Hawkinson J E, Shull L R, Joy R M
Department of Environmental Toxicology, University of California, Davis 95616.
Neurotoxicology. 1989 Spring;10(1):29-39.
The effect of lindane on 45Ca fluxes in synaptosomes was examined to determine whether modulation of calcium regulation can explain the lindane-induced enhancement in neurotransmitter release observed in other preparations. Lindane (0.03 - 4.6 microM) enhanced calcium uptake in non-depolarizing (low K+) medium: the effect was maximal at 0.1 microM lindane, which increased uptake by 15.8%. Lindane (11.5 microM) decreased calcium uptake in depolarizing (high K+) medium; lower concentrations were ineffective. In addition, lindane (9.2 microM) increased early 45Ca release from synaptosomes. However, lindane (2.4 or 5.9 microM) had no effect on calcium uptake by lysed synaptosomes in the presence or absence of mitochondrial poisons and/or ATP, indicating that lindane does not affect sub-cellular calcium storage. It is concluded that the lindane-induced changes in synaptosomal calcium flux are due to an increase in non-specific synaptic membrane permeability to calcium.
研究了林丹对突触体中45Ca通量的影响，以确定钙调节的调节是否可以解释在其他制剂中观察到的林丹诱导的神经递质释放增强。林丹（0.03 - 4.6 microM）在非去极化（低钾）培养基中增强了钙摄取：在0.1 microM林丹时效果最大，钙摄取增加了15.8%。林丹（11.5 microM）在去极化（高钾）培养基中降低了钙摄取；较低浓度无效。此外，林丹（9.2 microM）增加了突触体早期45Ca释放。然而，林丹（2.4或5.9 microM）在存在或不存在线粒体毒物和/或ATP的情况下对裂解的突触体的钙摄取没有影响，表明林丹不影响亚细胞钙储存。得出的结论是，林丹诱导的突触体钙通量变化是由于突触膜对钙的非特异性通透性增加。
