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. 2010 Jun 2;30(22):7672–7684. doi: 10.1523/JNEUROSCI.0290-10.2010

Figure 2.

Figure 2.

Voltage-dependent increases in tonic conductance were insensitive to inhibition of transporter-mediated or vesicular GABA release. A, Current responses to bicuculline application (Bic) (10 μm) under control conditions (left panel) and in the presence of SKF (40 μm) (right panel). Tonic current was increased by SKF. Holding potential was −40 mV. B, Mean tonic current density (in picoamperes/picofarad) versus voltage under control conditions and in presence of SKF (n = 6). Outward rectification was unaffected by SKF. C, Mean capacitance-specific conductance versus voltage (n = 6). There was a shift in the conductance curve, but the voltage dependence of tonic conductance was unaffected by SKF; the slopes of the solid lines are 0.31 and 0.33 pS/pF · mV−1 for control and SKF, respectively. The symbols are the same as in B. D, Current responses to Bic under control conditions (left panel) and with zero extracellular Ca2+/1 mm EGTA (right panel). As seen previously (Wu et al., 2006), phasic currents were reduced by zero extracellular Ca2+, but tonic currents were not (amplitudes of illustrated tonic currents were −31 pA for control and −38 pA for zero Ca2+). Holding potential was −60 mV. E, Tonic current density versus voltage for experiments with zero Ca2+/1 mm EGTA (n = 6). F, Capacitance-specific conductance versus voltage for all neurons tested in zero Ca2+/1 mm EGTA. The symbols are the same as in E. The voltage-dependent increase in tonic conductance was independent of extracellular Ca2+. The slopes of the solid lines are 0.30 and 0.23 pS/pF · mV−1 for control and zero Ca2+, respectively. Error bars represent SEM.