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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Neuronal and glial membrane potentials during sleep and paroxysmal oscillations in the neocortex.
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Neuronal and glial membrane potentials during sleep and paroxysmal oscillations in the neocortex.

机译:睡眠和新皮质阵发性振荡期间的神经元和神经胶质膜电位。

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This study investigated the fluctuations in the membrane potential of cortical neurons and glial cells during the slow sleep oscillation and spike-wave (SW) seizures. We performed dual neuron-glia intracellular recordings together with multisite field potential recordings from cortical suprasylvian association areas 5 and 7 of cats under ketamine-xylazine anesthesia. Electrical stimuli applied to the cortex elicited responses consisting of a biphasic depolarization in glial cells, which was associated with an EPSP-IPSP sequence in neurons. During the slow (<1 Hz) oscillation, extracellular measurements of the potassium concentration revealed periodic increases with an amplitude of 1-2 mm, similar in shape to glial activities. We suggest that, through their uptake mechanisms, glia cells modulate the neuronal excitability and contribute to the pacing of the slow oscillation. The slow oscillation often evolved into SW paroxysms, mimicking sleep-triggered seizures. This transition was associated with increased coupling between the depolarizing events in neurons and glial cells. During seizures, the glial membrane potential displayed phasic negative events related to the onset of the paroxysmal depolarizing shifts in neurons. These events were not voltage dependent and increased their incidence and amplitude with the development of the seizure. It is suggested that the intraglial transient negativities represent field reflections of synchronized neuronal potentials. We propose that the mechanisms underlying the neuron-glia communication include, besides the traditional neurotransmitter- and ion-mediated pathways, field effects crossing their membranes as a function of the state of the cortical network.
机译:这项研究调查了在缓慢的睡眠振荡和尖峰波(SW)发作期间皮质神经元和神经胶质细胞膜电位的波动。我们在氯胺酮-甲苯噻嗪麻醉下,进行了双神经元神经胶质细胞内记录以及猫皮上神经鞘缔合区5和7的多位场电位记录。施加到皮层的电刺激在神经胶质细胞中引起由双相去极化组成的反应,这与神经元中的EPSP-IPSP序列有关。在缓慢的(<1 Hz)振荡期间,钾浓度的细胞外测量显示周期性增加,幅度为1-2 mm,其形状类似于神经胶质活动。我们建议,通过其摄取机制,胶质细胞调节神经元兴奋性,并有助于缓慢振荡的起搏。缓慢的振荡常常演变成SW发作,模仿睡眠触发的癫痫发作。这种转变与神经元和神经胶质细胞中去极化事件之间增加的偶联有关。在癫痫发作期间,胶质细胞膜电位显示出与神经元中阵发性去极化移动的发作有关的阶段性负性事件。这些事件与电压无关,并随着癫痫发作的发展而增加其发生率和幅度。建议神经胶质内瞬态阴性代表同步神经元电位的场反射。我们提出,神经元-神经胶质细胞沟通的基础机制除了传统的神经递质和离子介导的途径外,还包括跨皮膜状态的皮层网络状态场效应。

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