Untreated (n) | +TrkB–IgG (n) | p value (ANOVA) | |
---|---|---|---|
EPSC amplitude | 1.0 ± 0.1 (31) | 0.9 ± 0.1 (34) | >0.5 |
Cell capacitance | 1.0 ± 0.1 (22) | 1.0 ± 0.0 (28) | >0.9 |
Sodium current | 1.0 ± 0.1 (15) | 1.0 ± 0.1 (21) | >0.9 |
Synapse number | 446 ± 63 (6) | 558 ± 93 (7) | >0.3 |
Synapse size (μm2) | 0.38 ± 0.02 (6) | 0.32 ± 0.02 (7) | >0.05 |
%PPD | 33 ± 7 (8) | 41 ± 6 (5) | >0.4 |
mEPSC rise time (msec) | 2.7 ± 0.3 (16) | 2.7 ± 0.2 (24) | >0.9 |
mEPSC τdecay(msec) | 2.8 ± 0.3 (16) | 2.2 ± 0.2 (24) | >0.1 |
EPSC rise time (msec) | 4.2 ± 0.3 (17) | 4.5 ± 0.4 (16) | >0.5 |
EPSC τdecay(msec) | 7.9 ± 0.7 (19) | 7.4 ± 0.7 (16) | >0.6 |
Cells treated long-term with TrkB–IgG were indistinguishable from untreated controls in EPSC amplitude, cell capacitance, peak sodium current, synapse number and size, paired-pulse depression (PPD), and rise and decay times of mEPSCs and EPSCs. Data were taken from experiments in which both TrkB–IgG-treated and untreated cells were measured. Values are normalized to untreated cells for parameters that varied in magnitude between experimental batches (EPSC amplitudes, sodium current amplitudes, and cell capacitance).