Hypocretin has a long-lasting effect on the target neuron, that helps to maintain daytime wakefulness, suppression of REM sleep, and therefore paralysis or dream-like hallucination, that is a REM sleep characteristic manifested during the day when it is deficient. Hypocretin producing neuron is active during wakefulness and stimulates cortex, basal forebrain, brain stem and hypothalamus producing norepinephrine, serotonin, dopamine, and histamine. There are two coned hypocretin receptors, HCRTR1 and HCRTR2, that are serpentine G-protein-coupled receptors. Prepro-hypocretin is enzymatically cleaved into two peptides, divided into hypocretin 1 and 2, and consists of 33 and 28 amino acids, respectively. Hypocretin is synthesized in the lateral hypothalamus and is derived from a protein precursor called prepro-hypocretin. Quality of life studies suggest the impact of narcolepsy is equal to Parkinson’s disease. In many patients with narcolepsy, sleepiness is severe, resulting in difficulty focusing and staying awake at school, work and during periods of inactivity. Hypnagogic hallucinations or sleep paralysis are mostly transient. Cataplexy may disappear spontaneously in some patients and it is presumed the patient adapts to his or her illness and avoids situations in which cataplexy can occur. Symptomatic fluctuations may appear in the clinical course and in general, EDS is the initial symptom and cataplexy occurs slowly over several months after onset and persists for life. Narcolepsy patients exhibit EDS, cataplexy (decreased muscle tone triggered by emotions) and abnormal transition to rapid eye movement (REM) sleep. Narcolepsy is characterized by decreased cerebrospinal fluid (CSF) hypocretin concentration associated with arousal, wakefulness and sleep regulation.
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