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Sleep and dreams

The Sleep/ Dream/ Wake Cycle

One of the small proteins (or peptides) involved in the modulation of wakefulness is corticotropin-releasing hormone (CRH). CRH is synthesized by the neurons of the hypothalamus and activates the pituitary and adrenal glands when an individual is subjected to stress.

The hormone ACTH and endorphins are other peptides that stimulate the wakefulness network. (Both ACTH and endorphins are derived from the same molecule: pro-opiomelanocortin.)

Prolactin is a hormone that has many different functions. It is associated with lactation in women but is also present in men. One of its many functions is to promote REM sleep.


Being awake results not from the activities of some “wakefulness centre” in the brain, but rather from the activation of a complex, redundant network of about ten groups of neurons distributed from the hypothalamus to the medulla oblongata.

These neurons communicate with one another by means of various neurotransmitters, but all have one property in common: they reduce or completely cease their activity when you are asleep.

One of these groups of neurons that activate wakefulness uses acetylcholine as its neurotransmitter. Located at the junction of the pons and the midbrain, these neurons project their axons to the thalamocortical cells of the thalamus, which they excite by means of acetylcholine.

Another group of neurons, which produce norepinephrine, also are involved in wakefulness. These neurons’ cell bodies are situated in the locus coeruleus and send projections to the cortex and the limbic system. Receiving sensory and vegetative signals, these noradrenergic neurons promote alertness and play an important role in reactions to stress.

The serotonergic neurons of the raphe nuclei also play an important role in wakefulness—for example, by blocking the activity of the neurons from which PGO waves originate during REM sleep. But serotonin also paradoxically plays a role in triggering sleep, by influencing the neurons of the preoptic hypothalamus.

A fourth group of neurons that play a role in wakefulness are scattered through the brainstem and other areas of the brain. These neurons, which use glutamate as their neurotransmitter, are highly active during periods of wakefulness and quiescent during non-REM sleep. However, some of them become active again during REM sleep, firing the neurons that prevent the body from moving during REM sleep.

In the posterior hypothalamus, some neurons that produce histamine become active as soon as you awaken but are completely silent during REM sleep. These neurons send their projections throughout the brain, and in particular to the other types of wakefulness neurons, which they help to activate.

Lastly, in the cortex, some neurons can also be activated by the removal of the inhibition exerted on them by other small cortical neurons that use the neurotransmitter GABA. During periods of wakefulness, the activity of these GABAergic neurons is attenuated by other GABAergic neurons located in the posterior hypothalamus and the basal telencephalon.

Awakening is thus the result of a general increase in the activity of the cortex which produces the unsynchronized firing of cortical neurons characteristic of periods of wakefulness. This neural activity is maintained by stimuli from both the external and the internal environments. Thus the activation of the brain’s wakefulness network can be said to be maintained, in part, by the state of wakefulness itself! A good example of this is when you force yourself to stay awake longer than usual, even though you are feeling tired.

But another, parallel mechanism also helps to maintain wakefulness: the inhibition of sleep. Interestingly, the two types of sleep—REM sleep and non-REM sleep—seem to be inhibited separately, by two distinct sets of wakefulness circuits in the brain.


Original modules
Tool Module: Brain Imaging Brain Imaging

Brain Rhythms: The Oscillations That Bind

The recording of an EEG is a completely pain-free, non-invasive procedure, because the electrodes are simply glued to the patient’s scalp. The various traces in an EEG represent the differences in electrical potential detected between these various electrodes.

Where do these differences come from? Mainly from the differences in the activity levels of the neurons in the various layers of the cerebral cortex when different areas of the cortex are compared. But the contribution of each individual neuron to the resulting signal is extremely small. Also, to reach the electrodes, this signal must pass through several layers of tissue, including the meninges, the skull, and the scalp, which attenuate this signal considerably. The signal will not be strong enough for the electroencephalograph to pick up unless several thousand neurons are firing simultaneously.


The electroencephalograph (follow the Tool module link to the left) is an instrument that provides information about the overall activity of large groups of neurons in the brain. The print-out from an electroencephalograph is called an electroencephalogram, or EEG. An EEG will never tell you what someone is thinking, but it will tell you whether they are thinking, or whether they are simply awake, or, for that matter, asleep.

Each electroencephalograph sensor consists of an electrode that is attached to a particular location on the scalp and that picks up a signal from the neurons in a given area of the cortex. The more synchronized the activity of these neurons, the greater the amplitude of the signal that the sensor receives. And the greater the amplitude of this signal, the greater the deflection (movement) of the pen that records the EEG trace.

Adapted from: Neurosciences, Bear, Connors, and Paradiso, Éditions Pradel, 2002

When a group of cortical neurons are excited simultaneously (that is, when all their dendrites receive stimuli at the same time), their weak individual signals are summed so that they become perceptible to the electrode attached to the adjacent portion of the scalp. Conversely, when the stimuli received by these neurons are not synchronized, their summed signals are weaker, and the amplitude of the resulting EEG trace will be smaller and more irregular.

Broadly speaking, when the cortex is busy analyzing information from a sensory stimulus or internal process, the activity of its neurons is relatively high but also relatively unsynchronized. Each little group of neurons is being activated by a different aspect of the cognitive task that the cortex is performing, so the activity of these groups is not highly synchronized, and the amplitude of the EEG trace is correspondingly small. In this state, high-frequency beta waves predominate.

In contrast, during non-REM sleep, the cortical neurons are no longer busy processing information. In addition, many of them are being stimulated by the same slow, rhythmic pulse from the thalamus, so their activity is highly synchronized. As a result, the EEG shows the high-amplitude, low-frequency trace characteristic of delta waves.

But what is the source of this rhythmic brain activity? Research indicates that the brain may synchronize these periodic oscillations in two different ways. In some cases, a group of neurons may be activated synchronously because all of them are influenced by a single generator, or pacemaker. In other cases, a group of neurons may set their own pace, by exciting or inhibiting one another.

If we compare groups of neurons to groups of musicians, we can say that in the first case, the neurons are like the members of an orchestra, all following instructions from the same conductor. In the second case, they are more like jazz musicians at a jam session, each constantly adjusting to the others by listening to and watching them.

Another good analogy for the second of these synchronization mechanisms is something that often happens at the end of a concert: the members of the audience start calling for an encore and then spontaneously start clapping their hands rhythmically, in unison. No one has to help them co-ordinate their clapping. People can clap their hands only within a narrow frequency range, so once a few people start clapping, it is easy for others to hear their rhythm, start clapping themselves, and then speed up or slow down until they are in phase with it.

Source: Neurosciences, Bear, Connors, and Paradiso, Éditions Pradel, 2002

A network of neurons interact in somewhat the same way, but through excitatory and inhibitory connections, rather than sight or sound. And because these neurons can generate action potentials only within a limited frequency range, though these potentials may be only partly synchronized at first, they can become more so until they develop major rhythmic oscillations.

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