PT - JOURNAL ARTICLE AU - Oded Fili AU - Itzhak Michaelevski AU - Yaniv Bledi AU - Dodo Chikvashvili AU - Dafna Singer-Lahat AU - Hassia Boshwitz AU - Michal Linial AU - Ilana Lotan TI - Direct Interaction of a Brain Voltage-Gated K<sup>+</sup>Channel with Syntaxin 1A: Functional Impact on Channel Gating AID - 10.1523/JNEUROSCI.21-06-01964.2001 DP - 2001 Mar 15 TA - The Journal of Neuroscience PG - 1964--1974 VI - 21 IP - 6 4099 - http://www.jneurosci.org/content/21/6/1964.short 4100 - http://www.jneurosci.org/content/21/6/1964.full SO - J. Neurosci.2001 Mar 15; 21 AB - Presynaptic voltage-gated K+ (Kv) channels play a physiological role in the regulation of transmitter release by virtue of their ability to shape presynaptic action potentials. However, the possibility of a direct interaction of these channels with the exocytotic apparatus has never been examined. We report the existence of a physical interaction in brain synaptosomes between Kvα1.1 and Kvβ subunits with syntaxin 1A, occurring, at least partially, within the context of a macromolecular complex containing syntaxin, synaptotagmin, and SNAP-25. The interaction was altered after stimulation of neurotransmitter release. The interaction with syntaxin was further characterized in Xenopus oocytes by both overexpression and antisense knock-down of syntaxin. Direct physical interaction of syntaxin with the channel protein resulted in an increase in the extent of fast inactivation of the Kv1.1/Kvβ1.1 channel. Syntaxin also affected the channel amplitude in a biphasic manner, depending on its concentration. At low syntaxin concentrations there was a significant increase in amplitudes, with no detectable change in cell-surface channel expression. At higher concentrations, however, the amplitudes decreased, probably because of a concomitant decrease in cell-surface channel expression, consistent with the role of syntaxin in regulation of vesicle trafficking. The observed physical and functional interactions between syntaxin 1A and a Kv channel may play a role in synaptic efficacy and neuronal excitability.