Abstract
It has been shown that endogenous prostaglandin D 2 and prostaglandin E 2 (PGE 2) are involved in sleep-wake regulation. Our recent experimental result that exogenously administered PGE 2 significantly reduces canine cataplexy (a pathological equivalent of rapid-eye-movement sleep atonia and a symptom of narcolepsy) suggests that PGE 2 is involved in the pathophysiology of canine narcolepsy. In order to further investigate the role of prostaglandins (PGs) in this disorder, PG levels in cerebrospinal fluid (CSF) of genetically homozygous narcoleptic, heterozygous (unaffected), and control Doberman pinschers were studied. PGE 2 levels were measured by direct radioimmunoassay (RIA) and after high-grade purification using PG affinity columns and high-performance liquid chromatography. PGD 2 and PGF 2α levels were measured by RIA after high-grade purification. There was no significant difference in PGE 2 levels between homozygous narcoleptic and heterozygous or controls dogs, and PGD 2 and PGF 2α levels were undetectable in most cases. Our results do not favor the hypothesis that central PGE 2 levels are modified in canine narcolepsy, assuming that PGE 2 levels in cisternal CSF properly reflect PGE 2 production in the brain.
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