Figure 2

Schema of the neuronal circuitry that is currently believed to be involved in the pontine regulation of rapid eye movement (REM) sleep and generation of motor atonia. Decreased discharge in dorsal raphé and locus coeruleus complex neurons preceding and during REM sleep progressively disinhibits pontine cholinergic neurones of the laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) via withdrawal of serotonin (5-HT)-mediated and noradrenaline-mediated inhibitory inputs. Activation of these LDT/PPT neurones then leads to increased acetylcholine (ACh) release into the pontine reticular formation, resulting in activation of the neuronal systems that mediate ascending and descending signs of REM sleep (e.g. cortical desynchronization and motor atonia, respectively). Exogenous application of a cholinergic agonist (e.g. carbachol) by microinjection into the pontine reticular formation is used to mimic this process and trigger REM-like neural events in reduced preparations (e.g. anaesthetized or decerebrate animals). Postural motor atonia in REM sleep is produced by postsynaptic inhibition of motor neurones by γ-aminobutyric acid (GABA) and glycine. Neurones of the medullary reticular formation are thought to drive this inhibition, themselves being driven by neurones in the pontine reticular formation (the reticular structures are indicated by the boxes). Whether hypoglossal (XII) motor neurones are also postsynaptically inhibited in REM sleep by similar mechanisms is uncertain. Hypoglossal motor neurones also receive excitatory inputs from the locus coeruleus complex and medullary raphé that may also contribute to reduced genioglossus muscle activity in sleep, especially REM sleep. Corelease of thyrotropin-releasing hormone (TRH) and substance P from raphé neurones may contribute to this process. The influences of other neural systems that are potentially modulated by sleep states are not included for clarity. See text for more details. +, excitation; -, inhibition; M, muscarinic.