Xenon (Xe) and other inert gases produce anesthesia via an inhibitory mechanism in neuronal networks. To better understand this mechanism, we measured the electrical signals from cultured rat cortical neuronal networks in a multi-electrode array (MEA) under an applied Xe pressure. We used the MEA to measure the firing of the neuronal network with and without Xe gas pressurized to 0.3 MPa. The MEA system monitored neuronal spikes on 16 electrodes (each 50 x 50 μm2) at a sampling rate of 20 kHz. The embryo rat cortical cells were first cultured on MEAs without Xe for approximately three weeks, at which time they produced synchronized bursts that indicate maturity. Then, with an applied Xe pressure, the synchronized bursts quickly ceased, whereas single spikes continued. The Xe-induced inhibition-recovery of neuronal network firing was reversible: after purging Xe from the system, the synchronized bursts gradually resumed. Thus, Xe did not inhibit single neuron firing, yet reversibly inhibited the synaptic transmission. This finding agrees with the channel-blocker and a modified-hydrate hypothesis of anesthesia, but not the lipid-solubility hypothesis.
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机译:氙气(Xe)和其他惰性气体通过神经网络中的抑制机制产生麻醉作用。为了更好地理解这种机制,我们在施加的Xe压力下测量了多电极阵列(MEA)中培养的大鼠皮质神经网络的电信号。我们使用MEA来测量在有和没有Xe气体加压到0.3 MPa的情况下神经网络的放电情况。 MEA系统以20 kHz的采样率监控16个电极(每个50 x 50μm2)上的神经元尖峰。首先在无Xe的MEA上培养胚胎大鼠皮层细胞大约三周,然后它们产生同步的爆发,表明成熟。然后,在施加Xe压力的情况下,同步突发迅速停止,而单个峰值继续。 Xe诱导的神经元网络放电的抑制恢复是可逆的:从系统清除Xe后,同步爆发逐渐恢复。因此,Xe不抑制单个神经元的放电,但可逆地抑制突触传递。这一发现与麻醉药的通道阻滞剂和修饰的水合物假说相符,但与脂质溶解性假说不符。
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