Regulation of inhibitory synaptic transmission by a conserved atypical interaction of GABA(A) receptor beta- and gamma-subunits with the clathrin AP2 adaptor.
Regulation of inhibitory synaptic transmission by a conserved atypical interaction of GABA(A) receptor beta- and gamma-subunits with the clathrin AP2 adaptor.
复制标题
通过 GABA(A) 受体 β 和 γ 亚基与网格蛋白 AP2 接头的保守非典型相互作用调节抑制性突触传递。
DOI：
10.1016/j.neuropharm.2008.06.072
复制
发表时间：
2008
影响因子：
4.7
通讯作者：
Kittler,JosefT
中科院分区：
文献类型：
--
作者：
Smith,KatharineR;McAinsh,Kristina;Chen,Guojun;Arancibia-Carcamo,ILorena;Haucke,Volker;Yan,Zhen;Moss,StephenJ;Kittler,JosefT
The number of surface and synaptic GABAAreceptors is an important determinant of inhibitory synapse strength. Surface receptor number is in part controlled by removal of receptors from the membrane by interaction with the clathrin adaptor AP2. Here we demonstrate that there are two binding sites for AP2 in the γ2-subunit: a Yxxϕ type motif specific to γ2-subunits and a basic patch AP2 binding motif, that is also found in GABAAreceptor β-subunits. Blocking GABAAreceptor–AP2 interactions using a peptide that inhibits AP2 binding to GABAAreceptors via the conserved basic patch mechanism increases synaptic responses within minutes, whereas simultaneously blocking both binding mechanisms has an additive effect. These data suggest that multiple AP2 internalization signals control the levels of surface and synaptic GABAAreceptors to regulate synaptic inhibition.
