Abstract
Calcium dynamics in presynaptic terminals regulate the response dynamics of most central excitatory synapses. However, this dogma has been challenged by the hypothesis that mobility of the postsynaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid subtype glutamate receptors (AMPAR) plays a role in tuning fast excitatory synaptic transmission. In this review, we reevaluate the factors regulating postsynaptic AMPAR mobility, reassess the modeling parameters, analyze the experimental tools, and end by providing alternative ideas stemming from recent results. In particular, newer methods of labeling AMPARs with small fluorophores in live neurons, combined with super-resolution microscopy and sub-second dynamics, lends support to the idea that AMPARs are primarily within the synapse, are greatly constrained, and have much slower mobility than previously thought. We discuss new experiments which may be necessary to readdress the role of postsynaptic AMPAR mobility in tuning fast excitatory synaptic transmission.
Highlights
Fast excitatory transmission at central nervous synapses depends on glutamate release from presynaptic terminals
Recent data shows that the majority of amino-3-hydroxy-5-methyl4-isoxazolepropionic acid subtype glutamate receptors (AMPAR) (∼86%) do not move more than 25 nm in 50 ms which supports the view that the postsynaptic densities (PSDs) is an environment of slow diffusion (Li et al, 2016)
When the authors set the average Dinst to 0.1 μm2/s, which we argue is too high, based on the current results, discussed above, the simulated AMPAR-mediated response showed that postsynaptic surface AMPAR mobility helped recover the synaptic response to about 70% of the first stimulus, experiencing some paired-pulse depression
Summary
Fast excitatory transmission at central nervous synapses depends on glutamate release from presynaptic terminals.
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