α1 and calcium/calmodulin-dependent protein kinase II (CaMKII) in the presynaptic fraction and between the NMDA receptor subunit NR2B and CaMKII in the postsynaptic density (PSD) fraction are important for neuronal function. Cav2.1α1, CaMKII, and NR2B are predominantly expressed in the hippocampus. To examine the above interactions and CaMKII activity in the hippocampal presynapse and PSD of Rolling Nagoya mice carrying a mutation in Cav2.1α1 subunit, we performed immunoprecipitation and Western blot analyses. In the presynapse, the interaction between Cav2.1α1 and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate Synapsin I (at Ser603) were decreased in mutant mice compared to wild-type mice. In the PSD, a similar pattern was observed for the interaction between NR2B and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate AMPA receptor subunit glutamate receptor 1 (at Ser831) between mutant and wild-type mice. Our data indicate that disruption of the interaction between Cav2. 1α1 and CaMKII may down-regulate presynaptic CaMKII activity and that Rolling Nagoya mice would be a useful model for examining presynaptic function.
AB - It has been reported earlier that interactions between Ca v2.1α1 and calcium/calmodulin-dependent protein kinase II (CaMKII) in the presynaptic fraction and between the NMDA receptor subunit NR2B and CaMKII in the postsynaptic density (PSD) fraction are important for neuronal function. Cav2.1α1, CaMKII, and NR2B are predominantly expressed in the hippocampus. To examine the above interactions and CaMKII activity in the hippocampal presynapse and PSD of Rolling Nagoya mice carrying a mutation in Cav2.1α1 subunit, we performed immunoprecipitation and Western blot analyses. In the presynapse, the interaction between Cav2.1α1 and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate Synapsin I (at Ser603) were decreased in mutant mice compared to wild-type mice. In the PSD, a similar pattern was observed for the interaction between NR2B and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate AMPA receptor subunit glutamate receptor 1 (at Ser831) between mutant and wild-type mice. Our data indicate that disruption of the interaction between Cav2. 1α1 and CaMKII may down-regulate presynaptic CaMKII activity and that Rolling Nagoya mice would be a useful model for examining presynaptic function.
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U2 - 10.1007/s12031-009-9216-5
DO - 10.1007/s12031-009-9216-5
M3 - Article
C2 - 19609731
AN - SCOPUS:77951623726
SN - 0895-8696
VL - 41
SP - 223
EP - 229
JO - Journal of Molecular Neuroscience
JF - Journal of Molecular Neuroscience
IS - 2
ER -