Guang-Zhe Huang1, Hisamitsu Ujihara1,*, Sei-ichi
Takahashi2,4, Hideto Kaba2,4, Takeshi Yagi3
and Shinpei Inoue1
Departments of 1Neuropsychiatry and 2Physiology,
Kochi Medical School, Nankoku, Kochi 783-8505, Japan
3Laboratory of Neurobiology, National Institute for Physiological
Sciences, Myodaiji, Okazaki, Aichi 444-8585, Japan
4CREST, Japan Science & Technology Corporation
*Corresponding author.ﾊﾊFAX:+81-88-880-2360
E-mail: ujiharah@med.kochi-ms.ac.jp
Abstract: An electrophysiological study was performed with mice lacking
complexinﾊII, a presynaptic protein. The long-term potentiation (LTP) by
high-frequency stimulation, recorded in the hippocampal CA1 area, was decreased
in complexinﾊII-lacking mice (CPXII KO mice). The overall postsynaptic currents
elicited by low frequency stimulation on the Schaffer collateral/commissural
fibers in the hippocampal CA1 pyramidal cells were not different between
wild-type and mutant mice. Excitatory postsynaptic currents (EPSCs) recorded
in the presence of 50ﾊmM bicuculline and inhibitory
postsynaptic currents (IPSCs) recorded in the presence of 50ﾊmM
AP-5 (DL-2-amino-5-phosphonopentanoic acid) +ﾊ30ﾊmM
CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) were also identical between
wild-types and mutants. Furthermore, the EPSCs following repetitive stimulation
(10ﾊHz) in CPXII KO mice did not show any difference with wild-types. These
findings suggest that complexinﾊ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.
Keywords: ComplexinﾊII-lacking mice, Long-term potentiation, Hippocampus,
CA1 pyramidal cell, Whole-cell recording
Copyrightｩ The Japanese Pharmacological Society 2000
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