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KMID : 0391519930010010033
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Journal of the Korean Child Neurology Society
1993 Volume.1 No. 1 p.33 ~ p.40
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An Experimental Study on the Effect of Diphenylhydantion and GABA on Na+, K+ -ATPASE in Microsomal Fraction of Rat Brain
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Abstract
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It has been widely accepted to exert antiepileptic activity, membrane-stabilize effect which has been attributed its ability to prevent the rise in intracelluar concentration of sodium upon freezing, electrical stimulation of the neuronal tissue.
The
mechanism by which in stimulated nerve are considered two possible explanations : 1) DPH could increase the rate of active transport of sodium out of the nerve cell, 2) DPH could inhibit the influx of sodium into cell during the stimulation of
neuronal
tissue.
In order to establish possible mechanism for the active role or non-role of Na+, K+, -APTase activity, The following serial experimental studies have been performed on. microsomal fraction of rat brain which prepared by Rawson and Pincus method,
Fiske-Subbarow method for measuremnt of enzyme activity and Lowry et al method for determination of protein faction.
@ES The following results were obtained :
@EN 1. Depending dose of DPH(0.01, 0.50, 1.00 mM), The inhibition or activation of Na+, K+, -ATPase activity was not observed in the presence of DPH.
2. Na+, K+, -ATPase activity was inhibited 55.3% by ouabain administration, and has no effect on Na+, K+, -ATPase activity adding. DPH.
3. Na+, K+, -ATPase activity was stimulated 24.7% by GABA administration, and no increase or decrease of enzyme activity was obsered in case of administration of GABA and DPH.
4. Depending on the different Na concentration, the effect of DPH on Na+, K+, -ATPase activities were not observed at 20 mM, 40 mM and 80mM Na concentration in the presence of 17mM K concetration respectively
5. Depending on the different K concentration, the effect of DPH on Na+, K+, -ATPase activities were not changed at 2 mM, 10 mM and 17 mM K concentration in presence of 80mM Na concentration respectively.
On the basis of our experiments, the following possible acition of DPH are able to be withdrawn. It is evidence indicating that the mechanism by DPH which stabilizes neuronal membrane and prevents the rise in intracelluar sodium in stimulated
nerve
tissue, which indicated that DPH has not propertity of extrusion of sodium by Na+,K+ -ATPase activation, but DPH interferes with the passive movement of sodium by passive diffusion during the stimulation of neuronal tissue.
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