Abstract
The plasticity of inhibitory transmission is expected to play a key role in the modulation of neuronal excitability and network function. Over the last two decades, the investigation of the determinants of inhibitory synaptic plasticity has allowed distinguishing presynaptic and postsynaptic mechanisms. While there has been a remarkable progress in the characterization of presynaptically-expressed plasticity of inhibition, the postsynaptic mechanisms of inhibitory long-term synaptic plasticity only begin to be unraveled. At postsynaptic level, the expression of inhibitory synaptic plasticity involves the rearrangement of the postsynaptic molecular components of the GABAergic synapse, including GABAA receptors, scaffold proteins and structural molecules. This implies a dynamic modulation of receptor intracellular trafficking and receptor surface lateral diffusion, along with regulation of the availability and distribution of scaffold proteins. This Review will focus on the mechanisms of the multifaceted molecular reorganization of the inhibitory synapse during postsynaptic plasticity, with special emphasis on the key role of protein dynamics to ensure prompt and reliable activity-dependent adjustments of synaptic strength.
Highlights
The plasticity of inhibitory transmission is expected to play a key role in the modulation of neuronal excitability and network function
While phasic inhibitory transmission is mainly mediated by the activation of α1-3β23γ GABAA receptors (GABAARs) clustered at synapses, tonic conductance arises from extrasynaptic GABAARs typically composed of α1/4/6βδ and α5βγ
ROLE OF GABAA RECEPTOR INTRACELLULAR TRAFFICKING IN THE EXPRESSION OF INHIBITORY SYNAPTIC PLASTICITY The initial demonstrations that GABAARs are brought to the neuronal surface by exocytosis and removed by clathrin-mediated endocytosis (Tehrani and Barnes, 1993; Kittler et al, 2000) represent the first indications that neurotransmitter receptors are not fixed at the neuronal membrane but exchange between surface and intracellular compartments
Summary
Diffusion dynamics of synaptic molecules during inhibitory postsynaptic plasticity. Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa, Italy. The expression of inhibitory synaptic plasticity involves the rearrangement of the postsynaptic molecular components of the GABAergic synapse, including GABAA receptors, scaffold proteins and structural molecules This implies a dynamic modulation of receptor intracellular trafficking and receptor surface lateral diffusion, along with regulation of the availability and distribution of scaffold proteins. This Review will focus on the mechanisms of the multifaceted molecular reorganization of the inhibitory synapse during postsynaptic plasticity, with special emphasis on the key role of protein dynamics to ensure prompt and reliable activity-dependent adjustments of synaptic strength. Other forms of inhibitory synaptic plasticity are expressed postsynaptically with persistent modifications of the abundance (Nusser et al, 1998; Kilman et al, 2002; Marsden et al, 2007; Kurotani et al, 2008; Bannai et al, 2009; Muir et al, 2010; Niwa et al, 2012; Saliba et al, 2012; Nahmani and Turrigiano, 2014; Petrini et al, 2014), assortment (Houston et al, 2008; Rajalu et al, 2009) and gating
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