Reticular Activating System

Cross references:   Dictionary     Figure Labels   Rhombencephalon    Medulla Oblongata   

Kolb & Whishaw give a fairly extensive discussion of the RAS on [K&W: 52 & 476-477].   

Reticular activating system (Wiki)   
    "The reticular activating system (RAS) is an area of the brain (including the reticular formation and its connections) responsible for regulating arousal and sleep-wake transitions."  
The RAS is composed of several neuronal circuits connecting the brainstem to the cortex. These pathways originate in the upper brainstem reticular core and project through synaptic relays in the rostral intralaminar and thalamic nuclei to the cerebral cortex.[4] As a result, individuals with bilateral lesions of thalamic intralaminar nuclei are lethargic or somnolent.[1] Several areas traditionally included in the RAS are:[5][6]

    The RAS consists of evolutionarily ancient areas of the brain, which are crucial to survival and protected during adverse periods. As a result, the RAS still functions during inhibitory periods of hypnosis.[7]"  
The neuronal circuits of the RAS are modulated by complex interactions between a few main neurotransmitters. The RAS contains both cholinergic and adrenergic components, which exhibit synergic as well as competitive actions to regulate thalamocortical activity and the corresponding behavioral state.

The reticular formation consists of more than 100 small neural networks, with varied functions"  

NOTE:  This is a very importnt part of the brain.  To learn more, click on the links. 


During the Spanish flu pandemic that raged after World War I ended in 1918, a Viennese neurologist, Constantin von Economo, observed that some flu patients fell into a state of lethargy or coma before dying, while others went several days without sleeping, and then died.

When von Economo autopsied the brains of these two types of patients, he found that they had different types of lesions. The patients who had been comatose before their deaths had lesions in the posterior hypothalamus or the upper part of the midbrain. Von Economo was thus the first scientist to use the term “wakefulness centre” to refer to these two parts of brain that seemed to be essential for wakefulness.

The patients who had experienced sleeplessness before dying had brain lesions in the
preoptic area of the anterior hypothalamus, which came to be known as the “sleep centre”.

Countless autopsies subsequently showed that when a person’s
brainstem suffers damage, whatever the cause, that person falls into deep sleep or a coma. This finding thus showed that the brainstem also plays an essential role in maintaining the state of wakefulness.


Some years later, in 1949, brain researchers Giuseppe Moruzzi and Horace Magoun successfully triggered comas in cats by using coagulation to destroy the central part of the brainstem, known as the reticular formation. From this result they concluded that these comas were due to an absence of wakefulness.

In other experiments, Moruzzi and Magoun found that by stimulating the reticular formation, they could awaken animals from normal sleep. The two researchers also knew that the reticular formation receives many incoming messages, in particular via the sensory pathways. From these two facts, Moruzzi and Magoun developed the concept of the “ascending activating reticular system”. The reticular formation in the brainstem then became the prime contender for the title of “wakefulness centre”.

But some of the conclusions drawn from these earlier, cruder, surgical interventions have since been invalidated by more selective experiments. In these experiments, neurotoxic substances were used to destroy the neurons of the posterior hypothalamus and the reticular formation, while leaving intact the axons that passed through these areas but arose from other structures elsewhere in the nervous system. The result: the wakefulness function was still diminished initially, but quickly returned to normal!

The researchers were thus forced to conclude that these other structures could take over the job of those that had been destroyed and that the wakefulness disorders created in past experiments had probably been attributable to damage to the axons arising from these other wakefulness-maintaining structures and passing through the structures that had been destroyed.

These results cast new doubt on a certain conception of sleep as a passive process, in which being deprived of sensory inputs was what caused people to fall asleep. In subsequent experiments, the application of electrical stimuli to the thalamus of cats while they were awake caused them to fall asleep, thus demonstrating that sleep is not simply a passive process, but rather involves interactions between the thalamus and the cortex.

Later, the finding that blocking the sensory messages reaching the brain in no way disturbed the cycles of sleeping and wakefulness contributed further to the abandonment of this passive model of the process of falling asleep. The discovery of the intense activity in the cortex during REM sleep also dealt a deadly blow to this model.  

Today, scientists instead regard sleep as an active phenomenon, and there is no longer any doubt about the important role that structures such as the anterior hypothalamus play in the onset of sleep. Other neurons heavily involved in controlling sleep and wakefulness belong to the various diffuse neuromodulation systems in the brainstem. By diffusing their neuromodulating substances throughout wide areas of the brain, the neurons in these systems act as switches that adjust the cortex’s sensitivity to sensory information.