慢性酒精刺激对大鼠伏核EEG及脑电功率谱的影响

观察慢性酒精刺激过程中大鼠伏核EEG及功率谱的变化 ,探索酒精依赖的神经机制。在伏核埋植记录电极后 ,给大鼠饮用 6 %酒精水溶液 30d。用脑电图机及计算机信号采集系统记录及分析饮酒期间及停饮后的伏核EEG及功率谱。结果表明 :在慢性饮酒过程中 ,α节律明显减小 ,散在的高幅慢活动δ波和θ波逐渐增多 ,功率谱分析表明δ频段功率百分比明显增加 ,而θ频段功率百分比明显减少 ,总功率减少。停饮后 ,出现棘波和棘慢综合波 ,并持续增多 ,δ频段功率百分比逐渐减少 ,而θ和α频段功率百分比逐渐增加 ,总功率增加 ,约在停饮 9～ 10d ,脑电逐渐恢复正常。提示 :伏核EEG和脑电功率谱的变化在一定程度上可反映慢性酒精刺激及撤除刺激对神经系统的影响。     

脑血管疾病的脑电功率谱研究

脑电功率谱分析技术主要用于对脑电信号在频域范围内各种变化的研究.借助脑电功率谱分析对临床脑血管疾病情况下脑生物电信号改变进行观察并提供大量目测脑电图无法获得的定量资料,是一项有意义的探讨.     

甲亢患者病程及血清T3,T4水平对脑电功率谱的影响

目的：对甲亢患者进行脑电功率谱的定量研究以观察甲亢对脑功能的影响，方法：采用计算机分析技术检测患者脑电功率谱，并测定血清Ｔ３，Ｔ４水平，结合病程综合研究。结果：甲亢患者脑电θ相对功率和（δ＋θ）／（α＋β）比值较正常对照组显著增高，α１＋α２较正常对照组显著降低，抗甲状腺药物治疗１个月后患得血清Ｔ３，Ｔ４恢复正常，但θ频段相对功率仍高于正常，甲亢患者的病程长短和血清Ｔ３，Ｔ４水平的增高与脑电功率谱     

酒精对大鼠伏核诱发电位的抑制

电刺激大鼠脑片嗅结节区,记录伏核神经元的诱发电位,观察酒精对该诱发电位的影响,并用氯胺酮和L-谷氨酸进行分析.结果表明 :酒精能使伏核神经元诱发电位的幅值降低22.1%,同时酒精亦能使外源性谷氨酸引起的诱发电位幅值降低32.7%.提示酒精抑制伏核神经元的诱发电位可能与NMDA受体有关.     

电刺激大鼠右侧尾壳核诱导皮层脑电高频振荡的特征

目的 探讨电刺激大鼠右侧尾壳核诱导皮层脑电高频振荡(HFO)功率谱特征.方法 实验共用雄性SD大鼠56只,体质量150?250 g,氨基甲酸乙酯麻醉下行气管插管和开颅术.将一根双极不锈钢同芯刺激电极植于右侧尾壳核,重复施加电刺激(60 Hz,2 s,0.4?0.6 mA);将两个不锈钢螺丝钉旋入双侧皮层的颅骨内,一个不...     

酒精对定量脑电图影响的研究和动态观察

目的 观察健康青年人饮用适量酒精（0.8 g/kg）后对各频段脑电功率的影响和动态观察.方法 记录20例健康青年志愿者饮酒前和饮酒后9 h的所有脑电数据并进行定量分析.结果 所有脑区α1频段相对功率百分比呈上升趋势,α3和δ频段呈下降趋势.平均酒精浓度于1.5 h达峰而脑电图平均相对功率百分比于2.5 h变化最明显.酒精浓度达峰后1 h内相应频段继续呈上升和下降趋势提示酒精对脑神经的作用有延迟效应.结论 适量酒精可使健康青年人各脑区α1频段相对功率百分比升高,而α3、δ频段相对功率百分比降低.酒精对脑神经的作用有延迟效应.     

酒精对大鼠伏核诱发电位的抑制

电刺激大鼠脑片嗅结节区,记录伏核神经元的诱发电位,观察酒精对该诱发电位的影响。并用氯胺酮和Ｌ－谷氨酸进行分析。结果表明：酒精能使伏核神经元诱发电位的幅值降低２２．１％,同时酒精亦能使外源性谷氨酸引起的诱发电位幅值降低３２．７％。提示酒精抑制伏核神经元的诱发电位可能与ＮＭＤＡ受体有关。     

脑深部电刺激对吗啡心理依赖大鼠伏核多巴胺受体的影响

目的探讨脑深部电刺激(DBS)对大鼠双侧伏核多巴胺D1A受体(D1AR)和D2受体(D2R)表达的影响以及多巴胺受体(DAR)在DBS治疗吗啡心理依赖中的作用。方法将60只SD大鼠随机分为假刺激组(ShS组)、电刺激组(DBS组)和生理盐水对照组(NS组),20只/组。用免疫组化法和RT-PCR法检测各组大鼠伏核多巴胺D1AR和D2R表达的变化。结果ShS组伏核D1AR阳性细胞数较NS组、DBS组明显增多(P0.01),而DBS组与NS组比较,差异无统计学意义(P0.05);三组间D1ARmRNA比较,差异无统计学意义(P0.05)。DBS组大鼠D2R阳性细胞数较NS组明显下降(P0.01),但较ShS组明显上升(P0.01);ShS组大鼠伏核D2RmRNA较NS组及DBS组显著上升(P0.01),而DBS组与NS组比较,差异无统计学意义(P0.05)。结论DBS对吗啡心理依赖大鼠伏核D1AR和D2R的表达起反向调节作用。     

脑电图功率谱和近似熵在人脑发育过程的研究

目的：研究人脑发育过程中脑电功率值和近熵的变化特征。方法：在一组共２０９例不同年龄组建康人中进行定量脑电图功率谱和近似熵计算。结果脑电图功率谱方面总的来说δ频率,θ频率等慢活动减少,α,β频率增加。近似熵随年龄增大表现为进行性增大,各年龄组以上各指标的差异用方差检测有显著性意义。     

基于EEG信号的卷积神经网络在癫痫检测中的应用价值研究

目的 探讨基于脑电图(Electroencephalogram,EEG)信号的卷积神经网络在癫痫检测中的应用价值。方法 本研究使用了来自癫痫EEG信号数据CHB-MIT数据库中的8例患者的EEG信号; EEG信号分为3类:发作间期、发作前期(发作前持续时间至10 min)和癫痫发作期状态; 开发了一种基于迁移学习和功率谱密度能量图的深度卷积神经网络(Deep convolutional neural network,DCNN)的癫痫EEG信号分类方法(EEG signal classification method,EEGC),并对癫痫状态进行分类; 将在线硬示例挖掘(Online hard example mining,OHEM)损失函数集成到EEGC方法中以获得较高的分类准确率。结果 本研究提出的EEGC方法对癫痫状态分类的准确度较高,但发作前期没有像其他两种状态那样准确分类; 当将OHEM损失函数集成到EEGC方法中时发作前期的分类准确度提高了3%,并且它对3种癫痫状态(发作间期、发作前期和癫痫发作)的分类具有很高的敏感度(97.8%、93.6%和95.8%)和特异度(99.2%、97.1%和99.3%)。结论 本研究提出的EEGC方法具有较高的癫痫状态分类准确率,可辅助临床医生了解患者癫痫状态的类别,从而有效地预防和治疗癫痫。     

Effects of d-amphetamine injected into the nucleus accumbens on ethanol reinforced behavior

Rats, initiated to self-administer 10% (v/v) ethanol in an operant situation using the sucrose-fading procedure, received bilateral n. accumbens microinjections of d-amphetamine prior to operant sessions. Doses of 4 micrograms, 10 micrograms and 20 micrograms/brain were administered and some animals also received a 4 microgram/brain dose of LY171555. Three different effects were observed: increased, decreased and no change in total session responding. There was no clear relation between injection area in the n. accumbens and type of effect observed. For either an increase or decrease in total session responding, momentary response rates were decreased. Both d-amphetamine and LY171555 produced similar results. The data support the hypothesis that dopamine in the n. accumbens is involved with ethanol reinforced operant responding but in a complex manner.     

Effect of lead exposure on dopaminergic receptors in rat striatum and nucleus accumbens

Haloperidol- and sulpiride-displaceable [3H]spiroperidol binding and the dopamine-inhibited adenylate cyclase were measured in rats chronically exposed to lead acetate. Haloperidol-displaceable [3H]spiroperidol binding was unmodified while sulpiride-displaceable binding was increased in striatum and decreased in nucleus accumbens. In addition, the decrease of sulpiride-displaceable binding in nucleus accumbens was paralleled by a reduced ability of bromocriptine to inhibit cAMP formation in presence of the D1 receptor antagonist SCH 23390. The results support the concept that in vivo lead treatment affects dopaminergic receptors and that the binding sites labelled by [3H]spiroperidol displaced by haloperidol may be different from those which recognize sulpiride.     

大鼠伏隔核神经元膜特性及乙醇对其影响

目的 :观察伏隔核神经元的膜特性及致醉剂量的乙醇 (44mmol L)对其影响。 方法 :在大鼠伏隔核脑片上 ,采用细胞内电流钳记录技术。结果 :所观察到的神经元包括五种类型 ,神经元的静息膜电位 (mV)为 - 79.1± 2 .4 ,输入阻抗 (MΩ)为 4 8.4± 2 .3,锋电位的幅度 (mV)平均为 98.5± 4 .1;致醉剂量的乙醇 (44mmol L)对大部分伏隔核神经元的膜电位、输入阻抗及I V曲线无明显影响。 结论 :在伏隔核内 ,存在多种膜特性类型的神经元 ;致醉剂量的乙醇对大鼠伏隔核神经元的膜特性无明显影响 ,说明乙醇对伏隔核神经元的抑制作用主要并不是通过影响膜特性来实现的。     

大鼠伏隔核神经元膜特性及乙醇对其影响

目的:观察伏隔核神经元的膜特性及致醉剂量的乙醇(44 mmol/L)对其影响.方法:在大鼠伏隔核脑片上,采用细胞内电流钳记录技术.结果:所观察到的神经元包括五种类型,神经元的静息膜电位(mV)为-79.1±2.4,输入阻抗(MΩ)为48.4±2.3,锋电位的幅度(mV)平均为98.5±4.1;致醉剂量的乙醇(44 mmol/L)对大部分伏隔核神经元的膜电位、输入阻抗及I/V曲线无明显影响.结论:在伏隔核内,存在多种膜特性类型的神经元;致醉剂量的乙醇对大鼠伏隔核神经元的膜特性无明显影响,说明乙醇对伏隔核神经元的抑制作用主要并不是通过影响膜特性来实现的.     

Effect of moderate ethanol dose on dopamine uptake in rat nucleus accumbens in vivo

The present study was designed to evaluate the effects of a moderate dose of ethanol (1 g/kg) on dopamine (DA) dynamics in rat nucleus accumbens (NAc) using fast-scan cyclic voltammetry. Voltammetric recordings were made every 100 ms at a carbon fiber microelectrode, positioned in the NAc core. Acute ethanol did not significantly alter DA uptake parameters (K(m) and V(max)), but amplitudes of the DA signals were decreased after the drug in both freely moving and anesthetized rats. Therefore, the present in vivo voltammetry results suggest that DA uptake changes are not involved in ethanol-induced increases in extracellular DA concentrations.     

Analysis of rat EEG using autoregressive power spectra

The main objective of this paper is to make the auto regressive (AR) power spectrum estimation method accessible to electrophysiologists and present some typical applications. The AR method is explained, choices of various parameters are explored and examples from the analysis of rat hippocampal EEG are given. We also provide the pseudocode for the computation of the AR coefficients and the AR spectrum. We compare the results from the AR method to the FFT-based power spectrum method and demonstrate the superiority of the AR method. We also show the differences in the spectra of the EEG of alcohol-preferring (P) and non-preferring (NP) rats in the baseline condition when no alcohol is infused. We found a statistically significant difference in peak theta frequency which was at 6.96 Hz for the P rats and at 7.74 Hz for the NP rats. There were also other observable differences in the shape of the spectra of the EEG of the P and NP rats.     

Effect of sleep deprivation on sleep and EEG power spectra in the rat

EEG power spectra of the rat were computed for consecutive 4-s epochs of the daily light period and matched with the scores of the vigilance states. Sleep was characterized by a progressive decline of low frequency spectral values (i.e. slow wave activity) in non-rapid eye movement (non-REM) sleep, and a progressive increase in the amount of REM sleep. During recovery from 24-h total sleep deprivation (TSD) the following changes were observed: an increase of slow wave activity in non REM sleep with a persisting declining trend; an enhancement of theta activity (7.25-10.0 Hz) both in REM sleep and waking; a decrease of non-REM sleep and an increase of REM sleep. In addition, a slow wave EEG pattern prevailed in the awake and behaving animal during the initial recovery period. In selective sleep deprivation paradigms, either REM sleep or slow wave activity in non-REM sleep was prevented during a 2-h period following upon 24-h TSD. During both procedures, non-REM sleep spectra in the lowest frequency band showed no increase. There was no evidence for a further enhancement of slow wave activity after its selective deprivation. The results indicate that: (1) slow wave activity in non-REM sleep and theta activity in REM sleep may reflect sleep intensity; and (2) REM sleep and active waking, the two states with dominant theta activity, may be functionally related.     

Effects of acute and chronic ethanol exposure on spatial cognitive processing and hippocampal function in the rat

Animals, including rats, have a predisposition to process and use spatial information to organize and guide behavior. The hippocampus and related structures are critically involved in this function, and, consequently, it has been proposed that one function of the hippocampus is to construct "spatial cognitive maps" of environments. Lesions to the hippocampus or its connections produce a pattern of alterations in behavior which include shifts from the use of spatial information to guide behavior to the use of cue- or taxon-based information to guide behavior. Recently it was demonstrated that ethanol interacts with a specific group of neurotransmitter systems, i.e., N-methyl-D-aspartate receptors and GABA(A) receptors that exist in high proportions in the hippocampus and related structures. In this review, we seek to summarize the literature demonstrating that one effect of acute and chronic ethanol exposure is to produce behavioral alterations that are strikingly similar to those found following lesions to the hippocampal system. Furthermore, cellular and anatomical alterations resulting from similar ethanol exposure paradigms will be reviewed and offered as possible mechanisms for producing the alterations in behavior. Finally, several unanswered questions concerning the interaction between ethanol and spatial cognitive processing will be identified.