The reticular formation plays a role in the rhythmical cycle of sleep and wakefulness. Evidence for its role can be obtained by using the electroencephalogram, or EEG, which is a surface recording of electrical patterns. Further evidence is obtained from experimental evidence based on lesioning of selected areas in the reticular formation.
The EEG obtained during sleep suggests that the brain passes through several stages of sleep. Wakefulness is characterized by high frequency, low voltage activity. During the early phases of sleep, after about 90 minutes, high frequency, low voltage activity is observed, accompanied by movements of the eyeball and dreaming. This is the so-called rapid eye movement (REM) sleep phase. With time during sleep, the EEG becomes progressively more low frequency, high voltage in character (so-called slow-wave sleep) until eventually the order is back to REM sleep. This sequence may be repeated about five or six times during each physiological sleep period. During the sleep period, intervals between REM episodes decrease, and the length of REM periods increases.
Stimulating the reticular formation can alter the pattern of EEG activity in conscious animals. The EEG shows high frequency, low voltage activity. If the ascending reticular formation efferents are interrupted through a lesion or a section of the mesencephalon, the animal loses consciousness, and stimulation of the reticular formation no longer produces any change in the EEG. The ascending reticular pathways which effect the changes in the EEG do not involve the participation of any of the major sensory inputs to the cerebral cortex, since they can be lesioned without altering the effects of stimulation of the reticular formation on the EEG. It is likely, however, that the changes seen in the EEG
Greenstein, Color Atlas of Neuroscience © 2000 Thieme after stimulation of the reticular formation involve the reticulothalamic pathway; stimulation of the intralaminar thalamic nuclei produces similar changes to the EEG as those seen after stimulation of the reticular formation.
The reticular formation is important also in the factors that cause the animal to fall asleep. If the reticular formation is le-sioned in the mid-pons, the animal is no longer able to fall asleep. Furthermore, if a hypnotic drug such as a barbiturate is applied selectively to the pontine-mesen-cephalon area, the animal becomes anesthetized and loses consciousness. The EEG pattern becomes synchronized for slow wave sleep. If, however, the drug is then restricted to the caudal area of the pons, the animal wakes up and the EEG pattern is desynchronized. This suggests that the rostral pontine-mesencephalic reticular formation activates and arouses from sleep, while the caudal pons reticular formation is sleep inducing.
The identity of the specific reticular formation nuclei involved in sleep is not known with certainty. There is evidence that the serotonergic raphe nuclei are involved, since the intracerebral injection of 5-HT induces sleep in cats. Nevertheless, lesioning of the raphe nucleus does not permanently abolish sleep. It is now known that the raphe nuclei are partly responsible for the inhibition of REM sleep.
1 second effects of stimulating the reticular formation on the EEG
EEG recordings from different areas of cat cerebral cortex electrical stimulation of reticular formation desïZn^
stage 1 stage 2 stage 3
REM sleep slow wave sleep brain stem rostral pons caudal pons
-► activating from sleep; EEG desynchronized sleep-inducing; EEG synchronized
EEG patterns in sleep
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