Figure 14.

Evidence that the REM sleep-related depression of activity in XII motoneurons is caused by a concurrent withdrawal of endogenous activation mediated by NE and 5-HT. When a cocktail containing the α₁-adrenergic receptor antagonist, prazosin, and a broad-spectrum 5-HT receptor antagonist, methysergide, is injected into the XII nucleus at multiple antero-posterior levels, spontaneous XII nerve activity is depressed to 20% to 30% of its control level and remains depressed for several hours (line graph at the top). This indicates that XII motoneurons are under a strong endogenous excitatory drive mediated by NE and 5-HT. The three sets of bar graphs at the bottom show XII nerve activity levels measured just before (B), during (D), and just after (A) REM sleep-like episodes elicited by pontine microinjections of carbachol. The first set of bars characterizes typical REM sleep-like depression elicited under the control conditions (before prazosin and methysergide injection into the XII nucleus; see Fig. 11A for a detailed time course and pattern of a typical REM sleep-like episode). Under these control conditions, XII nerve activity is depressed to 20% to 30% of the control. The second set of bars represents XII nerve activity during REM sleep-like episodes elicited 40 to 50 min after prazosin and methysergide microinjections, that is, when the antagonists exert maximal effect (cf. top graph). Under these conditions, there is no additional depression of XII nerve activity during the REM sleep-like episode beyond that already caused by the antagonists. The third set of bars shows XII nerve activity during the REM sleep-like episodes elicited when XII nerve activity partially recovered from the effect of the antagonists. At this time after the antagonist injections (about 170 min), XII nerve activity is again depressed during the REM sleep-like episodes. Thus, when endogenous activation of XII motoneurons mediated by NE and 5-HT is fully blocked (middle set of bars), no depression of XII nerve activity occurs during the REM sleep-like episodes. This indicates an occlusion between the depression caused by the antagonists and the effect of REM sleep-like state that takes place at the level of XII motoneurons. (Data from Ref. 142 visualized as Fig. 3 in Ref. 267 and republished with permission from Elsevier.)