Department of Critical Care Medicine, Affiliated Hospital of Zunyi Medical College, Zunyi, Guizhou, China.
Guizhou Key Laboratory of Anesthesia and Organ Protection, Zunyi Medical College, Dalian Road, Zunyi, Guizhou, 201, China.
BMC Anesthesiol. 2017 Aug 23;17(1):111. doi: 10.1186/s12871-017-0404-5.
Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC). Previous studies have demonstrated that thalamocortical system is critical for information transmission and integration in the brain. The ventral posteromedial nucleus (VPM) is a critical component of thalamocortical system. Glutamate is an important excitatory neurotransmitter in the brain and may be involved in ketamine-induced LOC.
The study used whole-cell patch-clamp to observe the effect of ketamine (30 μM-1000 μM) on glutamatergic neurotransmission in VPM slices.
Ketamine significantly decreased the amplitude of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs), but only higher concentration of ketamine (300 μM and 1000 μM) suppressed the frequency of sEPSCs. Ketamine (100 μM-1000 μM) also decreased the amplitude of glutamatergic miniature excitatory postsynaptic currents (mEPSCs), without altering the frequency.
In VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process.
氯胺酮是一种常用的静脉麻醉剂，可可逆地诱导意识丧失（LOC）。先前的研究表明，丘脑皮质系统对于大脑中的信息传递和整合至关重要。腹后内侧核（VPM）是丘脑皮质系统的重要组成部分。谷氨酸是大脑中一种重要的兴奋性神经递质，可能参与氯胺酮诱导的 LOC。
本研究使用全细胞膜片钳技术观察氯胺酮（30μM-1000μM）对 VPM 切片中谷氨酸能神经传递的影响。
氯胺酮显著降低了谷氨酸能自发性兴奋性突触后电流（sEPSC）的幅度，但只有较高浓度的氯胺酮（300μM 和 1000μM）才抑制了 sEPSC 的频率。氯胺酮（100μM-1000μM）也降低了谷氨酸能微小兴奋性突触后电流（mEPSC）的幅度，而不改变其频率。
在 VPM 神经元中，氯胺酮主要通过突触后机制减弱谷氨酸能神经传递，动作电位可能参与该过程。
