Figure 2.
Effects of bumetanide (BUM), serotonergic antagonist methysergide (MT), and 5HT on the spontaneous neuronal fictive swimming (whole-cell recordings). A, Representative traces of fictive swimming activity recorded in motoneurons before (control, top), after bumetanide (center), and in washout condition (bottom). The peaks of the spikes have been truncated. Bumetanide (3 min) caused clustering of fictive swim episodes that were separated by long quiescent intervals. This effect was reversible (washout). The asterisks point to expanded segments in D. B, 5HT (center) (Fig. 2C, center) reduced the duration of rest intervals compared with control (top). This effect was blocked by bumetanide (2 min), even in the presence of 5HT (bottom). C, Methysergide (bottom), similar to bumetanide, fragmented the robust fictive swimming induced by 5HT (center). D, Two superimposed fictive swim episodes, before (black line) and after bumetanide (gray line), taken from A (indicated by asterisk) to illustrate the similarity in their properties (duration, frequency, and area; illustrated by gray shade). These are summarized across all experiments in E-G. E, Box plots illustrating that the duration of fictive swim episodes across all experiments [before (C) and after 5HT, methysergide, bumetanide, 5HT plus bumetanide, and washout (W)] was conserved. F, The fictive swimming frequency (calculated from the large EPSPs, three of which are indicated by arrows in D; EPSPs could sometimes carry spikes) was similar across all experimental conditions as illustrated by box plots. G, The extent of depolarization during fictive swim episodes, calculated from the area under the curve (D, gray shade), was the same across all experiments, despite the pronounced effects of the drugs on the swim pattern. Error bars indicate SD.