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KMID : 0377519880130020249
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Chung-Ang Journal of Medicine
1988 Volume.13 No. 2 p.249 ~ p.259
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Influence of Tricyclic Antidepressant on Synaptosomal Calcium Transport
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Chung, Jin-Hee/정진희
Lee, Chung-Soo/Shin, Yong-Kyoo/Lee, Kwang-Soo/이정수/신용규/이광수
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Abstract
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Neurotransmitter release may be´associated ,with
entry of Ca´ + and a rise in the concentration of internal ionized calcium. Membrane depolarization opens the Ca+ + channels and causes a transient increase in the [Ca+ +]i. Many studies observed that central antidepressants affect transport of mono-amines at presynaptic terminals. In the present study, effects.of tricyclic antidepressant and MAO inhibitor on Ca´ + uptake by and -Na+-Ca+ + exchange in synaptosomes were investigated. In K+ rich medium, the amount of Ca+ + uptake by synaptosomes was 16.31 nmoles/2 min/mg protein. Tricyclic antidepressants, amitriptyline, imipramine and doxepin significantly inhibited K+ induced Ca uptake, and MAO inhibitor, tranylcypromine had a little inhibition. Tricyclic anti-depressants also inhibited the activity of Mg+ + independent Ca+ ` ATPase which was activated by cxtcrnal K-. K+ induced Ca++ uptake was inhibited by chlorpromazine and almost completely inhibited by chlorpromazine plus verapamil. Amitrip-1\ 1111c cnhibited an additional effect on inhibitory c llcct of either chlorpromazine or verapamil. Chlorportnazine inhibited the activity of Ca+ ´ ATPase. FOnnation rate of membrane depolarization by K+ \V .´IS reduced by amitriptyline, imipramine and doxcpin but not tranylcypromine. The amount of rckascd Ca - from Ca+ + loaded synaptosomes by 20 m´v1 Na-- was 9.50 nmoles/2 min/mg protein. :\11 drugs tested inhibited a Na+ -Ca+´exchange and activity of Na´-Ca´´ exchange and activity of
Na´-Ca ATPase. The results suggest that incyclic antidepressants may inhibit Ca´ ` uptake at presynaptic terminals ay olockade of Ca´ + channcl and by action on chlorprommazine sensitive sites. I n the presence of central antidepressants, it is assumcd that the return from excitated state to resting state in nerve cells may be delayed.
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