Article Figures & Data
Figures
- Figure 1.
Suppression of stimulus-evoked alkaline transients by XCA. Superimposed alkaline transients recorded in area CA1 stratum radiatum in response to 10 pulse, 100 Hz stimulation (black bar) of the Schaffer collaterals (recording depth, ∼100 μm) are shown. Control trace (CTL; black) and record after superfusion of XCA (gray) are shown.
- Figure 2.
Effect of XCA on single evoked EPSCs. A, Comparison of normalized control (CTL) versus XCA traces at a VH of −80 mV. Raw traces before normalization are shown in the inset, with calibration bars indicating the same time and current scale as in normalized records. B, Comparison of EPSCs at a VH of −30 mV. Note the shortening of the decay after addition of enzyme (gray). C, Comparison of superimposed EPSCs at a VH of −30 mV with 1 mm intracellular MK-801, 0 Mg2+ ACSF. Note the absence of effect after adding enzyme (gray overlay).
- Figure 3.
Effect of XCA on summated EPSCs. A, Summated currents in response to 10 pulse, 100 Hz stimulation of the Schaffer collaterals (VH = −30 mV). Records normalized to the peak control (CTL) current are shown. Note the shortening of decay with XCA (gray). B, Summated currents in 0 Mg2+ ACSF in response to a three pulse, 100 Hz stimulus train (VH = −80 mV). Note the shortening of decay with XCA (gray). C, Summated currents in 0 Mg2+ ACSF in response to a three pulse, 100 Hz stimulus train (VH = −80 mV). The pipette contained 1 mm MK-801. Note the absence of effect after addition of enzyme. Raw traces before normalization are shown in the insets, with calibration bars indicating the same time and current scale as in normalized records.
- Figure 4.
XCA curtailed the ADP. A, Current-clamp response to a five pulse, 12 Hz stimulus train. Note the marked shortening of the ADP after addition of XCA (gray). B, Current-clamp response to a 10 pulse, 100 Hz stimulus train. ADP was similarly shortened by XCA. C, APV reversibly curtailed the ADP after a 10 pulse, 100 Hz train. D, Suppression of the ADP was not attributable to run down. Responses to 10 pulse, 100 Hz stimulus shown for control train (CTL; black) and identical test train (gray) given after a 10 min interval are shown. Records shown here and in subsequent figures are averages of three to five raw traces. As a result, the apparent spike amplitudes are reduced, and the apparent spike frequency is increased, in the averaged traces.
- Figure 5.
Suppression of the ADP by XCA is NMDAR dependent. A, Responses to a three pulse, 100 Hz stimulus train (onset at arrowhead) in 0 Mg2+ ACSF. Note the marked curtailment of the ADP by XCA (gray). B, Responses to three pulse, 100 Hz stimulus train in 0 Mg2+ ACSF with 1 mm MK-801 in the pipette. Note the absence of effect after addition of enzyme. CTL, Control.
- Figure 6.
Suppression of the ADP by XCA requires functional enzyme. A, Responses to a 10 pulse, 100 Hz train in the presence of the poorly permeant carbonic anhydrase inhibitor benzolamide (20 μm). Note the absence of effect after adding enzyme. B, Responses to a 10 pulse, 100 Hz train. Addition of heat-inactivated enzyme had no effect on the ADP.
- Figure 7.
Suppression of ADP by XCA does not require GABAergic transmission or L-type Ca2+ channels. A, Responses to a 10 pulse, 100 Hz train in the presence of picrotoxin (PTX) and phaclofen (both 100 μm). Note the curtailment of the ADP after addition of enzyme (gray). B, Responses to a 10 pulse, 100 Hz train with 1 mm D-600 in the patch pipette. Note the curtailment of the ADP after addition of enzyme. CTL, Control.
