Abstract
GABAergic inhibitory neurotransmission contributes to diverse aspects of brain development and adult plasticity, including the expression of complex cognitive processes. This is afforded for in part by the dynamic adaptations occurring at inhibitory synapses, which show great heterogeneity both in terms of upstream signaling and downstream effector mechanisms. Single-particle tracking and live imaging have revealed that complex receptor-scaffold interactions critically determine adaptations at GABAergic synapses. Super-resolution imaging studies have shown that protein interactions at synaptic sites contribute to nano-scale scaffold re-arrangements through post-translational modifications (PTMs), facilitating receptor and scaffold recruitment to synaptic sites. Additionally, plasticity mechanisms may be affected by the protein composition at individual synapses and the type of pre-synaptic input. This mini-review article examines recent discoveries of plasticity mechanisms that are operational within GABAergic synapses and discusses their contribution towards functional heterogeneity in inhibitory neurotransmission.
Highlights
The plasticity of individual synapses occurs downstream of activity or neuro-modulatory signaling and must be reconciled with homeostatic mechanisms to maintain overall network function (Abbott and Nelson, 2000)
PV+ and SST+ synapses are regulated by distinct upstream signaling, with PV+ synapses being more affected by cell-autonomous firing and SST+ synapses affected by NMDA receptor (NMDAR)-driven glutamatergic input (Horn and Nicoll, 2018)
Activation of post-synaptic NMDARs signal downstream to the kinase CaMKIIα, which drives inhibitory long-term potentiation at SST+, but not PV+ synapses (Chiu et al, 2018)
Summary
The plasticity of individual synapses occurs downstream of activity or neuro-modulatory signaling and must be reconciled with homeostatic mechanisms to maintain overall network function (Abbott and Nelson, 2000). Even at the post-synaptic compartment level, individual synapses themselves exhibit functional diversity, and the cellular processes that facilitate this heterogeneity of function is currently an exciting topic of research. Unlike the mechanisms that have been described to influence specific aspects of excitatory postsynaptic plasticity, mechanisms operational at GABAergic postsynaptic terminals are relatively unexplored. Recent technological developments including single-particle tracking and superresolution imaging demonstrate that the inhibitory post-synapse is subject to dynamic activitydependent reorganization. Understanding the cellular mechanisms that contribute to dynamics at GABAergic synapses will help to explain emergent functional heterogeneity
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