Connection changes in somatosensory cortex induced by different doses of propofol.

Connection changes in somatosensory cortex induced by different doses of propofol.
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DOI:
10.1371/journal.pone.0087829
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Yu T
Yu T
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Li Z;Liu X;Zhang Y;Shi J;Zhang Y;Xie P;Yu T

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全身麻醉药广泛应用于临床已有160多年的历史,其对感觉反应性的影响机制至今仍不清楚。本研究通过电刺激大鼠胡须,探讨不同剂量异丙酚对大鼠躯体感觉皮层的影响。在固定笼中,大鼠用丙泊酚80 mg/kg腹腔内麻醉,然后用23 G金属针连接泵进行尾静脉插管。钻两个孔(直径2 mm),并将记录电极固定在初级躯体感觉皮层桶场(S1 BF)和次级躯体感觉皮层(S2)中。采用细胞外(20只大鼠)和细胞内(8只大鼠)记录方法,检测尾静脉泵注不同剂量异丙酚(20、40和80 mg/kg/h)对大鼠皮层神经元活动的影响。在丙泊酚20、40和80 mg/kg/h剂量下,每10 min检测一次触须反应、嗅觉反应、角膜反应(VOCR,镇静)和夹尾反应(TRP,镇痛)。异丙酚呈剂量依赖性降低VOCR和TRP。与S2相比,S1 BF的胡须刺激幅度更大,峰潜伏期更短。随着丙泊酚输注速率的增加,S1 BF和S2的反应潜伏期延长,在相同丙泊酚剂量下,S2的反应潜伏期长于S1 BF。随着丙泊酚输注速率的增加,S1 BF和S2之间的相关性降低。输入阻力随丙泊酚输注速率的增加而增加。异丙酚的镇静、镇痛作用呈剂量依赖性。不同剂量的异丙酚对S1 BF和S2之间的连接和本能振荡都有一定的调节作用。
The mechanism by which general anesthetics, widely used in clinical practice for over 160 years, effects on sensory responsiveness has been unclear until now. In the present study, the authors sought to explore the effect of different doses of propofol on somatosensory cortex by whisker stimulation in rats. In a fixed cage, rats were anesthetized with propofol 80 mg/kg intraperitoneally and then cathetered tail vein with 23-gauge metal needle connected with a pump. Two holes (2 mm diameter) were drilled and recording electrodes implantated in the primary somatosensory cortex barrel field (S1BF) and secondary somatosensory cortex (S2). The extracellular (20 rats) and intracellular (8 rats) recordings were used to test the neuron activity in both cortices at different doses of propofol (20, 40 and 80 mg/kg/h) through tail vein by pump. Meantime, vibrissal, olfactory, corneal responses (VOCR, sedation), and tail-pinch response (TRP, analgesia) were tested every 10 min during the doses of propofol 20, 40 and 80 mg/kg/h. VOCR and TRP were depressed by propofol in a dose-dependent manner. The amplitude by whisker stimulation in S1BF was stronger and the peak latency was shorter compared with that of in S2. The response latency of S1BF and S2 was increased by raising infusion rate of propofol with the response latency in S2 being longer than that in S1BF at the same doses of propofol. The cross-correlation between S1BF and S2 decreased as the propofol infusion rate increased. The input resistance was higher by increasing infusion rate of propofol. The sedation and analgesia effects of propofol were dose-dependent. Both the connectivity and instinctive oscillation between S1BF and S2 were proportionally modulated by the different doses of propofol.
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