Essential roles in synaptic plasticity for synaptogyrin I and synaptophysin I

208Citations
Citations of this article
113Readers
Mendeley users who have this article in their library.

Abstract

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.

Cite

CITATION STYLE

APA

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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free