The Neural Control of Slow-Wave and REM Sleep
Although sleep involves most of the brain, the basal forebrain region is particularly important to slow-wave and REM sleep. Sterman and Clemente found that electrical stimulation of this area produced drowsiness and the subjects of the study readily fell asleep. Evidence also suggests that the mechanisms involved in an animal’s ability to regulate its own body temperature (thermoregulation) are closely related to those involved in sleep. There are certain neurons that are extremely sensitive to changes in brain temperature. Warming of the preoptic area and the anterior hypothalamus (POAH) induces slow-wave sleep, similar to the effects of electrical stimulation shown by Strerman and Clemente. This could explain why people experience excessive sleepiness when they haver a high fever, or why people generally feel sleepy on hot summer days. It follows then, that sleep reduces brain temperature.
REM sleep consists of desynchronized EEG activity, muscular paralysis, rapid eye movements, and increased genital activity. REM sleep is controlled from within the pons. The executive mechanism activates the different components of REM sleep and consists of neurons that secrete acetylcholine. It has been discovered that people who are exposed to organophosphate insecticides (acting as acetylcholine agonists) spend higher amounts of time in REM sleep.
The brain contains several groups of acetylcholinergic neurons (which control the onset of REM sleep), the most important of these are found in the dorsalateral pons, in the PDT (pedunculopontine tegmental nucleus) and the LTD (laterodorsal tegmental nucleus). This region is commonly refered to as the peribrachial area. Certain neurons in the peribrachial area fire extremely fast during REM sleep; it is the high activity in the acetylcholinergic cells that is thought to kickstart a bout of REM sleep. Welter and Jones found through making lesions in the peribrachial area that the amount of REM sleep a person exhibits is directly related to the number of colinergic neurons that are functioning. Those who had kainic acid injected into their peribrachial areas experienced drastic reductions in their amounts of REM sleep.
The acetylcholinergic neurons of the peribrachial area send axons to the medial pontine reticular formation and to several regions of the forebrain, i.e., the basal ganglia, the thalamus, the the hypothalamus, the preoptic area, the hippocampus and the cingulate cortex. In addition they send axons to the brain stem regions involved in the control of eye movements. This explains how the acetylcholinergic neurons are responsible for the onset of REM sleep, including genital arousal, muscular paralysis, and rapid eye movements. Activation of the forebrain neurons causes arousal and rapid eye movements occur because of axons sent from the peribrachial area to the tectum. Muscular paralysis is interrupted by lesions to the brain stem – in these circumstances, people act out their dreams.