The potassium channel subunit K <sub>v</sub> β1 serves as a major control point for synaptic facilitation
In Ha Cho, Lauren C. Panzera, Morven Chin, Scott A. Alpizar, Genaro E. Olveda, Robert Hill, Michael B. Hoppa
Abstract
Significance Nerve terminals generally engage in two opposite and essential forms of synaptic plasticity (facilitation or depression) that play critical roles in learning and memory. While the molecular components of both types of terminals are similar with regards to vesicle fusion, much less is known about their molecular control of electrical signaling. Measurements of the electrical impulses (action potentials) underlying these two forms of plasticity have been difficult in small nerve terminals due to their size. In this study we deployed optical physiology measurements to overcome this size barrier. Here, we identify a unique mechanism (Kvβ1 subunit) that enables broadening of the presynaptic action potentials that selectively supports synaptic facilitation, but does not alter any other aspects of nerve terminal function.