The reciprocal interaction model

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McCarley and Hobson proposed the reciprocal interaction model to explain the transitions into and out of REM sleep states, described by the Lotka-Volterra equations, derived from population models of predator/prey interaction [136]. The limit cycle model, an update of the reciprocal interaction model, incorporated circadian and local GABAergic influences on REM sleep regulation [118,137].

As reviewed in Figure 2.5, select cholinergic neurons of LDT/PPT increase firing prior to and during REM sleep. These cholinergic neurons specifically direct the firing of reticular formation neurons

(SubC, parabrachial nucleus, and PnO), whose glutam-atergic output is responsible for the activation of the various components of REM sleep described above, including muscle atonia, PGO wave generation, and hippocampal theta activity. LDT/PPT neurons also project to GABAergic interneurons of RF. Therefore, inhibition of these GABAergic RF neurons, which inhibit REM-on RF neurons, provides positive feedback, where glutamatergic RF neurons are disinhibited as REM sleep begins. Cholinergic projections to both DR and LC have been described, although in vitro evidence only supports a direct excitatory role of acetylcholine on LC neurons [138]. The original model suggested that there was a very slow modulation of LC firing by LDT/PPT due to a slowly acting intracellular cascade leading to significant excitation. However it now seems much more likely that removal of a GABAergic input to LC/DR is important. We now postulate that, during REM sleep, GABAergic neurons, excited by LDT/PPT cho-linergic output, inhibit these serotonergic and nor-adrenergic REM-off neurons (evidence reviewed in [132]). In contrast, raphe serotonergic and locus coer-uleus noradrenergic neurons act as REM-off neurons, inhibiting the REM-on neurons of LDT/PPT during waking and NREM sleep. During wakefulness and NREM sleep, serotonergic and noradrenergic levels build up, activating autoreceptors that inhibit these systems, allowing REM state expression.

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Muscle atonia SubC

^ PGO Waves SubC/PB

Hippocampal theta PnO

Figure 2.5 Graphic depiction of the modified reciprocalinteraction modelof REM sleep control, originally proposed by McCarley and Hobson [136]. REM off neurons inhibit the REM on neurons during waking and NREM sleep. During NREM sleep, REM off cellfiring significantly decreases as a result of self inhibition of the REM off neurons; this results in disinhibition of REM on neurons, and REM sleep then occurs. As REM sleep progresses, REM on cells begin to excite the REM off cells, which become gradually more active and eventually terminate REM sleep. Cholinergic (REM on) LDT/PPT output excites local GABAergic interneurons that in turn inhibit REM off neurons. Also, this cholinergic output acts to inhibit local GABAergic REM off interneurons, which in turn inhibit the glutamatergic REM on reticular formation neurons.

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