Biogeographic and demographic changes in the distribution and abundance of scorpions inhabiting the Mediterranean region in northern Israel

A recent survey of the scorpion fauna in the Mediterranean region of northern Israel, has shown that the desert buthid, Leiurus quinquestriatus, formerly restricted to the arid and semi-arid regions in southern and eastern Israel, has penetrated through the Jordan Valley deep into the Mediterranean region, reaching into the northern Galil Mountains. At the same time, the oakwood scorpionid, Scorpio maurius fuscus, formerly the most abundant scorpion in the Mediterranean region, showed a marked decline in numbers. Various aspects of this apparent colonization and replacement in the scorpion fauna are discussed.     

Interaction of scorpion alpha-toxins with cardiac sodium channels: binding properties and enhancement of slow inactivation

The effects of the scorpion alpha-toxins Lqh II, Lqh III, and LqhalphaIT on human cardiac sodium channels (hH1), which were expressed in human embryonic kidney (HEK) 293 cells, were investigated. The toxins removed fast inactivation with EC(50) values of <2.5 nM (Lqh III), 12 nM (Lqh II), and 33 nM (LqhalphaIT). Association and dissociation rates of Lqh III were much slower than those of Lqh II and LqhalphaIT, such that Lqh III would not dissociate from the channel during a cardiac activation potential. The voltage dependence of toxin dissociation from hH1 channels was nearly the same for all toxins tested, but it was different from that found for skeletal muscle sodium channels (muI; Chen et al. 2000). These results indicate that the voltage dependence of toxin binding is a property of the channel protein. Toxin dissociation remained voltage dependent even at high voltages where activation and fast inactivation is saturated, indicating that the voltage dependence originates from other sources. Slow inactivation of hH1 and muI channels was significantly enhanced by Lqh II and Lqh III. The half-maximal voltage of steady-state slow inactivation was shifted to negative values, the voltage dependence was increased, and, in particular for hH1, slow inactivation at high voltages became more complete. This effect exceeded an expected augmentation of slow inactivation owing to the loss of fast inactivation and, therefore, shows that slow sodium channel inactivation may be directly modulated by scorpion alpha-toxins.