Figure 6.

Activity-dependent, long-term increases in Cl_i require Na⁺-K⁺-ATPase and NKCC1. All cells recorded with 9 mm Na_pipette. A, After a train of action potentials in the recorded cell (20 Hz, 2.5 min) (Fiumelli et al., 2005), Cl_i reaches a persistently higher steady state. Data from a single cell are shown as mean ± SD. B, Cl⁻ transport rate as a function of the magnitude of Cl⁻ depletion before (♦) and after postsynaptic action potentials (◇) for the cell in A. As in Figure 5 B, in control conditions, there is no relationship between the size of the Cl_i depletion and Cl⁻ transport rate. After the train of action potentials, Cl⁻ transport with 9 mm Na_pipette more closely resembles Cl⁻ transport with 0 mm Na_pipette (Fig. 5 B) in that larger Cl_i depletions correlate with slower NKCC1 Cl⁻ transport. C, The selective α2/α3 Na⁺-K⁺-ATPase antagonist DHO (10 μm) prevents the persistent increase in Cl_i after the train of action potentials. Data from a single cell are presented as mean ± SD. D, Inhibition of α2/α3 Na⁺-K⁺-ATPase (n = 4) or NKCC1 (n = 2) prevents the persistent increase in Cl_i after a train of action potentials. For each cell, Cl_i was normalized to its value before action potentials.