TY  - JOUR
KW  - Science & Technology
KW  -  Life Sciences & Biomedicine
KW  -  Cell Biology
KW  -  GABA(B) RECEPTOR INTERNALIZATION
KW  -  GAMMA-AMINOBUTYRIC-ACID
KW  -  CENTRAL-NERVOUS-SYSTEM
KW  -  PROTEIN-KINASE
KW  -  LATERAL MOBILITY
KW  -  INHIBITORY NEUROTRANSMISSION
KW  -  HETEROSYNAPTIC DEPRESSION
KW  -  SURFACE TRAFFICKING
KW  -  SYNAPTIC PLASTICITY
KW  -  SUSHI DOMAINS; AMPK; bungarotoxin binding site; Ca2+ signaling; excitotoxicity; GABA receptors; GABAB receptors; glutamate receptors; hippocampus; homeostatic signaling; lateral diffusion; NMDA receptors; phosphorylation; presynaptic terminal; quantum dots; receptor mobility; single-particle tracking; sushi domains
ID  - discovery1508144
N2  - Here, we uncover a mechanism for regulating the number of active presynaptic GABAB receptors (GABABRs) at nerve terminals, an important determinant of neurotransmitter release. We find that GABABRs gain access to axon terminals by lateral diffusion in the membrane. Their relative accumulation is dependent upon agonist activation and the presence of the two distinct sushi domains that are found only in alternatively spliced GABABR1a subunits. Following brief activation of NMDA receptors (NMDARs) using glutamate, GABABR diffusion is reduced, causing accumulation at presynaptic terminals in a Ca2+-dependent manner that involves phosphorylation of GABABR2 subunits at Ser783. This signaling cascade indicates how synaptically released glutamate can initiate, via a feedback mechanism, increased levels of presynaptic GABABRs that limit further glutamate release and excitotoxicity.
PB  - CELL PRESS
TI  - Phospho-dependent Accumulation of GABABRs at Presynaptic Terminals after NMDAR Activation
EP  - 1973
AV  - public
Y1  - 2016/08/16/
JF  - Cell Reports
A1  - Hannan, S
A1  - Gerrow, K
A1  - Triller, A
A1  - Smart, TG
SN  - 2211-1247
UR  - http://doi.org/10.1016/j.celrep.2016.07.021
N1  - © 2016 The Author(s). This is an open access article under the Creative Commons Attribution 4.0 International (CC BY 4.0) license (http://creativecommons.org/licenses/by/4.0/)
IS  - 7
VL  - 16
SP  - 1962
ER  -