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The Ascending Arousal system
The ascending arousal system has two major branches, which include discrete cell populations and neurotransmitters .
The first branch supplies nerves into the thalamus, activating neurons and nuclei essential for thalamocortical transmission.
The second branch of the ascending arousal system projects into the lateral hypothalamus, basal forebrain and cerebral cortex [2, 3, 4].
It comprises a number of cell populations (including noradrenergic, serotoninergic, dopaminergic and histaminergic neurons), lateral hypothalamic peptidergic neurons (orexin/hypocretin) and the basal forebrain (contains acetylcholine or GABA) .
Neurons in these monoaminergic systems discharge most rapidly during wakefulness, slow down during non-rapid eye movement (NREM) sleep and show a little activity during rapid-eye-movement (REM) sleep [6, 7, 8]. A similar effect is observed with the orexin/hypocretin neurons [9, 10].
In contrast, melatonin-concentrating neurons are strongly active during REM sleep .
In sum, all these systems together discharge in a specific and coordinated manner to promote cortical arousal .
The VLPO and the Sleep State
Sherin et al determined that a group of ventrolateral preoptic neurons is specifically activated during sleep .
The ventrolateral preoptic neuron (VLPO) efferents contain inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and galanin, which play a major role in keeping the ascending arousal system quiet during sleep [13, 14].
Neurons of the extended VLPO are connected with the various sites in the brain that are involved in REM sleep.
While the VLPO cluster provides output to the histaminergic neurons. Histaminergic neurons are active during waking, reduce firing during NREM sleep and stop discharge during REM sleep [15, 16].
Afferent neurons of the monoaminergic arousal system also connect with the VLPO .
Noradrenaline, acetylcholine, and serotonin are all neurotransmitters of wakefulness inhibit VLPO neurons . The reciprocal inhibitory interaction of the VLPO neurons with the noradrenergic, serotoninergic and cholinergic waking systems play a key role in regulating sleep .
Experiments in different animals showed that injury to the VLPO cluster and the extended VLPO decreased NREM and REM sleep [19, 20].
A familial advanced sleep phase syndrome (FASPS) mutation in location 2106 (A-G) of epsilon casein kinase 1 (CK1ε)-binding herp2 gene on chromosome 2 results in translocation of serine in amino-acid 662 with a glycine (56624) .
Phenotypes are a set of observable characteristics of an individual resulting from the interaction of its genotypes with the environment.
De novo synthesis refers to the synthesis of complex molecules from simple molecules such as sugars or amino acids as opposed to recycling after partial degradation.
DAT is a membrane-spanning protein that pumps the neurotransmitter dopamine out of the synapse back into the cytosol, from which other transporters sequester DA into vesicles and storage for later release.
Cataplexy is a symptom of narcolepsy in which patients experience abrupt transitions from waking to a state akin to REM sleep, with complete muscle atonia .
An efferent organ or body part carries impulses from the central nervous system to the effector.
Noradrenaline and serotonin inhibit the activity of orexin through the activation of G-protein-regulated inwardly rectifying K+ (GIRK or Kir3) channels via α2-adrenoceptors and 5HT1A-receptors .
An afferent nerve fiber or organ carries nerve impulses from the sensory organs to the central nervous system (CNS).
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