In the article “Expression and Function of SNAP-25 as a Universal SNARE Component in GABAergic Neurons,” by Lawrence C. R. Tafoya, Manuel Mameli, Teiko Miyashita, John F. Guzowski, C. Fernando Valenzuela, and Michael C. Wilson, which appeared on pages 7826–7838 of the July 26, 2006 issue, the calibration for the series of scale bars for electrophysiological studies presented in Panels A, B, D, and F of Figure 2 were inadvertently omitted during the preparation of this figure for submission. The corrected figure is reprinted here. Also, on page 7829, the concentration of TTX should have read TTX (0.5 μm), instead of TTX (0.5 mm).
GABAergic transmission could not be evoked in SNAP-25-deficient mutant neurons, although spontaneous currents persist. A, Whole-cell patch-clamp recordings of field stimulation ePSCs obtained from cortical slices of E17.5 control and Snap25-null mutant fetuses. GABAergic responses were isolated by recording in the presence of NBQX (10 μm) plus APV (100 μm) to block glutamatergic transmission. Representative tracings are presented on the left with respective calibrations. The trace (dotted) obtained after application of 20 μm bicuculline to control slices is superimposed over the recording in the absence of GABAA receptor inhibition and indicates GABAergic origin of the response. Mutant slices did not show any detectable response to stimulation. B, Recordings of sPSCs in the absence of TTX. C, sPSCs from Snap25-null mutant slices (n = 9) were decreased in frequency (26.1-fold) and amplitude (6.0-fold) compared with controls (n = 5; ∗∗∗p < 0.001). Error bars represent SEM. D, mPSCs recorded in the presence of TTX (0.5 μM). E, Both the amplitude (5.2-fold) and frequency (12.9-fold) of TTX-resistant mPSCs were decreased in Snap25-null mutants (n = 3) compared with controls (n = 3; ∗∗∗p < 0.001). TTX treatment, however, did not significantly reduce the frequency or amplitude of mPSCs recorded from SNAP-25-deficient slices (see Results) indicating that action potential-dependent responses that contribute to the sPSCs of control slices are completely absent in Snap25-null mutants. Error bars represent SEM. F, Response of Snap25-null mutant (n = 5) and control slices (n = 5) to bath application of GABA (50 μm). Note that the response to exogenous GABA in Snap25-null mutant slices was more robust than control (8.4-fold; p < 0.001; n = 8), suggesting that the decreased amplitude for mIPSCs recorded from mutant slices was not attributable to inherent receptor defects and that GABAA receptors may be upregulated in SNAP-25-deficient fetal brain.
