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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 >Matrix metalloproteinase-9 activity increased by two different types of epileptic seizures that do not induce neuronal death: a possible role in homeostatic synaptic plasticity.
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Matrix metalloproteinase-9 activity increased by two different types of epileptic seizures that do not induce neuronal death: a possible role in homeostatic synaptic plasticity.

机译：两种不引起神经元死亡的癫痫发作的类型增加了基质金属蛋白酶9的活性：可能在稳态突触可塑性中发挥作用。

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摘要

Matrix metalloproteases (MMPs) degrade or modify extracellular matrix or membrane-bound proteins in the brain. MMP-2 and MMP-9 are activated by treatments that result in a sustained neuronal depolarization and are thought to contribute to neuronal death and structural remodeling. At the synapse, MMP actions on extracellular proteins contribute to changes in synaptic efficacy during learning paradigms. They are also activated during epileptic seizures, and MMP-9 has been associated with the establishment of aberrant synaptic connections after neuronal death induced by kainate treatment. It remains unclear whether MMPs are activated by epileptic activities that do not induce cell death. Here we examine this point in two animal models of epilepsy that do not involve extensive cell damage. We detected an elevation of MMP-9 enzymatic activity in cortical regions of secondary generalization after focal seizures induced by 4-aminopyridine (4-AP) application in rats. Pro-MMP-9 levels were also higher in Wistar Glaxo Rijswijk (WAG/Rij) rats, a genetic model of generalized absence epilepsy, than they were in Sprague-Dawley rats, and this elevation was correlated with diurnally occurring spike-wave-discharges in WAG/Rij rats. The increased enzymatic activity of MMP-9 in these two different epilepsy models is associated with synchronized neuronal activity that does not induce widespread cell death. In these epilepsy models MMP-9 induction may therefore be associated with functions such as homeostatic synaptic plasticity rather than neuronal death.
机译：基质金属蛋白酶（MMP）降解或修饰大脑中的细胞外基质或膜结合蛋白。 MMP-2和MMP-9通过导致持续神经元去极化的治疗被激活，并被认为有助于神经元死亡和结构重塑。在突触中，MMP对细胞外蛋白的作用有助于学习过程中突触功效的变化。它们在癫痫发作中也被激活，并且MMP-9已经与海藻酸盐治疗诱导的神经元死亡后异常突触连接的建立有关。尚不清楚MMP是否被不诱导细胞死亡的癫痫活动所激活。在这里，我们在两种不涉及广泛细胞损伤的癫痫动物模型中检验了这一点。我们检测到大鼠4-氨基吡啶（4-AP）引起的局灶性癫痫发作后，继发性皮层皮质区域MMP-9酶活性升高。 Wistar Glaxo Rijswijk（WAG / Rij）大鼠（普遍性失神癫痫的遗传模型）中的Pro-MMP-9水平也高于Sprague-Dawley大鼠，并且这种升高与昼夜出现的尖峰波放电相关在WAG / Rij大鼠中。在这两个不同的癫痫模型中，MMP-9的酶活性增加与同步神经元活性有关，后者不会引起广泛的细胞死亡。因此，在这些癫痫模型中，MMP-9的诱导可能与稳态突触可塑性而不是神经元死亡等功能有关。

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