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

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 complex in II-lacking mice (CPXII KO mice). The overall postsynaptic currents elici ted by low frequency stimulation on the Schaffer collateral/commissural fib ers 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 (IP SCs) recorded in the presence of 50 muM Af-5 (DL-2-amino-5-phosphonopentano ic acid) + 30 muM CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) were also ide ntical between wild-types and mutants. Furthermore, the EPSCs following rep etitive stimulation (10 Hz) in CPXII KO mice did not show any difference wi th wild-types. These findings suggest that complexin II does not play a cru cial role in ordinary neural transmission, short-term synaptic plasticity o r synaptic transmission during high-frequency repetitive stimulation. There fore, the protein is thought to be involved in the LTP process following te tanic stimulation, including the induction and/or maintenance of the LTP.