氯胺酮可抑制去抑制杏仁核切片中的同步放电。
Ketamine suppresses synchronized discharges in the disinhibited amygdala slice.
作者信息
Gean P W, Chang F C
机构信息
Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan City, Taiwan, R.O.C.
出版信息
Brain Res Bull. 1991 Jun;26(6):923-7. doi: 10.1016/0361-9230(91)90258-l.
The effect of ketamine on the paroxysmal depolarizing shift (PDS) induced by bicuculline was studied in rat amygdala slices using intracellular recording techniques. Stimulation of the ventral endopyriform nucleus evoked an excitatory postsynaptic potential (EPSP). After exposure to bicuculline (20 microM), the same stimulus intensity evoked burst firing. Superfusion of ketamine reversibly reduced the duration of PDS. Pretreatment of amygdala slices with DL-2-amino-5-phosphonovaleate (DL-APV, 50 microM) occluded the effect of ketamine suggesting that ketamine shortened the burst duration via its blocking action on the NMDA receptors. In all neurons tested, a large depolarizing shift remained in the presence of ketamine. The ketamine-resistant component was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 8 microM) indicating its mediation by the non-NMDA receptors.
采用细胞内记录技术，在大鼠杏仁核切片中研究了氯胺酮对荷包牡丹碱诱导的阵发性去极化漂移（PDS）的影响。刺激腹侧梨状内皮层核诱发兴奋性突触后电位（EPSP）。暴露于荷包牡丹碱（20微摩尔）后，相同的刺激强度诱发爆发性放电。氯胺酮灌流可可逆地缩短PDS的持续时间。用DL-2-氨基-5-磷酸戊酸（DL-APV，50微摩尔）预处理杏仁核切片可阻断氯胺酮的作用，表明氯胺酮通过对N-甲基-D-天冬氨酸（NMDA）受体的阻断作用缩短爆发持续时间。在所有测试的神经元中，在氯胺酮存在的情况下仍存在较大的去极化漂移。氯胺酮抗性成分被6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX，8微摩尔）阻断，表明其由非NMDA受体介导。
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