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 serotonin reuptake inhibitors, tricyclics, and monoamine oxidase inhibitors) and stimulants (such as amphetamine, methylphenidate and cocaine) interfere with REM sleep by stimulating the monoamine neurotransmitters which must be suppressed for REM sleep to occur. Administered at therapeutic doses, these drugs may stop REM sleep entirely for weeks or months. Withdrawal causes a REM rebound. Sleep deprivation stimulates hippocampal neurogenesis much as antidepressants do, but whether this effect is driven by REM sleep in particular is unknown. Although it manifests differently in different animals, REM sleep or something like it occurs in all land mammals as well as in birds. The