Leil Tarek A, Chen Zi-Wei, Chang Chang-Sheng S, Olsen Richard W
Department of Molecular and Medical Pharmacology, Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095-1735.
J Neurosci. 2004 Dec 15;24(50):11429-38. doi: 10.1523/JNEUROSCI.3355-04.2004.
The trafficking of GABA(A) receptors is an important component of the pathway that regulates plasticity of inhibitory synapses. The 17 kDa GABA(A) receptor-associated protein (GABARAP) has been implicated in the trafficking of GABA(A) receptors because of its ability to interact not only with the gamma2 subunit of the receptor but also with microtubules and the N-ethylmaleimide-sensitive factor (NSF). To elucidate the role of GABARAP in the trafficking of GABA(A) receptors, we have constructed a yellow fluorescent protein (YFP) fusion protein of GABARAP and expressed it in neurons using adenovirus, so that its function may be examined. YFP-GABARAP colocalized with gamma2 subunit-containing GABA(A) receptors and NSF to the perinuclear cytoplasm in cultured hippocampal neurons and to the proximal regions of dendrites that are making synaptic contact. Expression of YFP-GABARAP in Cos7 cells and cultured hippocampal neurons was able to increase the level of GABA(A) receptors detected at the plasma membrane, even at low levels of YFP-GABARAP expression. This effect is specific to the function of GABARAP on GABA(A) receptor trafficking, because point mutations in the gamma2-binding domain of YFP-GABARAP interfered with the ability of YFP-GABARAP to increase GABA(A) receptor surface levels. These mutations also disrupted the colocalization of YFP-GABARAP with the gamma2 subunit and with NSF in hippocampal neurons. The results of this study show for the first time that GABARAP has a functional effect on the trafficking of GABA(A) receptors and provide decisive evidence for the role of GABARAP in transporting GABA(A) receptors to the plasma membrane in neurons.
γ-氨基丁酸A(GABA(A))受体的转运是调节抑制性突触可塑性通路的重要组成部分。17 kDa的GABA(A)受体相关蛋白(GABARAP)因其不仅能与受体的γ2亚基相互作用,还能与微管和N-乙基马来酰亚胺敏感因子(NSF)相互作用,而被认为与GABA(A)受体的转运有关。为了阐明GABARAP在GABA(A)受体转运中的作用,我们构建了GABARAP的黄色荧光蛋白(YFP)融合蛋白,并使用腺病毒在神经元中表达,以便研究其功能。YFP-GABARAP在培养的海马神经元中与含γ2亚基的GABA(A)受体和NSF共定位于核周细胞质,以及正在形成突触联系的树突近端区域。即使在YFP-GABARAP低水平表达时,YFP-GABARAP在Cos7细胞和培养的海马神经元中的表达也能增加质膜上检测到的GABA(A)受体水平。这种效应是GABARAP对GABA(A)受体转运功能所特有的,因为YFP-GABARAP的γ2结合域中的点突变会干扰YFP-GABARAP增加GABA(A)受体表面水平的能力。这些突变还破坏了YFP-GABARAP与海马神经元中γ2亚基和NSF的共定位。本研究结果首次表明GABARAP对GABA(A)受体的转运具有功能作用,并为GABARAP在神经元中将GABA(A)受体转运到质膜中的作用提供了决定性证据。