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. 2003 Dec;555(Pt 1):45–59. doi: 10.1113/jphysiol.2003.053900

Figure 2. The CN-induced inward current (ICN) is carried by Na+ influx.

Figure 2

The magnitude of the inward current induced by 2 mm CN (ICN) in hypoglossal MNs held at –60 or –70 mV was compared under different experimental conditions (A and C). A, no significant difference (n.s.) in the amplitude of ICN was found when TTX was present in the aCSF compared to the control condition (control, –51 ± 9 pA, n= 8; TTX, –56 ± 13 pA, n= 7). Blockade of K+ currents with TEA and replacement of intracellular K+ by Cs+ did not change the magnitude of ICN either (TTX, TEA, CsCl, –62 ± 15 pA, n= 10). Similarly, additional wash-in of Cd2+ to block Ca2+ conductances did not change ICN amplitude (TTX, TEA, CsCl, CdCl2, –46 ± 8 pA, n= 4). B, recording of MN membrane potential (Vm) in the presence of TTX. CN depolarized Vm even when Ca2+ was completely removed from the extracellular solution (containing 1 mm EGTA), further indicating that Ca2+ was not the charge carrier of ICN. C, reducing the extracellular Na+ concentration from 144 to 26 mm decreased ICN to 40 ± 13% of the control value (ICN: control, 45 ± 9 pA; low Na+, 18 ± 9; P < 0.05, n= 4); re-addition of Na+ increased ICN back to 76 ± 10%, identifying Na+ as the main charge carrier of ICN at the given membrane potential. (A and B, intracellular solution contained 100 μm fura-2.)