Abstract
Kainate receptors (KARs) are glutamate-gated ion channels that play fundamental roles in regulating neuronal excitability and network function in the brain. After being cloned in the 1990s, important progress has been made in understanding the mechanisms controlling the molecular and cellular properties of KARs, and the nature and extent of their regulation of wider neuronal activity. However, there have been significant recent advances towards understanding KAR trafficking through the secretory pathway, their precise synaptic positioning, and their roles in synaptic plasticity and disease. Here we provide an overview highlighting these new findings about the mechanisms controlling KARs and how KARs, in turn, regulate other proteins and pathways to influence synaptic function.
Highlights
Glutamate is the major excitatory neurotransmitter in the CNS and participates in most aspects of brain function
Using the RUSH system, which allows the synchronous release and visualization of cargo proteins trafficking through the secretory pathway [65, 66], it has been demonstrated that GluK2-containing kainate receptors (KARs) utilise these local secretory pathway systems for their delivery to the cell surface [48] (Fig. 1)
There is a strong base of knowledge about the activity-dependent regulation of KAR endocytosis and recycling [13, 15, 67,68,69,70,71], compared to AMPARs [72] and tsVSVG cargo [73], little is known about the activitydependence of secretory pathway trafficking of KARs
Summary
Glutamate is the major excitatory neurotransmitter in the CNS and participates in most aspects of brain function. Some neurons, including CA1 pyramidal neurons and dispersed hippocampal cultures display robust KAR currents following Despite their classical ion channel structure, KARs can signal via a non-canonical G-protein coupled metabotropic cascade [11]. Postsynaptic metabotropic KAR signalling is much more widespread than ionotropic KAR signalling [12, 13] and recent discoveries have highlighted their previously unsuspected roles in neuromodulation. They regulate inhibitory transmission by controlling surface expression of the chloride transporter KCC2 [14] and mediate certain forms of synaptic plasticity [15, 16]. We highlight what is known, what remains to be established, and outline the future perspectives for KAR research and how it will impact on our understanding of brain function and dysfunction in disease
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