Reduced hippocampal LTP in mice lacking a presynaptic protein: complexin II

The SNAP receptor (SNARE) complex is a core complex specialized for synapti c vesicle exocytosis, and the binding of SNAPs to the complex is an essenti al step for neurotransmitter release. Complexin I and II have been identifi ed as SNARE-complex-associated proteins. Importantly, complexins compete wi th alpha-SNAP for binding to the complex, suggesting that complexins may mo dulate neurotransmitter release process. To examine this possibility and to understand the physiological function of complexins, we generated complexi n II knockout mice. The complexin-II-deficient mice (-/-) were viable and f ertile, and appeared normal. Electrophysiological recordings in the mutant hippocampus showed that ordinary synaptic transmission and paired-pulse fac ilitation, a form of short-term synaptic plasticity, were normal. However, long-term potentiation (LTP) in both CA1 and CA3 regions was impaired, sugg esting that complexin II may not be essential for synaptic vesicle exocytos is, but it does have a role in the establishment of hippocampal LTP.