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. 2003 Jul 23;552(Pt 1):89–107. doi: 10.1113/jphysiol.2003.044263

Figure 7. EPSC prolongation produced by block of GLT-1 is larger when more fibres are stimulated.

Figure 7

A, specimen parallel fibre EPSCs of different amplitude evoked by molecular layer stimulation in the same GLAST knock-out cell. B, EPSCs in the same cell and with the same stimulus strength as A, after application of 200 μM DHK. C and D, data in A and B normalised to have the same peak. E, weighted decay time constant for different stimulation intensities, in the absence and presence of DHK, measured as in A-D and normalised to the value (4.83 ± 0.44 ms) for an EPSC amplitude near 640 pA in control solution, in 7 knock-out cells. The amplitudes and time constants of the fast and slow exponential components of the EPSC decay (in the order Afast, τfast, Aslow, τslow) were as follows. For low stimulation, in control: 118 ± 12 pA, 3.69 ± 0.19 ms, 3.05 ± 2.07 pA, 22.8 ± 8.1 ms (4 out of 7 cells showed a slow component); in DHK: 76.4 ± 11.0 pA, 3.07 ± 0.41 ms, 20.4 ± 8.9 pA, 25.1 ± 10.6 ms (5 out of 7 cells showed a slow component). For medium stimulation, in control: 539 ± 44 pA, 4.09 ± 0.47 ms, 66.5 ± 35.5 pA, 17.4 ± 6.1 ms (5 out of 7 cells showed a slow component); in DHK: 482 ± 44 pA, 4.37 ± 0.68 ms, 124 ± 35 pA, 36.3 ± 7.9 ms (all cells showed a slow component). For high stimulation, in control: 1060 ± 196 pA, 4.40 ± 0.67 ms, 451 ± 187 pA, 21.4 ± 10.6 ms (6 out of 7 cells showed a slow component); in DHK: 1102 ± 61 pA, 5.91 ± 0.62 ms, 338 ± 52 pA, 50.9 ± 8.7 ms (all cells showed a slow component).