![]() ![]() Raven, New York, pp 199–233īertilsson L, Tuck JR, Siwers B (1980) Biochemical effects of Zimelidine in man. In: DJ McGinty, Drucker-Collin R, Morrison A, Parmeggiani P (eds) Brain mechanisms of sleep. Pharmacol Biochem Behav 5:599–602.īaker T, Dement WC (1985) Canine narcolepsy-cataplexy syndrome evidence for an inherited monoaminergic-cholinergic imbalance. Synapse 6:33–44īabcock DA, Narver EL, Dement WC, Mitler MM (1976) Effects of imipramine, chlorimipramine, and fluoxetine on cataplexy in dogs. Eur J Pharmacol 166:493–504Īppel NM, Mitchell WMM, Contrera JF, De Souza EB (1990) Effects of high dose fenfluramine treatment on monoamine uptake sites in rat brain: assessment using quantitative autoradiography. GBR 12909: selectivity and molecular mechanism of action. Neurology 42:34–43Īndersen PH (1989) The dopamine uptake inhibitor. Our findings also demonstrate that canine narcolepsy is a useful tool in assessing the pharmacological specificity of antidepressant drugs.Īldrich M(1992) Narcolepsy. Our results demonstrate the preferential involvement of adrenergic systems in the control of cataplexy and, presumably, REM sleep atonia. All compounds affecting noradrenergic transmission completely suppressed canine cataplexy at low doses in all dogs tested, whereas compounds which predominantly modified serotoninergic and dopaminergic transmission were either inactive or partially active at high doses. Some additional compounds interesting clinically but with less pharmacological selectivity, i.e., cocaine, dextroamphetamine, methylphenidate, nomifensine and pemoline, were also included in the study. A total of 14 compounds acting on the adrenergic (desipramine, nisoxetine, nortriptyline, tomoxetine, viloxazine), serotoninergic (fenfluramine, fluoxetine, indalpine, paroxetine, zimelidine) and dopaminergic (amfonelic acid, amineptine, bupropion, GBR 12909) systems were tested. ![]() ![]() In order to determine which monoamine is selectively involved in the therapeutic effect of these compounds, we examined the effects of selective monoamine uptake inhibitors and release enhancers on cataplexy using a canine model of the human disorder. Both stimulant and antidepressant drugs presynaptically enhance monoaminergic transmission but both classes of compounds lack pharmacological specificity. Cell 98, 365–376.Narcolepsy is currently treated with antidepressants to control REM-related symptoms such as cataplexy and with amphetamine-like stimulants for the management of sleepiness. The Sleep Disorder Canine Narcolepsy Is Caused by a Mutation in the Hypocretin (Orexin) Receptor 2 Gene. Lin, L., Faraco, J., Li, R., Kadotani, H., Rogers, W., Lin, X., Qiu, X., de Jong, P.J., Nishino, S., and Mignot, E. Identification and Functional Analysis of Mutations in the Hypocretin (Orexin) Genes of Narcoleptic Canines. Hungs, M., Fan, J., Lin, L., Lin, X., Maki, R.A., and Mignot, E. Small-breed dogs seem to be more severely affected. Symptoms usually appear by the dog’s 6 months of age. Predisposed breeds include the Labrador Retriever, Poodle, Dachshund and the Doberman Pinscher. Sudden loss of muscle tone triggered mainly by positive emotions that share some physiological similarities with REM sleep atonia, called cataplexy is the most valuable clinical feature used to diagnose narcolepsy. Narcolepsy has been diagnosed in many breeds and has an established hereditary component. Symptoms appear suddenly, and the recovery is spontanious as well. Dog narcolepsy Labrador type is a disabling sleep disorder characterized by daytime sleepiness, sleep fragmentation, striking transitions from wakefulness into rapid eye movement (REM) sleep, and symptoms of abnormal REM sleep, such as cataplexy, sleep paralysis, and hypnagogic hallucinations.
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