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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The decreases in calcium binding proteins and neurofilament immunoreactivities in the Purkinje cell of the seizure sensitive gerbils.
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The decreases in calcium binding proteins and neurofilament immunoreactivities in the Purkinje cell of the seizure sensitive gerbils.

机译：癫痫敏感沙鼠的浦肯野细胞中钙结合蛋白和神经丝免疫反应性的降低。

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In previous studies, it has been reported that Purkinje cell degeneration during seizure is evoked by excitotoxicity due to an increase in the intracellular Ca(2+) level, though calbindin D-28k (CB) and parvalbumin (PV), intracellular free calcium buffers, are abundantly colocalized in these cells. In the present study, we investigated the expressions of CB, PV, neurofilament (NF) 68, 150, 200, and polyphosphorylated epitope in NF (RT 97), in the cerebellum of gerbils to identify the mechanism of Purkinje cell damages induced by seizure. In seizure resistant gerbils, nearly all the Purkinje cells showed CB, PA, NF 150, NF 200 and RT 97 immunoreactivity. In SS gerbils, however, a clear decrease in the number of CB(+) and PV(+) Purkinje cells was observed. The NF and RT 97 immunoreactivities, in the Purkinje cells was also lower (except NF 68), but not absent. These results suggest several points. First, the decrease in the concentrations of CB and PV may render the Purkinje cells more susceptible to intermittent Ca(2+) fluctuations and more prone to accumulating intolerable quantities of Ca(2+). Second, during the Ca(2+)-PV interaction PV plays an important role in facilitating donations of Mg(2+), which is a potent enzyme activator in phosphorylation. Thus the decline in PV concentration also implicated the defects of phosphorylation in the NF. Third, increases in both the intracellular Ca(2+) level and dephosphorylation trigger the degradation of the NF, particularly NF 200. Finally, these degradations in the NF induce the functional defects in Purkinje cell, which then cause Purkinje cell degeneration.
机译：在以前的研究中，据报道，尽管钙结合蛋白D-28k（CB）和小白蛋白（PV），细胞内游离钙缓冲剂引起了癫痫发作期间浦肯野细胞的变性是由于细胞内Ca（2+）水平升高引起的兴奋性毒性引起的。在这些细胞中大量共定位。在本研究中，我们调查了沙鼠小脑中CB，PV，神经丝（NF）68、150、200和NF（RT 97）中多磷酸化表位的表达，以确定癫痫发作引起的浦肯野细胞损伤的机制。在抗癫痫的沙鼠中，几乎所有的浦肯野细胞都具有CB，PA，NF 150，NF 200和RT 97免疫反应性。然而，在沙鼠沙鼠中，观察到CB（+）和PV（+）Purkinje细胞的数量明显减少。浦肯野细胞中的NF和RT 97免疫反应性也较低（NF 68除外），但不存在。这些结果表明了几点。首先，CB和PV浓度的降低可能使Purkinje细胞更容易受到间歇性Ca（2+）波动的影响，并且更容易累积无法忍受的Ca（2+）量。第二，在Ca（2 +）-PV相互作用期间，PV在促进Mg（2+）的捐赠中起重要作用，Mg（2+）是磷酸化中的一种强大的酶激活剂。因此，PV浓度的下降也牵涉到NF中磷酸化的缺陷。第三，细胞内Ca（2+）水平和去磷酸化水平的升高都会触发NF（尤其是NF 200）的降解。最后，NF中的这些降解会诱导浦肯野细胞功能缺陷，进而导致浦肯野细胞变性。

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