EFFECTS OF SODIUM ON PKC TRANSLOCATION - RELATIONSHIP TO NEUROTRANSMITTER RELEASE

被引：9

作者：

BASUDEV, H

ROMANOSILVA, MA

BRAMMER, MJ

CAMPBELL, IC

机构：

[1] INST PSYCHIAT,DEPT NEUROSCI,LONDON SE5 8AF,ENGLAND

[2] UNIV FED MINAS GERAIS,ICB,DEPT BIOCHEM,BR-30161 BELO HORIZONT,MG,BRAZIL

[3] UNIV FED MINAS GERAIS,ICB,DEPT IMMUNOL & PHARMACOL,BR-30161 BELO HORIZONT,MG,BRAZIL

来源：

NEUROREPORT | 1995年 / 6卷 / 05期

关键词：

NA+ INFLUX; TITYUSTOXIN; GRAMICIDIN D; GLUTAMATE RELEASE; PKC; SYNAPTOSOME;

D O I：

10.1097/00001756-199503270-00026

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

OUR previous work using Nac channel activators such tityustoxin (TsTX), indicated that local increases in Na+ modulate glutamate release from synaptosomes. We have now investigated the role of the Ca2+/phospholipid-dependent protein kinase (PKC) in mediating this effect. TsTX and KCI stimulate 'fast' glutamate release to the same extent but TsTX is more effective than KCI in enhancing the 'slow' phase of release. KCI greatly stimulates PKC translocation. However, TsTX inhibits basal and phorbol ester-induced translocation while the Na+-ionophore, gramicidin D, has no effect. Taken together, these data suggest TsTX mediated localized Na+ entry inhibits PKC translocation and that this effect may be associated with recruitment of vesicles to the readily releasable pool.

引用

页码：809 / 812

页数：4

共 15 条

[1] AN ION CHANNEL LOCUS FOR THE PROTEIN-KINASE-C POTENTIATION OF TRANSMITTER GLUTAMATE RELEASE FROM GUINEA-PIG CEREBROCORTICAL SYNAPTOSOMES [J].