Superfusion of bumetanide blocked the formation of hippocampal LTP in a dose dependent manner.

(A) From Left to right, representative superimposed traces of fEPSPs recorded extracellularlly under control conditions and after exposure to 0, 5, 10, and 20 µM bumetanide. Application of 10 µM bumetanide blocked LTP formation in hippocampus CA1 Schaffer collateral fiber. Bumetanide was applied from −10 min∼10 min. n = 10 for each trial (B) fEPSP recorded in the stratum radiatum and evoked by stimulation of the Schaffer collateral—commissural pathway with different intensities in vehicle-treated and bumetanide-treated slices (10 µM). fEPSP slopes are comparable between vehicle-treated (filled circle, n = 8) and bumetanide-treated (open circle, n = 8) for a given range of stimulus intensities. (C) Fiber volley amplitudes are similar between vehicle-treated and bumetanide-treated (10 µM) slices for a given range of stimulus intensities.