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 activity in REM sleep as in wakefulness. The amygdala is also active during REM sleep and may participate in generating the PGO waves, and experimental suppression of the amygdala results in less REM sleep. The amygdala may also cardiac function in lieu of the less active insular cortex. 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