FUNCTION AND METABOLISM OF CATECHOLAMINES IN THE BRAIN
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概要
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The various pathways for the metabolism of exogenous and endogenous catecholamines have been repeatedly and extensively studied in recent years (1-12). It has been established that circulating catecholamine initially undergoes O-methylation rather than deamination in both man and animals (13, 14). The metabolic pathways of brain catecholamines is a little difference from that of circulating catecholamines. The relative importance of catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) in the inactivation of catecholamines in the brain has been a matter of debate. In the present study it was attempted to investigate the metabolism of noradrenaline which was injected into the cisterna of the rabbit.<BR> Noradrenaline is present in all sympathetic neurons. In recent years electronmicroscopic studies have demonstrated that noradrenaline resides in the electron-dense core of the granulated vesicle in preterminal axons and synaptic endings in the hypothalamus of the rat (15) and of the rabbit (16). The uneven distribution of catecholamines in the brain (17-21) suggests that catecholamines have roles to play in the specialized function of those ragions where its concentration is high. However the precise role for brain catecholamines has not been clearly understood. Reserpine, α-methyl-m-tyrosine, Su 5171, Win 18501-2 and monoamine oxidase inhibitors have been used to try to obtain informations on the function of catecholamines in the brain (22-28). It is well established that the sedative action of reserpine is closely associated with loss of noradrenaline and that of serotonin in the brain (29, 30). However, lack of which amines is responsible for the sedative action of reserpine is open to question. The present experiments were performed on rabbits and mice in order to obtain a better understanding of the central action of reserpine, Win 18501-2, Catron and iproniazid.
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