Involvement of complexin II in synaptic plasticity in the CA1 region of the hippocampus: The use of complexin II-lacking mice

被引:19
作者
Huang, GZ
Ujihara, H [1 ]
Takahashi, S
Kaba, H
Yagi, T
Inoue, S
机构
[1] Kochi Med Sch, Dept Neuropsychiat, Nankoku, Kochi 7838505, Japan
[2] Kochi Med Sch, Dept Physiol, Nankoku, Kochi 7838505, Japan
[3] Natl Inst Physiol Sci, Neurobiol Lab, Okazaki, Aichi 4448585, Japan
关键词
complexin II-lacking mice; long-term potentiation; hippocampus; CA1 pyramidal cell; whole-cell recording;
D O I
10.1254/jjp.84.179
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
An electrophysiological study was performed with mice lacking complexin II, a presynaptic protein. The long-term potentiation (LTP) by high-frequency stimulation, recorded in the hippocampal CAI area, was decreased in complexin II-lacking mice (CPXII KO mice). The overall postsynaptic currents elicited by low frequency stimulation on the Schaffer collateral/commissural fibers in the hippocampal CAI pyramidal cells were not different between wild-type and mutant mice. Excitatory postsynaptic currents (EPSCs) recorded in the presence of 50 muM bicuculline and inhibitory postsynaptic currents (IPSCs) recorded in the presence of 50 muM Af-5 (DL-2-amino-5-phosphonopentanoic acid) + 30 muM CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) were also identical between wild-types and mutants. Furthermore, the EPSCs following repetitive stimulation (10 Hz) in CPXII KO mice did not show any difference with wild-types. These findings suggest that complexin II does not play a crucial role in ordinary neural transmission, short-term synaptic plasticity or synaptic transmission during high-frequency repetitive stimulation. Therefore, the protein is thought to be involved in the LTP process following tetanic stimulation, including the induction and/or maintenance of the LTP.
引用
收藏
页码:179 / 187
页数:9
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