The Journal of Neuroscience, August 24, 2005, ():
Trafficking of GABAA Receptors, Loss of Inhibition, and a Mechanism for Pharmacoresistance in Status Epilepticus
J. Neurosci. Naylor et al.
25: 7724
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Supplemental Material
Files in this Data Supplement:
- Supplemental Fig. 1
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Supplementary Figure 1. Distribution shift of mIPSC peak amplitudes during SE. The peak amplitude distributions for control (solid) and SE cells (dashed) were generated with binomial probability functions using parameters for postsynaptic receptor numbers, single channel currents, and Popenmax obtained from fits of mIPSCs (Table 1; Fig. 3C for examples from individual cells including data histograms). The solid vertical bar (at 18 pA) represents the peak amplitude threshold detection that would explain the difference between control and SE mIPSC frequencies as a greater loss of small events below detection levels with SE. Since the lowest detected mIPSC peak amplitude averages 15 ± 3 pA across cells, thepredicted 18 pA detection threshold may exceed the actual detection threshold slightly, but not substantially.
- Supplemental Fig. 2
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Supplementary Figure 2. Amplitude of GABAA mIPSC and tonic currents recorded in dentate gyrus granule cells relative to time of sacrifice. A, Note the larger absolute peak amplitudes of mIPSCs for control cells (left; n=26) compared to SE cells (right; n=50) with a slow trend for SE cells to increase peak amplitudes towards control values with greater incubation times. Due to the large total number of cells, control and SE cells were presented on separate plots. B, Note the greater amplitude for SE (n=12) compared to control (n=14) cells for recordings within 2 hours of sacrifice, with a progressive reduction in the difference between the two populations of cells after 2 hours of sacrifice. The tonic currents were measured with GABA (1 µM) and the GABA uptake inhibitor NO711 (10 µM) in the perfusate.
