發(fā)布時間：2018-04-25 17:36

  本文選題：工作記憶 + 局部場電位��； 參考：《天津醫(yī)科大學(xué)》2014年碩士論文

【摘要】：研究目的： 丙泊酚是臨床常用靜脈麻醉藥,丙泊酚麻醉對大腦認(rèn)知功能的影響是麻醉臨床關(guān)注的熱點(diǎn)。工作記憶是一類重要的認(rèn)知功能,前額葉皮層是工作記憶的關(guān)鍵腦區(qū)之一。本論文基于在體植入式微電極記錄的兩類不同模態(tài)神經(jīng)信號：局部場電位(Local field potential, LFP)和動作電位(Action potential, AP),分析LFPs功能連接網(wǎng)絡(luò)特性和和神經(jīng)元群體的電活動,研究丙泊酚麻醉對工作記憶的抑制機(jī)制,為臨床丙泊酚麻醉提供理論支持。 研究方法： 1.實(shí)驗(yàn)動物為8-10周齡雄性SD大鼠14只,體重300-350g; 2.大鼠進(jìn)行Y迷宮工作記憶任務(wù)訓(xùn)練,直到連續(xù)三天平均正確率達(dá)到85%; 3.丙泊酚麻醉大鼠模型的制備：大鼠隨機(jī)分為兩組,丙泊酚組(n=7,麻醉劑量為0.9mg/kg·min尾靜脈注射丙泊酚2h)和對照組(n=7); 4.在大鼠前額葉皮層植入16通道微電極陣列,應(yīng)用在體植入式微電極陣列記錄技術(shù),記錄大鼠在Y迷宮工作記憶過程中前額葉皮層多通道神經(jīng)信號,從中獲取兩種不同模態(tài)神經(jīng)信號：多通道LFPs和神經(jīng)元集群的動作電位時空序列； 5.LFPs的時頻分析,獲取工作記憶的特征頻段； 6.研究丙泊酚麻醉對工作記憶LFPs的0頻段、γ頻段功能連接網(wǎng)絡(luò)特性的抑制作用； 7.計算工作記憶參考點(diǎn)前2s的神經(jīng)元群體平均發(fā)放頻率,將高于平均頻率的神經(jīng)元募集為編碼工作記憶事件的神經(jīng)元集群。研究丙泊酚麻醉對工作記憶神經(jīng)元群體集群電活動和群體中每個神經(jīng)元電活動的抑制作用。 研究結(jié)果： 1.劑量為0.9mg/kg·min,2h的丙泊酚麻醉后24、48、72h對大鼠Y迷宮工作記憶行為學(xué)影響的結(jié)果：與對照組比較,麻醉后24h丙泊酚組57%±5%,對照組90%±3%(p0.01);麻醉后48h丙泊酚組75%±4%,對照組91%±2%(p0.05)；麻醉后72h:丙泊酚組88%±3%,對照組90%±3%(p0.05)。 2.丙泊酚麻醉后24、48、72h對大鼠工作記憶LFPs特征分量的影響 大鼠在工作記憶任務(wù)過程中,LFPs能量曲線的峰值發(fā)生在工作記憶參考點(diǎn)前2s時間段內(nèi),峰值前后各0.5s時段內(nèi)工作記憶LFPs的0和γ頻段的能量明顯高于其它時間段(p0.05)。丙泊酚組與對照組結(jié)果相比,麻醉后24h:丙泊酚組LFPs的0頻段能量峰值下降(p0.05),Y頻段能量峰值顯著下降(p0.01);麻醉后48h:丙泊酚組LFPs的0頻段能量下降(p0.05),γ頻段能量下降(p0.05)；麻醉后72h兩組大鼠LFPs的0頻段和γ頻段能量峰值無差異(p0.05)。 3.丙泊酚麻醉后24、48、72h對工作記憶LFPs功能連接的影響 麻醉后24h,LFPs的0頻段分量DTF值：丙泊酚組為0.0082±0.0021,對照組為0.0162±0.0012(p0.01)；LFPs的γ頻段分量DTF值：丙泊酚組為0.0032±0.0011,對照組為0.0122±0.0013(P0.01)。麻醉后48h,LFPs的0頻段分量DTF值：丙泊酚組為0.0140±0.0023,對照組為0.0165±0.0019(p0.05)；LFPs的丫頻段分量DTF值：丙泊酚組為0.0065±0.0013,對照組為0.0119±0.0028(p0.01)。麻醉后72h,LFPs的0頻段分量DTF值：丙泊酚組為0.0157±0.0029,對照組為0.0165±0.0014(p0.05)；LFPs的γ頻段分量DTF值：丙泊酚組為0.0117±0.0024,對照組為0.0121±0.0015(p0.05)。 4.丙泊酚麻醉后24、48、72h對工作記憶LFPs網(wǎng)絡(luò)特性的影響 (1)丙泊酚麻醉對工作記憶LFPs網(wǎng)絡(luò)連接密度D的影響： 麻醉后24h, LFPs的θ頻段分量：丙泊酚組為0.22±0.03,對照組為0.42±0.07(p0.01):LFPs的γ頻段分量：丙泊酚組為0.12±0.03,對照組為0.63±0.05(p0.01)。麻醉后48h,LFPs的0頻段分量：丙泊酚組為0.30±0.04,對照組為0.48±0.06(p0.05);LFPs的γ頻段分量：丙泊酚組為0.48±0.04,對照組為0.62±0.03(p0.05)。麻醉后72h,LFPs的0頻段分量：丙泊酚組為0.41±0.02,對照組為0.47±0.05(p0.05)；LFPs的γ頻段分量：丙泊酚組為0.61±0.05,對照組為0.63±0.04(p0.05)。 (2)丙泊酚麻醉對工作記憶LFPs網(wǎng)絡(luò)信息傳遞效率Eglobal的影響： 麻醉后24h, LFPs的0頻段分量：丙泊酚組為0.57±0.02,對照組為0.62±0.04(p0.05);LFPs的γ頻段分量：丙泊酚組為0.24±0.02,對照組為0.72±0.06(p0.01)。麻醉后48h,LFPs的0頻段分量：丙泊酚組為0.58±0.04,對照組為0.67±0.02(p0.05)；LFPs的γ頻段分量：丙泊酚組為0.49±0.07,對照組為0.73±0.02(p0.05)。麻醉后72h, LFPs的0頻段分量：丙泊酚組為0.62±0.02,對照組為0.66±0.02(p0.05)；LFPs的γ頻段分量：丙泊酚組為0.69±0.04,對照組為0.73±0.04(p0.05)。 5.丙泊酚麻醉后24、48、72h對工作記憶大鼠神經(jīng)元群體電活動的影響 (1)丙泊酚麻醉對工作記憶神經(jīng)元集群頻率編碼的影響： 與對照組結(jié)果相比,麻醉后24、48h丙泊酚組編碼工作記憶事件的神經(jīng)元集群個數(shù)顯著下降(p10.01,p20.05)；麻醉后72h兩組無差異(p0.05)。 (2)丙泊酚麻醉對工作記憶神經(jīng)元群體中每個神經(jīng)元電活動的影響： 與對照組結(jié)果相比,編碼工作記憶事件的神經(jīng)元集群中神經(jīng)元電活動占神經(jīng)元群體比例在麻醉后24h:丙泊酚組為24.3%±4.7%,對照組為80.6%±13.5%(p0.01)；麻醉后48h:丙泊酚組為48.6%±11.2%,對照組為81.2%±11.4%(p0.05)；麻醉后72h:丙泊酚組為78.3%±10.2%,對照組為82.6%±15.1%(p0.05)。 研究結(jié)論： 1.劑量為0.9mg/kg·min,2h的丙泊酚麻醉,在48h內(nèi)對大鼠工作記憶任務(wù)的執(zhí)行存在明顯抑制作用,72h后無抑制作用： 2.大鼠LFPs的0(4-12HZ)和γ頻段(30-60HZ)分量在編碼工作記憶過程起關(guān)鍵作用。劑量為0.9mg/kg·min,2h的丙泊酚麻醉,在48h內(nèi)對LFPs的γ頻段特征分量抑制作用顯著,72h后無抑制作用； 3.LFPs的γ頻段分量功能連接在丙泊酚麻醉后48h內(nèi)被顯著抑制,72h后無抑制作用；而0頻段分量的功能連接僅在丙泊酚麻醉后24小時內(nèi)被抑制； 4.丙泊酚麻醉后48h內(nèi)顯著抑制LFPs的θ和γ頻段網(wǎng)絡(luò)連接密度,72h后無抑制作用； 5.丙泊酚麻醉后48h內(nèi)顯著抑制LFPs的γ頻段分量的網(wǎng)絡(luò)信息傳遞效率,72h后無抑制作用,劑量為0.9mg/kg·min,2h的丙泊酚麻醉對θ頻段的網(wǎng)絡(luò)信息傳遞效率無抑制作用； 6.丙泊酚麻醉后48h內(nèi)明顯抑制神經(jīng)元集群電活動與群體中每個神經(jīng)元的電活動,72h后無抑制作用。
[Abstract]:The purpose of the study is:
Propofol is a commonly used intravenous anesthetic. The effect of propofol on cognitive function of the brain is the focus of clinical attention. Working memory is one of the most important cognitive functions. The prefrontal cortex is one of the key brain regions of working memory. This paper is based on two different modal neural signals recorded in body implantable microelectrodes: local The field potential (Local field potential, LFP) and action potential (Action potential, AP) are used to analyze the characteristics of the functional connection network of LFPs and the electrical activity of the neuronal population, and to study the mechanism of the suppression of working memory by propofol anesthesia, and provide theoretical support for the clinical propofol anesthesia.
Research methods:
1. the experimental animals were 14 male SD rats aged 8-10 weeks, weighing 300-350g.
2. rats were trained in Y maze task memory task until the average three day accuracy rate was 85%.
3. the rat model of propofol anesthetized: rats were randomly divided into two groups, propofol group (n=7, anesthetic dose of 0.9mg/kg min caudal intravenous propofol 2H) and control group (n=7).
4. the 16 channel microelectrode arrays were implanted in the prefrontal cortex of the rat, and the multichannel neural signals were recorded in the prefrontal cortex of the Y labyrinth labyrinth of rats, and two different modal neural signals were obtained from the body embedded microelectrode array recording technique, and the action potential spatiotemporal sequence of the multichannel LFPs and the God Jing Yuan cluster was obtained.
5.LFPs's time-frequency analysis is used to get the characteristic frequency of working memory.
6. to study the inhibitory effect of propofol anesthesia on the 0 band and gamma band functional connectivity network of working memory LFPs.
7. the average frequency of neuronal population distribution before the working memory reference point 2S was calculated, and the neurons raised above the average frequency were collected as the neurons of the coded working memory events. The inhibitory effect of propofol anesthesia on the group electrical activity of working memory neurons and the electrical activity of each neuron in the group was investigated.
The results of the study:
1. dose of 0.9mg/kg. Min, the effect of 24,48,72h on the working memory behavior of Y maze after anaesthesia of 2h in rats: compared with the control group, 24h propofol group after anesthesia was 57% + 5%, and the control group was 90% + 3% (P0.01); 48h propofol group was 75% + 4% after anesthesia, and the control group was 91% + 2% (P0.05); 72h: propofol group after anesthesia was 88% + 57%, and the control group 90% + 3% (p0.0) 5).
2. effects of propofol 24,48,72h on LFPs characteristic components of working memory in rats
During the working memory task, the peak of the LFPs energy curve occurred in the 2S period before the working memory reference point. The energy of the 0 and the gamma band of the working memory LFPs in the 0.5s period of the peak before and after the peak was significantly higher than that of the other time periods (P0.05). The 0 frequency band energy peak of the LFPs in the 24h: propofol group after anaesthesia was compared with the control group. The energy peak of Y band decreased significantly (P0.01), the 0 band energy of LFPs in 48h: propofol group decreased (P0.05), and the energy of gamma frequency band decreased (P0.05) after anesthesia, and there was no difference between the 0 band and the gamma band energy peak of 72h two rats after anesthesia (P0.05).
3. the effect of 24,48,72h on functional connectivity of working memory LFPs after propofol anesthesia
The 0 band component DTF value of 24h and LFPs after anesthesia was 0.0082 + 0.0021 in propofol group and 0.0162 + 0.0012 in control group (P0.01), and the DTF value of LFPs was 0.0032 + 0.0011 in propofol group and 0.0122 + 0.0013 (P0.01) in control group. The 0 frequency component DTF value of 48h and LFPs after anesthesia: Propofol group 0.0140 + 0.0023 and control group 0.0165 + 0.001 9 (P0.05); the DTF value of the frequency segment of LFPs: the propofol group was 0.0065 + 0.0013, the control group was 0.0119 + 0.0028 (P0.01). The DTF value of the 0 band components of 72h and LFPs after anesthesia was 0.0157 + 0.0029 in the propofol group and 0.0165 + 0.0014 (P0.05) in the control group; the DTF value of the gamma frequency component of LFPs: Propofol group was 0.0117 + 0.0024, and the control group was 0.0121 + 0.001 5 (P0.05).
4. effects of propofol anesthesia on 24,48,72h working memory LFPs network characteristics
(1) the effect of propofol anesthesia on the D density of working memory LFPs network:
After anaesthesia, 24h, LFPs was 0.22 + 0.03, and the control group was 0.42 + 0.07 (P0.01): the gamma frequency component of LFPs was 0.12 + 0.03 in the propofol group and 0.63 + 0.05 (P0.01) in the control group. The 0 band components of 48h and LFPs after anesthesia were 0.30 + 0.04, and the control group was 0.48 + 0.06 (P0.05); and the gamma frequency component of LFPs: propofol. The group was 0.48 + 0.04 and the control group was 0.62 + 0.03 (P0.05). The 0 band components of 72h and LFPs after anesthesia were 0.41 + 0.02 in propofol group and 0.47 + 0.05 (P0.05) in the control group; the gamma frequency component of LFPs was 0.61 + 0.05 in propofol group and 0.63 + 0.04 in the control group (P0.05).
(2) the effect of propofol anesthesia on the information transmission efficiency Eglobal of working memory LFPs network:
The 0 band components of 24h and LFPs after anesthesia were 0.57 + 0.02 in propofol group and 0.62 + 0.04 (P0.05) in the control group; the gamma frequency component of LFPs was 0.24 + 0.02 in propofol group and 0.72 + 0.06 (P0.01) in the control group. The 0 band components of 48h and LFPs after anesthesia: Propofol group was 0.58 + 0.04, and the control group was 0.67 + P0.05; and LFPs's gamma frequency component: propos The phenol group was 0.49 + 0.07 and the control group was 0.73 + 0.02 (P0.05). The 0 band components of 72h and LFPs after anesthesia were 0.62 + 0.02 in propofol group and 0.66 + 0.02 (P0.05) in the control group. The gamma frequency component of LFPs was 0.69 + 0.04 in propofol group and 0.73 + 0.04 in the control group (P0.05).
5. effects of propofol anesthesia on the electrical activity of neurons in working memory rats after 24,48,72h
(1) the effect of propofol anesthesia on the frequency coding of working memory neurons.
Compared with the control group, the number of neuron clusters in the 24,48h propofol group coded working memory events after anesthesia was significantly decreased (p10.01, p20.05), and there was no difference in the 72h two groups after anesthesia (P0.05).
(2) the effect of propofol anesthesia on the electrical activity of each neuron in the working memory neuron population.
Compared with the control group, the proportion of neuron electrical activity in the neuron group in the neurons of the coded working memory event was 24.3% + 4.7% in the 24h: propofol group after anesthesia and 80.6% + 13.5% (P0.01) in the control group, 48.6% + 11.2% in the 48h: propofol group after anesthesia and 81.2% + (P0.05) in the control group, and 78.3% + in the 72h: propofol group after anesthesia. 10.2%, the control group was 82.6% + 15.1% (P0.05).
The conclusions are as follows:
1. doses of 0.9mg/kg? Min, 2h propofol anesthesia, 48h in the implementation of working memory tasks in rats significantly inhibited, after 72h no inhibition effect:
The 0 (4-12HZ) and gamma band (30-60HZ) components of LFPs in 2. rats play a key role in coding working memory process. The dose of 0.9mg/kg. Min, 2h in propofol anesthesia, in 48h has significant inhibitory effect on the characteristic component of LFPs frequency band, and there is no inhibition after 72h.
The functional connection of 3.LFPs's gamma band components was significantly inhibited in 48h after propofol anesthesia and no inhibition after 72h, while the functional connection of the 0 band components was inhibited only within 24 hours after propofol anesthesia.
4. after anesthesia with propofol, 48h significantly inhibited the network density of LFPs theta and gamma band, and had no inhibitory effect after 72h.
After 5. propofol anaesthesia, 48h significantly inhibited the network information transmission efficiency of the gamma frequency component of LFPs, no inhibition after 72h, the dose of 0.9mg/kg. Min, and 2H's propofol anesthesia had no inhibitory effect on the network information transmission efficiency of the theta frequency band.
6. after propofol anesthesia, 48h significantly inhibited the electrical activity of neurons and the electrical activity of each neuron in the population, but 72h had no inhibitory effect.

【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R614

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相關(guān)期刊論文 前1條

1 張環(huán)環(huán);汪萌芽;;異丙酚對離體大鼠下丘腦視上核神經(jīng)元的抑制作用[J];生理學(xué)報;2012年02期

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