经颅电刺激咀嚼肌诱发电位的检测方法与正常值

目的　对健康个体进行经颅电刺激咀嚼肌运动诱发电位的研究 ,建立评估皮质脑干束的检查方法。方法　对 5 6名健康志愿者进行经颅电刺激 ,在双侧咀嚼肌同时接受 ,分别记录同侧的根运动诱发电位 ( R- MEP)和对侧的皮层运动诱发电位 ( C- MEP)的潜伏期、波幅。结果　在同侧记录的是兴奋同侧的三叉神经根所产生的动作电位 ,因此称为“root”MEP( R- MEP) ;在对侧轻收缩状态下记录的是兴奋对侧的皮质延髓束所产生的动作电位 ,因此称为“cortical”MEP( C- MEP)。 R- MEP的潜期为 3.5 5± 0 .44 ms,波幅为 3.49± 2 .73m V;C- MEP的潜期为5 .83± 1.40 ms,波幅为 5 6 3.84± 5 2 5 .0 7μV。C- MEP的潜期与年龄无明显相关性 ( P>0 .1)。结论　 C- MEP是一种非创伤性评估皮质脑干束的检测方法。     

Calcium-dependent action potentials in mouse spinal cord neurons in cell culture

Following blockade of membrane potassium conductance with tetraethylammonium ions or 3-aminopyridine, long-duration action potentials were recorded from mouse spinal cord neurons in primary dissociated cell culture. The action potentials were calcium-dependent since they: (1) were not blocked by the sodium-channel blocker tetrodotoxin, (2) could be recorded in sodium-free, calcium-containing medium (3) could not be evoked in sodium-containing, calcium-free medium, (4) were blocked by calcium channel blockers manganese and cobalt and (5) had overshot amplitudes that varied linearly with the log of the extracellular calcium concentration (slope of 27.5 mV/decade change in calcium concentration).     

Erythropoietin prevents early and late neuronal demise through modulation of Akt1 and induction of caspase 1, 3, and 8

Erythropoietin (EPO) modulates primarily the proliferation of immature erythroid precursors, but little is known of the potential protective mechanisms of EPO in the central nervous system. We therefore examined the ability of EPO to modulate a series of death-related cellular pathways during anoxia and free radical induced neuronal degeneration. Neuronal injury was evaluated by trypan blue, DNA fragmentation, membrane phosphatidylserine exposure, protein kinase B phosphorylation, cysteine protease activity, mitochondrial membrane potential, and mitogen-activated protein (MAP) kinase phosphorylation. We demonstrate that constitutive neuronal EPO is insufficient to prevent cellular injury, but that signaling through the EPO receptor remains biologically responsive to exogenous EPO administration. Exogenous EPO is both necessary and sufficient to prevent acute genomic DNA destruction and subsequent phagocytosis through membrane PS exposure, because neuronal protection by EPO is completely abolished by co-treatment with an anti-EPO neutralizing antibody. Through pathways that involve the initial activation of protein kinase B, EPO maintains mitochondrial membrane potential. Subsequently, EPO inhibits caspase 8-, caspase 1-, and caspase 3-like activities linked to cytochrome c release through mechanisms that are independent from the MAP kinase systems of p38 and JNK. Elucidating some of the novel neuroprotective pathways employed by EPO may further the development of new therapeutic strategies for neurodegenerative disorders.     

Suppression of hippocampal synaptic plasticity during slow-wave sleep

The influence of behavioral state on the induction of long-term enhancement (LTE) of hippocampal synapses was studied in chronically prepared animals. Perforant path evoked field potentials and EEG were recorded from fascia dentata during slow-wave sleep (SWS) and waking. LTE was strongly suppressed during SWS, suggesting that hippocampal information storage may be inactivated at certain phases of the sleep cycle. Normal LTE was observed in the same animals while awake.     

Relation of olfactory bulb and cortex. II. Model for driving of cortex by bulb

The major projection pathway of the olfactory bulb is by way of the lateral olfactory tract (LOT) to the olfactory cortex. Oscillatory bursts of extracellular potential appear during inspiration in both bulb and cortex. Based on anatomical and physiological considerations, a model was proposed, consisting of a bulbar transmitter, a conduction line representing axons in the LOT, and a cortical receiver. The model predicted the relation between phase and frequency of bulbar and cortical burst pairs, based on the expectation that the bulb drives the cortex. Experimental phase-frequency plots were computed from bursts of 9 bulbocortical electrode site pairs from each of 10 rabbits. For each site pair, the model predicted the expected range of the joint variation of phase and frequency, using the known distance between the bulbar and cortical sites. The model was highly successful (greater than 95% prediction accuracy) for one quarter of the total number of site pairs examined. The wide range of variation for the rest of the data suggested that higher order interactions are responsible for the phase relation between bulb and cortex. Convergence of input, independence of the cortical generator, cortical feedback to the bulb and synchronization by an outside source are all discussed as possible contributors to this variation.     

血管性帕金森综合征和帕金森病患者智能与事件相关电位的对比研究

目的:对血管性帕金森综合征(VP)患者和帕金森病(PD)患者的智能和事件相关电位(ERP)进行对比研究,以期探讨两者智能障碍及其电生理变化的特点。方法:用简易智能状态量表对51例VP及50例PD进行评分,并检测其ERP各波的潜伏期及波幅,并与32例正常者作对照。结果:1.VP组痴呆的发生串明显高于PD组;重症痴呆发生率高,提示症状重。2.VP组的N_2、P 300潜伏期较PD组、正常对照组均明显延长,P_(300)波幅较两者均明显降低。3.VP组痴呆者较非痴呆者N_2、P_(300)潜伏期明显延长,P_(300)波幅明显降低,4.VP组痴呆者较PD组痴呆者N_2、P_(300)潜伏期明显延长,P_(300)波幅明显降低。结论:VP与PD比较,智能障碍发生率高,程度重,电生理改变更明显。     

Cajal 间质细胞与胃肠起搏

近年的研究发现,Cajal间质细胞(ICC)是胃肠起博细胞。ICC呈星状,有长的突起。均表达c-kit,ICC之间、ICC与周围平滑肌形成缝隙连接,可自发产生起博电位。ICC起博的机制可能是:ICC自发产生的单元电位总和达阈值,激活电压依赖的Ca2 可通透的离子通道,形成起博电位的初始部分;Ca2 内流,激活对细胞内Ca2 敏感的酶,使IP3生成增加;从而增高IP3的浓度,引起Ca2 从内源性Ca2 库瞬间释放,使细胞内Ca2 浓度上升,活化细胞膜上Ca2 活化的Cl-通道,细胞膜去极化产生平台部分;Ca2 的进入使局部Ca2 浓度上升,通道失活,起搏电位终止。     

血管性认知障碍的分子机制和遗传学

随着对血管性认知障碍概念认识的加深以及对其发病机制的深入研究,近年来有关血管性认知障碍的研究报道日益增多。文章就血管性认知障碍的分子机制和遗传学等方面做了综述。     

Effects of successful cardioversion of persistent atrial fibrillation on right ventricular refractoriness and repolarization.

AIM: Changes in ventricular refractoriness and repolarization after successful electrical cardioversion to sinus rhythm in persistent atrial fibrillation (AF) patients were studied. METHODS AND RESULTS: In 33 AF patients with controlled ventricular response, right ventricular ERP (VERP) at three basic cycle lengths (600, 500, 400 ms), as well as monophasic action potential duration (MAPd(90)) at a drive cycle length of 500 ms, were measured just before, 20 min and 24 h after cardioversion. VERP at 600 ms changed from 241+/-19 ms to 249+/-21 ms to 253+/-24 ms (P<0.001), VERP at 500 ms changed from 234+/-19 ms to 242+/-22 ms to 246+/-23 ms (P<0.001) and VERP at 400 ms changed from 224+/-20 ms to 232+/-23 ms to 236+/-24 ms (P<0.001). MAPd(90) changed from 247+/-16 ms preconversion to 252+/-17 ms 20 min postconversion to 253+/-19 ms after 24 h (P<0.05). Change in refractoriness at 500 ms was well correlated with change of mean RR interval before and 20 min after conversion (R=0.616, P<0.001). There was no correlation between RR variability and VERP before cardioversion. CONCLUSION: Restoration of sinus rhythm in persistent AF patients is followed by significant effects on ventricular refractoriness and repolarization related to cycle length change. No AF related ventricular electrophysiological alterations were found.     

肌萎缩侧索硬化患者膈肌运动诱发电位

目的 初步探讨膈股运动诱发电位（DMEP）在肌萎缩侧索硬化（ALS）患者的应用及特点。方法 以表面电极在肋间隙处记录37例ALS患者及31例正常对照者经颅及经项磁刺激时产生的膈肌复合肌肉动作电位潜伏期和波幅,并计算中枢运动传导时间（CMCT）。22例ALS患者同时接受了用力肺活量百分比（％FVC）测定。结果 ALS患者较对照者颈及皮层潜伏期延长,颈及皮层波幅对数降低,CMCT延长,皮层潜伏期、皮层波幅对数、CMCT均与锥体束受累相关;皮层潜伏期和CMCT与临床呼吸困难相关,颈潜伏期与％FVC相关。结论 CMCT、颈及皮层潜伏期是DMEP参数中反映ALS患者呼吸功能障碍的敏感指标。CMCT反映ALS患者与呼吸功能相关的皮质脊髓束功能,CMCT与颈潜伏期结合有助于全面准确地揭示ALS患者呼吸受累的本质。