Mandel Mauricio, Talamoni Fonoff Erich, Bor-Seng-Shu Edson, Teixeira Manoel Jacobsen, Chadi Gerson
Department of Neurology, University of São Paulo School of Medicine, São Paulo, Brazil.
Funct Neurol. 2012 Oct-Dec;27(4):207-16.
Neurogenic neuroprotection is a promising approach for treating patients with ischemic brain lesions. In rats, stimulation of the deep brain nuclei has been shown to reduce the volume of focal infarction. In this context, protection of neural tissue can be a rapid intervention that has a relatively long-lasting effect, making fastigial nucleus stimulation (FNS) a potentially valuable method for clinical application. Although the mechanisms of neuroprotection induced by FNS remain partially unclear, important data have been presented in the last two decades. A 1-h electrical FNS reduced, by 59%, infarctions triggered by permanent occlusion of the middle cerebral artery in Fisher rats. The acute effect of electrical FNS is likely mediated by a prolonged opening of potassium channels, and the sustained effect appears to be linked to inhibition of the apoptotic cascade. A better understanding of the neuronal circuitry underlying neurogenic neuroprotection may contribute to improving neurological outcomes in ischemic brain insults.
神经源性神经保护是治疗缺血性脑损伤患者的一种有前景的方法。在大鼠中,已证明刺激深部脑核可减少局灶性梗死的体积。在这种情况下,神经组织保护可以是一种具有相对持久作用的快速干预措施,使得小脑顶核刺激(FNS)成为一种具有潜在临床应用价值的方法。尽管FNS诱导神经保护的机制仍部分不明,但在过去二十年中已有重要数据公布。1小时的电FNS可使Fisher大鼠大脑中动脉永久性闭塞引发的梗死减少59%。电FNS的急性效应可能由钾通道的延长开放介导,而持续效应似乎与凋亡级联反应的抑制有关。更好地理解神经源性神经保护背后的神经元回路可能有助于改善缺血性脑损伤的神经学预后。