Baker R E, Ruijter J M, Bingmann D
Netherlands Institute for Brain Research, Amsterdam.
Int J Dev Neurosci. 1991;9(4):339-45. doi: 10.1016/0736-5748(91)90055-q.
Chronic depolarization is inimical to neuronal growth and synaptogenesis so that spontaneous action potential generation appears to be required for the normal cytomorphological maturation of neocortical networks. The efficacy of 25 mM K in suppressing spontaneous bioelectric activity was monitored by extra- and intracellular recording from the explants. Intracellular recording from individual neurons showed that membrane potentials were reduced to ca -30 mV in potassium cultures but rapidly repolarized to ca -50 mV when returned to normal growth medium. Though action potentials could be readily evoked from these explants, spontaneous discharges and postsynaptic potentials were absent from potassium-treated cultures. Both spontaneous bioelectric activity and postsynaptic potentials returned to the cultures by 5 days after returning the explants to normal growth medium. Extracellular recordings also showed that the explants were bioelectrically silent in the presence of 25 mM K or 25 mM K plus tetrodotoxin. In contrast to tetrodotoxin alone, bioelectric activity was absent when the cultures (with or without tetrodotoxin) were returned to normal growth medium. The explants gradually began to evince spontaneous bioelectric activity between 3 and 5 days after being returned to normal growth medium. Massive cell death induced by chronic exposure to tetrodotoxin was totally prevented by concomitant addition of 25 mM potassium, though these explants were significantly thinner than controls due to a large decrease in neuropil. We conclude that chronic depolarization of neonatal cortical explants by potassium results in a delayed return of spontaneous bioelectric discharges. Chronic depolarization results in a retardation of network formation in these explants apparently due to a lack of neurite and/or synapse formation.(ABSTRACT TRUNCATED AT 250 WORDS)
慢性去极化不利于神经元生长和突触形成，因此新皮层网络的正常细胞形态成熟似乎需要自发动作电位的产生。通过对外植体进行细胞外和细胞内记录，监测25 mM钾抑制自发生物电活动的效果。对单个神经元的细胞内记录显示，在钾培养基中膜电位降至约-30 mV，但回到正常生长培养基后迅速复极化至约-50 mV。虽然这些外植体能够轻易诱发动作电位，但钾处理的培养物中没有自发放电和突触后电位。将外植体放回正常生长培养基5天后，自发生物电活动和突触后电位都恢复到培养物中。细胞外记录还显示，在存在25 mM钾或25 mM钾加河豚毒素的情况下，外植体没有生物电活动。与单独使用河豚毒素不同，当培养物（无论有无河豚毒素）回到正常生长培养基时，没有生物电活动。外植体在回到正常生长培养基后3至5天逐渐开始出现自发生物电活动。同时添加25 mM钾可完全防止因长期暴露于河豚毒素而诱导的大量细胞死亡，尽管由于神经毡大量减少，这些外植体明显比对照组薄。我们得出结论，钾导致新生皮层外植体慢性去极化，导致自发生物电放电延迟恢复。慢性去极化导致这些外植体中网络形成延迟，显然是由于缺乏神经突和/或突触形成。（摘要截短至250字）
