Cortico-subcortical relationships in the sleep-wake cycle

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 sense 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 direct descending inhibitory influences to the sleep centers located in the posterior hypothalamus.

Result: due to descending cortical inhibition, the hypothalamic sleep centers lose their ability to block the midbrain reticular formation. Thus, the functional loop closes to maintain stable activity.

Development of slow-wave and paradoxical sleep

The transition to sleep and the shift of its stages are caused by a systemic reorganization of cortico-subcortical connections.

Slow-wave 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. Breaking free from 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 the slow sleep stage.

During the paradoxical (rapid eye movement) sleep phase, the mechanism changes dramatically. The process is carried out through close morphofunctional connections of the hypothalamic centers with limbic structures. It is this complex that assumes the function of generating ascending activating influences on the cortex. The most important feature of this stage is that intense cortical activation (EEG activation, dream formation) proceeds against the background of a complete absence of stimulating influences from the brainstem reticular formation.

P.K. 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.

The theory relies on a number of classic experimental and clinical justifications:

• Hess's experiments. Electrical stimulation of the posterior hypothalamus in cats induced deep sleep. It was established that the excitation of hypothalamic neurons leads to direct inhibition of reticular formation cell activity.
• Decortication and sleep in newborns. Animals with a removed cortex and infants lack descending inhibitory control from the frontal lobes. Therefore, the hypothalamic "sleep centers" transition into an actively dominant state and inhibit the brainstem.
• Mechanism of awakening in newborns. Infant sleep is interrupted exclusively by the excitation of hunger centers localized in the lateral hypothalamus. They suppress the "sleep centers," which lifts the block from the reticular formation — the cortex receives ascending activation once again. Wakefulness lasts precisely until nutritional needs are met.
• Sensory deafferentation. Classical 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 turns off cortical activation and causes immediate sleep.

Role of the brainstem (Hobson and McCarley's theory)

An alternative view on sleep generation is presented in the works of American psychiatrists J. Hobson and R. McCarley, who associate the onset of sleep cycles primarily with brainstem structures.

A key role in their concept is played by giant neurons located in the anterior reticular formation of the brainstem. Through their long axons, these cells are able to exert a direct activating effect on the cerebral cortex. The regulation of state transitions is explained by the fact that these reticular formation cells are in complex reciprocal relationships with other brainstem neuronal groups, forming an internal sleep-wake oscillator.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of EEG activation formation during rapid eye movement sleep.
• Neurophysiology of giant neurons in the anterior brainstem reticular formation.
• Interaction of the lateral hypothalamus (hunger center) and sleep centers.
• Reciprocal inhibitory interactions of brainstem structures according to the Hobson-McCarley theory.

Other topics in the "Sleep" section

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