RT Journal Article
SR Electronic
T1 Protein Kinase C Regulates the Interaction between a GABA Transporter and Syntaxin 1A
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 6103
OP 6112
DO 10.1523/JNEUROSCI.18-16-06103.1998
VO 18
IS 16
A1 Matthew L. Beckman
A1 Eve M. Bernstein
A1 Michael W. Quick
YR 1998
UL http://www.jneurosci.org/content/18/16/6103.abstract
AB Syntaxin 1A inhibits GABA uptake of an endogenous GABA transporter in neuronal cultures from rat hippocampus and in reconstitution systems expressing the cloned rat brain GABA transporter GAT1. Evidence of interactions between syntaxin 1A and GAT1 comes from three experimental approaches: botulinum toxin cleavage of syntaxin 1A, syntaxin 1A antisense treatments, and coimmunoprecipitation of a complex containing GAT1 and syntaxin 1A. Protein kinase C (PKC), shown previously to modulate GABA transporter function, exerts its modulatory effects by regulating the availability of syntaxin 1A to interact with the transporter, and a transporter mutant that fails to interact with syntaxin 1A is not regulated by PKC. These results suggest a new target for regulation by syntaxin 1A and a novel mechanism for controlling the machinery involved in both neurotransmitter release and reuptake.