Non-rapid eye movement sleep activation occurs during NREM that is comparable to the type that occurs during REM. It is this sub-cortical activation that results in dreaming during the NREM stage during the morning hours. During non-REM sleep, the tonic drive to most respiratory muscles of the upper airway is inhibited. This has two consequences: However, because the diaphragm is largely driven by the autonomous system, it is relatively spared of non-REM inhibition. As such, the suction pressures it generates stay the same. This narrows the upper airway during sleep, increasing resistance and making airflow through the upper airway turbulent and noisy. For example,
Rapid eye movement sleep from unavailability of monoamine neurotransmitters (restraining the abundance of acetylcholine in the brainstem) and perhaps from mechanisms used in waking muscle inhibition. The medulla oblongata, located between pons and spine, seems to have the capacity for organism-wide muscle inhibition. Some localized twitching and reflexes can still occur. Pupils contract. Lack of REM atonia causes REM behavior disorder, sufferers of which physically act out their dreams, or conversely "dream out their acts", under an alternative theory on the relationship between muscle impulses during REM and associated mental imagery (which would also apply to people without the condition, except that commands to