Mechanism of Wakefulness Maintenance
The state of active wakefulness is based on the continuous circulation of nerve impulses between the cortex and subcortical structures. The primary trigger is active afferentation—a powerful stream of sensory information from all sensory organs entering the brain.
This afferentation stimulates the structures of the reticular formation (formatio reticularis). The activated reticular formation generates powerful ascending activating influences that spread to the cerebral cortex, maintaining it in a state of functional readiness. In response, excited neurons of the frontal cortex send descending inhibitory influences to the sleep centers located in the posterior hypothalamus.
Result: Due to descending cortical inhibition, the hypothalamic sleep centers lose the ability to block the midbrain reticular formation. Thus, the functional loop closes to maintain stable activity.
Development of NREM and REM Sleep
The transition to sleep and the succession of its stages are driven by a systemic reorganization of cortico-subcortical connections.
Non-rapid eye movement (NREM) sleep begins with the elimination of sensory afferentation (e.g., in silence and darkness). This leads to a drop in the tone of the reticular formation and a decrease in its ascending activating influences on the cortex. As a result, the frontal cortex ceases to inhibit the neurons of the posterior hypothalamic sleep center. Escaping control, the posterior hypothalamus begins to actively inhibit the reticular formation of the brainstem. A complete blockade of ascending activation occurs, marking the onset of NREM sleep.
During the phase of rapid eye movement (REM) sleep, the mechanism changes drastically. The process is carried out through close morphofunctional connections between hypothalamic centers and limbic structures. It is this complex that assumes the function of generating ascending activating influences on the cortex. A crucial feature of this stage is that intense cortical activation (EEG activation, dreaming) proceeds against the background of a complete absence of stimulating influences from the brainstem reticular formation.
Anokhin's Cortico-Subcortical Theory of Sleep
P.K. Anokhin formulated a concept explaining the nature of normal sleep and its disorders. The leading postulate of the theory states: whatever the cause of falling asleep, sleep is always a direct consequence of a decrease in ascending activating influences from subcortical formations on the cerebral cortex.
This theory is supported by several classic experimental and clinical findings:
- Hess's experiments. Electrical stimulation of the posterior hypothalamus in cats induced deep sleep. It was established that excitation of hypothalamic neurons leads to direct inhibition of reticular formation cell activity.
- Decortication and newborn sleep. In animals with a removed cortex and in infants, descending inhibitory control from the frontal lobes is absent. Therefore, the hypothalamic "sleep centers" transition into an actively dominant state and inhibit the brainstem.
- Mechanism of newborn arousal. Infant sleep is interrupted exclusively by the excitation of hunger centers localized in the lateral hypothalamus. They suppress the "sleep centers," which removes the block on the reticular formation—the cortex receives ascending activation anew. Wakefulness lasts precisely until nutritional needs are met.
- Sensory deafferentation. Classic clinical observations by A. Strümpell and S.P. Botkin showed that the complete loss of sensory input fatally reduces the tone of the reticular formation. This shuts down cortical activation and induces immediate sleep.
Role of the Brainstem (Hobson-McCarley Theory)
An alternative view on sleep generation is presented in the works of American psychiatrists J.A. Hobson and R.W. McCarley, who attribute the genesis of sleep cycles predominantly to brainstem structures.
A key role in their concept is played by giant neurons located in the anterior parts of the brainstem reticular formation. Through their long axons, these cells are capable of exerting a direct activating effect on the cerebral cortex. The regulation of state transitions is explained by the fact that these reticular formation cells exist in complex reciprocal relationships with other brainstem neuronal groups, forming an internal sleep-wake oscillator.