Klinik und Poliklinik für Neurochirurgie, Westfälische Wilhelms-Universität Münster, Germany.
Cephalalgia. 2012 Jan;32(2):116-24. doi: 10.1177/0333102411431308. Epub 2011 Dec 15.
Cortical spreading depression (CSD) has an important role in migraine with aura. Prolonged neuronal depression is followed by a late excitatory synaptic plasticity after CSD.
Intra- and extracellular recordings were performed to investigate the effect of CSD on intracellular properties of mouse neocortical tissues in the late excitatory period.
During CSD, changes in the membrane potentials usually began with a relatively short hyperpolarization followed by an abrupt depolarization. These changes occurred roughly at the same time point after CSD as the beginning of the negative extracellular deflection. Forty-five minutes after CSD, neurons showed significantly smaller amplitude of afterhyperpolarization and a reduced input resistance. Depolarization and hyperpolarization of the cells by constant intracellular current injections in this period significantly changed the frequency of the action potentials.
These data indicate higher excitability of the neocortical neurons after CSD, which can be assumed to contribute to hyperexcitability of neocortical tissues in patients suffering from migraine.
皮质扩散性抑制（CSD）在有先兆偏头痛中起重要作用。CSD 后会出现长时间的神经元抑制和随后的晚期兴奋性突触可塑性。
采用细胞内和细胞外记录的方法，研究 CSD 对晚期兴奋性期小鼠新皮质组织细胞内特性的影响。
CSD 期间，膜电位的变化通常以相对短暂的超极化开始，随后是突然的去极化。这些变化大致发生在 CSD 后与负细胞外偏转开始相同的时间点。CSD 后 45 分钟，神经元的后超极化幅度明显减小，输入电阻降低。在此期间通过恒定的细胞内电流注入使细胞去极化和超极化，显著改变了动作电位的频率。
这些数据表明 CSD 后新皮质神经元的兴奋性增加，这可能导致偏头痛患者的新皮质组织过度兴奋。
