Please use this identifier to cite or link to this item:
Title: Inhibition of sodium-dependent uptake processes in purified rat brain synaptosomes by lophozozymus pictor toxin and palytoxin
Authors: Lau, C.O.
Ng, F.H.
Khoo, H.E. 
Yuen, R.
Tan, C.H.. 
Issue Date: 1996
Citation: Lau, C.O., Ng, F.H., Khoo, H.E., Yuen, R., Tan, C.H.. (1996). Inhibition of sodium-dependent uptake processes in purified rat brain synaptosomes by lophozozymus pictor toxin and palytoxin. Neurochemistry International 28 (4) : 385-390. ScholarBank@NUS Repository.
Abstract: To get an insight into the mechanism of neurotoxicity exhibited by Lophozozymus pictor toxin (LPTX) and the toxin isolated from P. caribaeorum (C-PTX) studies were carried out on the effect of these toxins on the uptake of selected substrates (neurotransmitters, amino acids and glucose) in isolated nerve endings. The toxins were found to inhibit the uptake of γ-aminobutyric acid (GABA), noradrenaline, choline, L-leucine and 2-deoxy-D-glucose in rat brain synaptosomes. LPTX- or C-PTX-induced inhibition of synaptosomal uptake was reduced in the absence of Na+ in the assay medium. Synaptosomes exposed to LPTX and C-PTX release K+ in a dose-dependent manner. Ouabain, a selective inhibitor of the plasma membrane Na+, K+-ATPase could inhibit LPTX- and C-PTX-induced K+ efflux from synaptosomes and alleviate the toxin-induced inhibition of synaptosomal GABA uptake. It appears that the induction of ionic flux is the primary cause of toxicity by these toxins leading to the inhibition of Na+-dependent uptake processes in synaptosomes. The antagonistic action of ouabain suggests the involvement of the membrane sodium pump in the development of cytotoxicity.
Source Title: Neurochemistry International
ISSN: 01970186
DOI: 10.1016/0197-0186(95)00107-7
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Jul 22, 2021


checked on Jul 22, 2021

Page view(s)

checked on Jul 10, 2021

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.