Chemicals in the brain
>>><<<Compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves. The monoamine neurotransmitters norepinephrine, serotonin and histamine are completely unavailable. Injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. Carbachol, which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monoamine neurotransmitters have already been depleted.[3][22][23][24][25]
Two other neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.[3][26]
Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.[27]
Models of REM regulation
According to the activation-synthesis hypothesis proposed by Robert McCarley and Allan Hobson in 1975–1977, control over REM sleep involves pathways of "REM-on" and "REM-off" neurons in the brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep.[3][22][24][28] They used Lotka–Volterra equations to describe this cyclical inverse relationship.[10]: §12.2 369–373 Kayuza Sakai and Michel Jouvet advanced a similar model in 1981.[26] Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.[29] The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters;[30]: 16 researchers in recent years increasingly include GABA regulation in their models.
Two other neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.[3][26]
Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.[27]
Models of REM regulation
According to the activation-synthesis hypothesis proposed by Robert McCarley and Allan Hobson in 1975–1977, control over REM sleep involves pathways of "REM-on" and "REM-off" neurons in the brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep.[3][22][24][28] They used Lotka–Volterra equations to describe this cyclical inverse relationship.[10]: §12.2 369–373 Kayuza Sakai and Michel Jouvet advanced a similar model in 1981.[26] Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.[29] The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters;[30]: 16 researchers in recent years increasingly include GABA regulation in their models.