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. 2019 Jun 7;8:e45946. doi: 10.7554/eLife.45946

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© 2019, Grassmeyer et al

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Figure 5. — Example I_A(Glu) recordings from control and Syt1-deficient cones in response to 2 (A), 5 (B), and 25 (C) ms depolarizing steps (−70 to −10 mV). (D) Example I_A(Glu) recordings from a control cone evoked by 25 ms steps in control conditions and following bath application of the glutamate transport inhibitor, TBOA (100 μM). (E) I_A(Glu) charge transfer as a function of step duration in control cones, Cone^Syt1CKO cones, and control cones in the presence of 100 μM TBOA. Charge transfer was measured from the end of the test step. 2 ms: control: 1415 ± 463 pC, n = 7 cones; Cone^Syt1CKO: 20.7 ± 7.6 pC, n = 9 cones; control vs. Cone^Syt1CKO, p=0.0039. 5 ms: control: 3675 ± 646 pC, n = 19 cones; Cone^Syt1CKO: 49.8 ± 11.3 pC, n = 8 cones; control +TBOA: 160.3 ± 51.3 pC, n = 7 cones; Cone^Syt1CKO vs. control: p=0.0014, TBOA vs. control: p=0.0033. 25 ms: control: 4507 ± 734 pC, n = 17 cones; Cone^Syt1CKO: 64.9 ± 29.9 pC, n = 10 cones; control +TBOA: 455 ± 139 pC, n = 9 cones; Cone^Syt1CKO vs. control: p=0.0003, TBOA vs. control: p=0.0012 (t-tests corrected for multiple comparisons).