Fig. 3. The electrographic features of rapid eye movement (REM) sleep are elicited by microinjection of cholinergic agonists (  e.g. , carbachol) or acetylcholinesterase inhibitors into medial regions of the pontine reticular formation (mPRF). The traces in  A illustrate 80 s of recording from an intact, unanesthetized cat during the transition from non-REM sleep to REM sleep (  arrow ) after saline (control) microinjection into the medial pontine reticular formation. Note the onset of muscle atonia in the electromyogram (EMG). The cortical electroencephalogram (EEG) shows the normal transition from the high-amplitude waves of non-REM sleep to the low-amplitude, fast-frequency waves of REM sleep. Recordings from depth electrodes placed in the left and right lateral geniculate bodies (LGB) reveal the onset of field potentials that comprise a state-specific marker of REM sleep. These potentials are named  PGO waves for the brain locations (pons, geniculate, occipital cortex) from which they can be recorded.  Microinjecting nanogram amounts of carbachol (  B ) into the mPRF causes a REM sleep–like state characterized by the same electrographic features of REM sleep (  A ). One difference is that microinjection of cholinomimetics into the mPRF causes onset of a REM sleep–like state to occur directly from wakefulness, with no intervening non-REM sleep (  B ). EOG = electrooculogram. From Baghdoyan  et al. ;  modified with permission.  C indicates that, compared with wakefulness, acetylcholine (ACh) release in the mPRF (see  inset ) significantly increases during both REM sleep and during the cholinergically evoked REM sleep–like state (Carbachol REM). From Leonard and Lydic  and Lydic  et al. ;  modified with permission. These findings demonstrate a role for pontine cholinergic transmission in the generation of REM sleep.