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KMID : 0365819730130010177
Journal of Pusan Medical College
1973 Volume.13 No. 1 p.177 ~ p.185
Studies on Phosphorylase Activity of Rat Brain

Abstract
Many biochemical and pharmacological studies have suggested a possible involvement of the phospho¡©rylase enzyme of the brain in the synthesis of norepinephrine, and several drugs have been studied for the action on brain phosphorylase, but only a few have been found to have consistant effect. Some drugs such as insulin caused a significant increase in the activity of the enzyme in the brain but the activity for reserpine administration to the rat could not be confirmed in experimental groups.
Some investigators showed that the hallucinogenic agents in combination with the anxiety-producing drugs depressed phosphorylase activity in the brain but other investigators suggested that antidepressant drugs might increase active catecholamine.
The present investigation was conducted in an attempt to study the effects of some hypnotics, tran¡©quilizers and antidepressants on phosphorylase activity of rat brain in vitro and in vivo, and the results are summarized as the follows.
1. Brain phosphorylase activity was slightly depressed by phenobarbital, amobarbital and reserpine in vitro.
2. Diazepam, promazine and chlorpromazine depressed brain phosphorylase activity in vitro markedly.
3. Brain phosphorylase activity was depressed by phenobarbital, diazepam, reserpine, promazine and chlorpromazine in vivo in the following order: reserpine>chlorpromazine>phenobarbital>prom¡© azinepdiazepam.
4. Brain phosphorylase activity was slightly increased by iproniazid, imipramine and amphetamine in vivo.
5. The increased effect of the brain phosphorylase activity by antidepressants was more remarkable when the rat was treated with reserpine before or after the drugs.
Consequently, these results suggested that a possible relationship between the phosphorylase level and the action of these drugs might exist in reference to active catecholamine, particularly norepinephrine, responsible for functional extracellular release.
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