Departments of Pain Care.
Anesthesiology, Southwest Hospital, Army Medical University, Chongqing, China.
Neuroreport. 2020 Dec 9;31(17):1242-1248. doi: 10.1097/WNR.0000000000001540.
Propofol anesthesia rapidly causes loss of consciousness, while the neural mechanism underlying this phenomenon is still unclear. Glutamatergic neurons in the basal forebrain play an important role in initiation and maintenance of wakefulness. Here, we selectively recorded the activity of glutamatergic neurons in vGlut-2-Cre mice. Propofol induced outward currents in a concentration-dependent manner. Bath application of propofol generated membrane hyperpolarization and suppressed the firing rates in these neurons. Propofol-induced stable outward currents persisted after blockade of the action potentials, implying a direct postsynaptic effect of propofol. Furthermore, propofol selectively increased the GABAergic inhibitory synaptic inputs via affecting the GABAARs, but did not affect the glutamatergic transmissions. Together, propofol inhibits the excitability of the glutamatergic neurons via direct influencing the membrane intrinsic properties and the inhibitory synaptic transmission. This inhibitory effect might provide a novel mechanism for the propofol-induced anesthesia.
异丙酚麻醉会迅速导致意识丧失，但其背后的神经机制尚不清楚。基底前脑的谷氨酸能神经元在觉醒的启动和维持中起着重要作用。在这里，我们选择性地记录了 vGlut-2-Cre 小鼠中谷氨酸能神经元的活动。异丙酚以浓度依赖的方式诱导外向电流。灌流应用异丙酚会产生膜超极化，并抑制这些神经元的放电频率。异丙酚诱导的稳定外向电流在阻断动作电位后仍然存在，这表明异丙酚具有直接的突触后效应。此外，异丙酚通过影响 GABAAR 选择性地增加 GABA 能抑制性突触输入，但不影响谷氨酸能传递。总之，异丙酚通过直接影响膜固有特性和抑制性突触传递来抑制谷氨酸能神经元的兴奋性。这种抑制作用可能为异丙酚诱导麻醉提供了一种新的机制。
