Gorelova N A, Koroleva V I, Amemori T, Pavlík V, Burĕs J
Electroencephalogr Clin Neurophysiol. 1987 Apr;66(4):440-7. doi: 10.1016/0013-4694(87)90213-6.
The failure to elicit cortical spreading depression (SD) under ketamine anesthesia has been examined in 25 rats. SD was elicited by microinjection of K+ acetate (1 microliter, 0.15 mol/l) into the cerebral cortex and monitored by recording the accompanying slow-potential waves. I.p. injection of ketamine HCl (50 mg/kg) elicited after 5-10 min blockade of SD propagation lasting 30-40 min. SD penetration into a cortical area superfused with 10(-4) and 10(-3) mol/l ketamine was partly or completely blocked, respectively. Systemic ketamine doses eliciting SD blockade only slightly reduced spontaneous activity of cortical units recorded with carbon fiber microelectrodes and did not increase but rather decreased the rate of K+ removal from a KCl pool (30 microliters, 40 mmol/l) contacting a 12.5 mm2 area of exposed cortical surface. The results indicate that the ketamine-induced SD blockade is due neither to epileptic activity nor to enhanced active transport of ions but rather to interference with chemically gated ionic channels and/or to stabilization of postsynaptic membranes.
在25只大鼠中研究了氯胺酮麻醉下未能诱发皮层扩散性抑制（SD）的情况。通过向大脑皮层微量注射醋酸钾（1微升，0.15摩尔/升）诱发SD，并通过记录伴随的慢电位波进行监测。腹腔注射盐酸氯胺酮（50毫克/千克）5 - 10分钟后可诱发SD传播阻断，持续30 - 40分钟。SD分别部分或完全被阻止进入用10⁻⁴和10⁻³摩尔/升氯胺酮灌流的皮层区域。引起SD阻断的全身氯胺酮剂量仅轻微降低了用碳纤维微电极记录的皮层神经元的自发活动，并且没有增加而是降低了与12.5平方毫米暴露皮层表面接触的氯化钾池（30微升，40毫摩尔/升）中钾离子的清除率。结果表明，氯胺酮诱导的SD阻断既不是由于癫痫活动，也不是由于离子主动转运增强，而是由于对化学门控离子通道的干扰和/或突触后膜的稳定。
