We have generated mice lacking synaptogyrin I and synaptophysin I to explore the functions of these abundant tyrosine-phosphorylated proteins of synaptic vesicles. Single and double knockout mice were alive and fertile without significant morphological or biochemical changes. Electrophysiological recordings in the hippocampal CA1 region revealed that short-term and long-term synaptic plasticity were severely reduced in the synaptophysin/synaptogyrin double knockout mice. LTP was decreased independent of the induction protocol, suggesting that the defect in LTP was not caused by insufficient induction. Our data show that synaptogyrin I and synaptophysin I perform redundant and essential functions in synaptic plasticity without being required for neurotransmitter release itself.
Janz, R., Südhof, T. C., Hammer, R. E., Unni, V., Siegelbaum, S. A., & Bolshakov, V. Y. (1999). Essential roles in synaptic plasticity for synaptogyrin I and synaptophysin I. Neuron, 24(3), 687–700. https://doi.org/10.1016/S0896-6273(00)81122-8