Figure 3. Simulations: effects of iGluSnFR on glutamate concentration and receptor activation.
(A) Simulated glutamate waveforms (i), peak glutamate concentration (ii), AMPAR activation (iii), NMDAR activation (iv) and mGluR activation (v) in the synaptic cleft (≤110 nm from the release site). Trace colors correspond to different iGluSnFR concentrations, as indicated in i. (B) As in A, but in the perisynaptic region (160–260 nm from the release site). (C) As in A, but in the extrasynaptic region 400–500 nm from the release site. (D) When iGluSnFR was also present within the synaptic cleft, it influenced cleft glutamate concentration waveforms (i) and produced sizeable signals within the cleft (ii), but did not strongly influence receptor activation within the cleft (iii-v).
Figure 3—source data 1. Peak free glutamate concentration as a function of iGluSnFR concentration.
Peak [glu] within the center of the synaptic cleft (110 nm) (Figure 3Aii). Peak [glu] in the perisynaptic region (160–260 nm from release site) (Figure 3Bii). Peak [glu] in a neighboring synapse (400–500 nm from release site) (Figure 3Cii).
elife-54441-fig3-data1.xlsx (13.6KB, xlsx)
Figure 3—figure supplement 1. Simulations: receptor activation and iGluSnFR signals at a lower diffusion coefficient.
(A) Simulated glutamate waveforms (i), peak glutamate concentration (ii), AMPAR activation (iii), NMDAR activation (iv) and mGluR activation (v) in the synaptic cleft (≤110 nm from the release site). Trace colors correspond to different iGluSnFR concentrations, as indicated in i. Diffusion coefficient is 5 × 10−7 cm2s−1. (B) As in A, but in the perisynaptic region (160–260 nm from the release site). (C) As in A, but 400–500 nm from the release site. (D-E) A 5-fold change in the diffusion coefficient had little effect on iGluSnFR signals (D) or the time course of glutamate uptake (E). Solid lines indicate simulations with D = 2.5 × 10−6 cm2 s−1, dashed lines indicate D = 5 × 10−7 cm2 s−1.