氯胺酮诱导促进谷氨酸能兴奋性突触传递的NMDA受体介导机制。
NMDA receptor-mediated mechanism of ketamine-induced facilitation of glutamatergic excitatory synaptic transmission.
作者信息
Narimatsu Eichi, Kawamata Yurie, Kawamata Mikito, Fujimura Naoyuki, Namiki Akiyoshi
机构信息
Department of Anesthesiology, Sapporo Medical University School of Medicine, South 1, West 16, Chuo-ku, Sapporo, Hokkaido 060-8543, Japan.
出版信息
Brain Res. 2002 Oct 25;953(1-2):272-5. doi: 10.1016/s0006-8993(02)03375-9.
The effect of ketamine on CA1-field EPSPs (fEPSPs) in rat hippocampal slices was investigated. Ketamine (100 microM) facilitated fEPSPs at 0.05 Hz. The fEPSP facilitation was suppressed completely by AP-5 and partially by propranolol, and also by an increase in stimulation frequency. These results indicate that ketamine facilitates excitatory synaptic transmission by activating NMDA receptors via beta-adrenoceptors under conditions in which NMDA receptor channel block is slight.
研究了氯胺酮对大鼠海马脑片CA1区场兴奋性突触后电位（fEPSPs）的影响。氯胺酮（100微摩尔）在0.05赫兹时促进fEPSPs。AP-5可完全抑制fEPSP的促进作用，普萘洛尔和刺激频率增加可部分抑制。这些结果表明，在NMDA受体通道阻断轻微的条件下，氯胺酮通过β-肾上腺素能受体激活NMDA受体来促进兴奋性突触传递。
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