Figure 8.

KCC2 and NCKK1 are involved in the production of biphasic and RD responses. A1, Single (left) and averaged (n = 6; right) biphasic responses triggered by glutamate (30 μm, 30 s, arrowhead) in control condition (full line) and in the presence of furosemide (Furo.; 100 μm, dotted line). Note that only the second part of the optical signal (increase of the phase shift) was blocked by furosemide. A2, Single (left) and averaged (n = 6; right) RD response triggered by glutamate (30 μm, 30 s, arrowhead) in control condition (full line) and in the presence furosemide (dotted line). The amplitude of RD response is strongly decreased by furosemide. A3: Concentration–response curves of the inhibitory effect of furosemide on biphasic (full square and full line; IC₅₀ = 580 nm) and RD (empty square and dotted line; IC₅₀ = 550 nm) responses. B1, Single (left) and averaged (n = 6; right) biphasic responses triggered by glutamate (30 μm, 30 s, arrowhead) in control condition (full line) and in the presence of bumetanide (Bume.; 20 μm, dotted line). With this blocker, there were no modifications of the biphasic responses. B2, Single (left) and averaged (n = 14; right) RD responses triggered by glutamate (30 μm, 30 s, arrowhead) in control condition (Cont.; full line) and in the presence of bumetanide (dotted line). The amplitude of the RD response is decreased by bumetanide to a smaller degree than by furosemide. B3, Concentration–response curves of the inhibitory effect of bumetanide on biphasic (Biph.; full square and full line; IC₅₀ not determined) and RD (empty square and dotted line; IC₅₀ = 55 nm) responses. Note that an inhibitory effect of bumetanide was observed from 100 μm on for the biphasic response, a concentration 2000-fold higher than the IC₅₀ observed for the RD response. Calibration: 2 min and 2°.