Neuropathogenic properties of Argas (Persicargas) walkerae larval homogenates

被引:8
作者
Maritz, C
Louw, AI
Gothe, R
Neitz, AWH [1 ]
机构
[1] Univ Pretoria, Dept Biochem, ZA-0002 Pretoria, South Africa
[2] Univ Munich, Inst Trop Med & Parasitol, Munich, Germany
来源
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR AND INTEGRATIVE PHYSIOLOGY | 2001年 / 128卷 / 02期
基金
新加坡国家研究基金会;
关键词
H-3]glycine; neurotransmitter release; synaptosomes; tick paralysis toxin;
D O I
10.1016/S1095-6433(00)00307-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
Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure. This form of paralysis is commonly confused with Guillain-Barre syndrome, botulism and myasthenia gravis and although the clinical symptoms of these diseases are similar, it is not clear whether the pathogenesis is also the same. During this study we investigated the mechanism of paralysis by the tick Argas (Persicargas) walkerae by determining the effect of larval humogenates on both potassium-stimulated (calcium-dependent) and veratridine-stimulated (external calcium-independent) release of [H-3]glycine from crude rat brain synaptosomes. The results indicated that larval homogenates inhibited both processes. These findings are reconcilable with the results obtained for two other paralysis-causing tick species. Ixodes holocyclus and Drumacentor andersoni, which were indicated to cause paralysis by decreasing the synthesis or release of acetylcholine at the neuromuscular junction. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:233 / 239
页数:7
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