ALPHA-LATROTOXIN RELEASES BOTH VESICULAR AND CYTOPLASMIC GLUTAMATE FROM ISOLATED NERVE-TERMINALS

被引:57
作者
MCMAHON, HT
ROSENTHAL, L
MELDOLESI, J
NICHOLLS, DG
机构
[1] UNIV DUNDEE, DEPT BIOCHEM, DUNDEE DD1 4HN, SCOTLAND
[2] CNR, CTR CYTOPHARMACOL, DEPT PHARMACOL, I-20133 MILAN, ITALY
[3] UNIV MILAN, SCI INST S RAFFAELE, I-20122 MILAN, ITALY
基金
英国惠康基金;
关键词
Calcium; Exocytosis; Glutamate; Synaptosomes; α‐Latrotoxin;
D O I
10.1111/j.1471-4159.1990.tb05793.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Abstract: α‐Latrotoxin causes a massive release of endogenous glutamate from guinea‐pig cerebrocortical synaptosomes. There appear to be two components to the release. In the first 2 min following addition of 1.3 nMα‐latrotoxin, glutamate release is largely energy dependent. Superimposed upon this release is a more slowly developing but ultimately much more extensive release of cytoplasmic glutamate together with γ‐aminobutyric acid and nonvesicular amino acids such as aspartate and α‐aminoisobutyrate. In parallel with this cytoplasmic release there is an extensive depletion of ATP, a massive rise in cytoplasmic free Ca2+ concentration, and a severe restriction of synaptosomal respiratory capacity. The cytoplasmic release is only partially Na+ dependent. eliminating a simple reversal of the plasma membrane acidic amino acid carrier. It is concluded that α‐latrotoxin releases both transmitter and cytoplasmic pools of amino acids in synaptosomes and causes a major disruption of terminal integrity. Copyright © 1990, Wiley Blackwell. All rights reserved
引用
收藏
页码:2039 / 2047
页数:9
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