Role for calcium in heat shock-mediated synaptic thermoprotection in Drosophila larvae

被引:17
作者
Barclay, JW [1 ]
Robertson, RM [1 ]
机构
[1] Queens Univ, Dept Biol, Kingston, ON K7L 3N6, Canada
来源
JOURNAL OF NEUROBIOLOGY | 2003年 / 56卷 / 04期
关键词
calcium; Drosophila; heat shock; synaptic plasticity; thermotolerance;
D O I
10.1002/neu.10247
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Chemical synaptic transmission is the mechanism for fast, excitation-coupled information transfer between neurons. Previous work in larval Drosophila has shown that transmission at synaptic boutons is protected by heat shock exposure from subsequent thermal stress through pre- and postsynaptic modifications. This protective effect has been, at least partially, ascribed to an up-regulation in the inducible heat shock protein, hsp70. Effects of hsp70 are correlated with changes to intracellular calcium handling, and the dynamics of intracellular calcium regulate synaptic transmission. Consistent with such a relationship, synaptic plasticity increases at locust neuromuscular junctions following heat shock, suggesting an effect of heat shock on residual presynaptic calcium. Intracellular recording from single abdominal muscle fibers of Drosophila larvae showed that prior heat shock imparts thermoprotection by increasing the upper temperature limit for synaptic transmission. Heat shock exposure enhances short-term synaptic plasticity and increases its thermosensitivity. Increasing extracellular calcium levels eliminates the physiological differences between control and heat shock preparations; excess calcium itself induces thermoprotection at elevated concentrations. These data support the hypothesis that stress-induced neuroprotection at the nerve terminal acts, at least partially, through an alteration to the physiological effects of residual presynaptic calcium. (C) 2003 Wiley Periodicals.
引用
收藏
页码:360 / 371
页数:12
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