Abstract
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 CA1 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 CA1 pyramidal cells were not different between wild−type and mutant mice.Excitatory postsynaptic currents(EPSCs)recorded in the presence of 50μM bicuculline and inhibitory postsynaptic currents(IPSCs)recorded in the presence of 50μM AP−5(DL−2−amino−5−phosphonopentanoic acid)+ 30μM 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.
