侧脑室注射氟桂嗪对马桑内酯诱发大鼠皮层和海马痫样放电的抑制作用

采用皮层应用马桑内酯的方法致痫大鼠，观察侧脑室注射钙通道阻滞药氟桂嗪对致痫动物皮层脑电图、海马电图和皮层诱发电位的影响。结果显示，马桑内酯致痫时，皮层脑电图、海马电图发生痫样放电，皮层诱发电位呈高振幅变化。侧脑室注射氟桂嗪能明显地抑制致痫大鼠皮层诱发电位的振幅和脑电图、海马电图痫样放电。结果提示，氟桂嗪的抗癫痫作用与抑制中枢神经元Ｃａ＾２＋内流有关。     

电刺激蓝斑对马桑内酯诱发大鼠大脑皮层痫样放电的影响

采用皮层应用马桑内酯的方法致痫大鼠 ,观察电刺激蓝斑对皮层脑电图痫样波频率、振幅和大脑皮层诱发电位的影响。结果表明 ,电刺激蓝斑明显抑制马桑内酯诱发的痫样放电活动 ,侧脑室注射α受体阻断药酚妥拉明可明显抑制电刺激蓝斑的效应 ,注射 β受体阻断药心得安对电刺激蓝斑的效应影响不明显     

电刺激蓝斑对马桑内酯诱发大鼠大脑皮层痫？…

采用皮民桑内酯的方法致痫大鼠，观察电刺激蓝斑对皮层脑电图痫样波频率、振幅和大脑皮层诱发电位的影响。结果表明，电刺激蓝斑明显抑制马桑内酯诱发的痫样放电活动，侧脑室注射α受体阻断药酚妥拉明可明显抑制电刺激蓝斑的效应，注射β受体阻断药心得安对电刺激蓝斑的效应影响不明显。     

马桑内酯致痫大鼠海马IL-2免疫反应性的变化

目的:探求细胞因子中的白细胞介素2(Interleukin-2,IL-2)与癫痫发病之间的关系。方法:将Wistar大鼠分成三组,第一组侧脑室注入马桑内酯(Coriari Lactone,CL)2μL,第二组注入等量的生理盐水,第三组不做任何处理。然后运用免疫组织化学方法,对大鼠海马IL-2的免疫反应性进行分析;同时对实验中大鼠的行为及脑电图(eletroencepalograph,EEG)进行观察和记录。结果:第一组大鼠侧脑室注射CL过程中即诱发癫痫,且测到痫性脑电图,第二组、第三组无癫痫症状且未记录到痫性脑电图;第一组大鼠海马IL-2免疫反应性较第二组及第三组显著增强(P<0.01),表现在其海马CA_1、CA_2、CA_3区细胞数目增多,突起及其分支增多,着色明显加深;而第二、三组之间无明显差别(P>0.05)。结论:IL-2参与癫痫的发病过程,二者之间存在着一定的联系。     

强直电刺激海马致痫后大鼠大脑皮质NOS神经元变化研究

采用强直电刺激大鼠海马建立致痫模型,观察NOS神经元在致痫大鼠和正常大鼠大脑皮质的分布特征,探讨NO在癫痫发作中的作用。实验结果表明,建模组大脑皮质的阳性细胞数较正常组明显增多NOS神经元弥散分布于致痫大鼠大脑皮质,细胞胞体较大,并借突起相互交织成网。由此可得到如下结论：癫痫发生时脑内NO作用明显,这可能与癫痫引起的神经元损伤及NO介导的痫性放电的发生、传播、汇集有关;NOS—NO途径可能参与癫痫的启动与传播。     

睡眠中抽搐患者常规脑电图和动态脑电图比较

目的:比较睡眠中抽搐(含睡眠+清醒抽搐)患者常规脑电图(REEG)和24 h动态脑电图(AEEG)检出痫样放电及痫性放电率,从而指导临床医生选择脑电图检查方法。方法:常规脑电图组(I组)268例,描记清醒期30 min,动态脑电图组(II组)103例(其中75例由I组检查阴性转至),描记包括清醒期和睡眠期在内的24 h脑电图,统计两组的痫样放电率及痫性放电率并进行比较。结果:I组痫样放电56例(20.90%),II组痫样放电73例(70.87%);I组痫性放电3例(1.12%),Ⅱ组痫性放电13例(12.62%)。结论:动态脑电图组痫样放电及痫性放电率明显高于常规脑电图组(P<0.01),睡眠中抽搐(含睡眠+清醒抽搐)患者行24 h动态脑电图检查明显优于常规脑电图检查。     

慢性酒精中毒大鼠学习记忆及星形胶质细胞的变化

目的:研究酒精致大鼠学习记忆障碍与星形胶质细胞变化的关系。方法:将24只雄性Wister大鼠随机均分成对照组和酒精中毒组,酒精中毒组大鼠隔日胃内注入含酒精(2.5g/kg)的蒸馏水2ml共90d,对照组则注入不含酒精的蒸馏水2ml。然后采用Morris水迷宫和免疫组织化学技术,分析大鼠学习记忆能力的变化和额叶皮层、海马星形胶质细胞的改变。结果:酒精中毒组大鼠Morris水迷宫潜伏期明显延长,额叶皮层和海马的星形胶质细胞数目反应性增生。结论:酒精致大鼠学习记忆能力障碍与星形胶质细胞的改变有关。     

安定在颞叶癫痫病灶的脑电图定侧定位中的应用

目的：总结安定在63例颞叶癫痫病灶的脑电图(elctroencephalogram EEG)定侧定位中的应用。方法：通过癫痫导联检查，明确63例患EEG表现双侧同步痫样放电，再进行美解眠诱发试验，当EEG显示示双侧同步痫样放电或临床发作时，停止注射美解眠，缓慢推注安定，持续描记EEG。结果：当安定注射到一定剂量，双侧同步痫样放电频率逐渐减少，能量降低，直至消失，但病灶侧侵于镜灶侧。当停止注射安定后，痫放电逐渐恢复，但病灶侧先于镜灶侧。结论：利用安定对痫灶放电的扩散产生抑制，但不能消除痫灶异常放电的作用原理，可以安全有效地对颞叶癫痫病灶进行定侧定位。     

复合颞叶癫痫手术治疗40例分析

目的：通过对40例致痫灶位于颞叶加其它脑叶的难治性癫痫病人进行手术治疗的经验总结，以提高对复合型颞叶癫痫的认识。方法：共选择了40例复合颞叶癫痫患者，其中致痫灶位于颞叶加额叶的27例，颞叶加顶叶的6例，颞叶加枕叶的3例，同时位于颞叶，额叶和顶叶的4例，手术方法采取全麻下开颅在皮层脑电图监测下行前颞叶切除，功能区软膜下横纤维切断和致痫灶皮层切除。结果：本组无死亡病例，轻瘫6例，不全失语5例，术后随访半年～3年，发作完全消失23例，基本消失10例，发作次数减少50%或变型小发作5例，无效2例。有效率达95%。结论：对复合颞叶癫痫，除作前颞叶切除，再加其它脑叶的致痫灶处理，更能有效地提高治愈率。     

慢性应激性抑郁发生中海马糖皮质激素对BDNF的影响

为证明慢性应激性抑郁的发生与应激引起的糖皮质激素(Glucocorticoids,GCs)分泌增加,导致海马脑源性神经营养因子(Brain Derived Neurothrophic Factor,BDNF)表达抑制有关.实验用大鼠通过建立慢性不可预见性温和应激(Chronic Unpredictable Mild Stress,CUMS)抑郁模型,通过海马微量注射皮质酮及糖皮质激素受体拮抗剂米司非酮,然后测量体重,观测行为学表现,并用酶联免疫吸附法检测海马内GCs和BNDF含量.结果显示:CUMS明显诱发大鼠抑郁样行为,海马组织中皮质酮明显升高,BDNF水平明显下降.海马微量注射米司非酮,使CUMS诱发的大鼠抑郁样行为明显改善,且BDNF水平明显升高.正常大鼠海马微量注射皮质酮后,表现出与CUMS组相似的抑郁样行为,且海马组织中BDNF明显下降.以上结果表明,慢性应激引起大鼠海马皮质酮明显升高,使海马BDNF表达明显减少,导致抑郁发生.糖皮质激素Ⅱ型受体(Glucocorticoids Receptor,GR)起着重要作用.     

NMDA receptors in the visual cortex of young kittens are more effective than those of adult cats

Acidic amino acids, such as glutamate and aspartate, are thought to be excitatory transmitters in the cerebral neocortex and hippocampus. Receptors for these amino acids can be classified into at least three types on the basis of their agonists. Quisqualate-preferring receptors and kainate-preferring receptors are implicated in the mediation of synaptic transmission in many regions including the hippocampus and visual cortex, whereas N-methyl-D-aspartate (NMDA)-preferring receptors are thought to be involved in modulating synaptic efficacy, for example in longterm potentiation, a form of synaptic plasticity in the hippocampus. In the visual cortex of the cat and monkey, it is well established that synaptic plasticity, estimated by susceptibility of binocular responsiveness of cortical neurons to monocular visual deprivation, disappears after the 'critical' period of postnatal development. Here we report that during the critical period in young kittens, a selective NMDA-receptor antagonist blocks visual responses of cortical neurons much more effectively than it does in the adult cat. This suggests that NMDA receptors may be involved in establishing synaptic plasticity in the kitten visual cortex.     

中央上核向大脑皮质的纤维投射——HRP逆行标记法研究

本文用辣根过氧化物的酶(HRP)逆行标记法对中央上核(CS)向大脑皮质的纤维投射进行了研究。观察结果表明;CS向大脑皮质投射的范围很广泛,除压上回和视区以外的大部分大脑皮质都接受CS的投射纤维,但从整体上看前半皮质多于后半皮质。在各脑区的注射例中,海马的标记细胞最多,其次是隔区,前乙状回,后乙状回和扣带回。标记细胞为中等大小的卵圆形细胞,位于核的中央部。     

Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential

Traditionally, neuronal operations in the cerebral cortex have been viewed as occurring through the interaction of synaptic potentials in the dendrite and soma, followed by the initiation of an action potential, typically in the axon. Propagation of this action potential to the synaptic terminals is widely believed to be the only form of rapid communication of information between the soma and axonal synapses, and hence to postsynaptic neurons. Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca2+-dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals.     

Activation of NMDA receptors blocks GABAergic inhibition in an in vitro model of epilepsy

The application of tetanic electrical stimuli to the stratum radiatum fibre pathway in the hippocampus in vitro produces an NMDA (N-methyl-D-aspartate) receptor-dependent enhancement of synaptic efficacy. Repeated application of such stimuli produces a progressive enhancement of synaptic efficacy leading to the genesis of spontaneous and stimulation-evoked epileptiform discharges. We have used this in vitro approach to explore the cellular mechanisms which underlie the kindling model of epilepsy. Kindling of the stratum radiatum fibre pathway in vitro induced a progressive, long-lasting reduction of both spontaneous and stimulation-evoked GABAergic (gamma-aminobutyric acid-mediated) inhibitory postsynaptic potentials (i.p.s.ps). The reduction of i.p.s.ps by kindling was associated with a profound decrease in the sensitivity of CA1 pyramidal neurons to ionophoretically applied GABA and an increase in sensitivity to NMDA. The reduction of i.p.s.ps and GABA sensitivity was prevented by kindling in the presence of the NMDA receptor antagonist D-2-amino-5-phosphonovalerate (D-APV). These results demonstrate that kindling-like stimulus patterns produce a reduction of GABAergic inhibition in the hippocampus resulting from a stimulus-induced postsynaptic activation of NMDA receptors. The modulation of GABAergic inhibition by NMDA receptors may cause the synaptic plasticity which underlies the kindling model of epilepsy.     

初孵扬子鳄大脑皮层组织学结构观察

本文用光镜对扬子鳄大脑皮层的组织学结构进行了研究 .扬子鳄大脑皮层可分为外网状层、细胞层和内网状层三层 ,神经细胞绝大多数集中于细胞层内 ,内、外网状层中零星分布一些小细胞 .从内侧到外侧 ,大脑皮层可分为海马、新皮质和梨状皮质三部分 ,三者之间无明显界线 ,细胞排布有所区别 .本文对扬子鳄的大脑皮层同其他脊椎动物的进行了比较讨论 .     

Cholinergic-rich brain transplants reverse alcohol-induced memory deficits

Alcohol-induced memory impairment in man has been attributed to deficiencies in subcortical noradrenergic and cholinergic systems, as well as to damage in midbrain structures. Korsakoff's psychosis, a disease in which alcohol poisoning causes apparently irreversible memory defects, is characterized by lesions in cholinergic and noradrenergic nuclei and by a decrease in the activity of choline acetyltransferase (ChAT) and the content of noradrenaline (NA) in forebrain areas such as cerebral cortex and hippocampus, innervated by these nuclei. Prolonged intake of ethanol in rodents similarly produces signs of noradrenergic and cholinergic deafferentation in the cortex and hippocampus, as well as persistent memory deficits. To test whether alcohol-induced memory impairments depend on cholinergic deafferentation, we transplanted cholinergic-rich fetal basal forebrain cell suspensions into the cortex and hippocampus of alcohol-treated rats. The substantial and persistent memory losses produced in our rats by ethanol intake were associated with an impairment of cholinergic function, and were reversed by cholinergic-rich transplants into cortex and hippocampus.     

5-HT3 receptors mediate inhibition of acetylcholine release in cortical tissue

The release of cerebral acetylcholine from terminals in the cerebral cortex has been shown to be regulated by 5-hydroxytryptamine (5-HT) but it is not known which subtype of the 5-HT receptor is involved. 5-HT receptor agonists increase acetylcholine levels in vivo, indicating a reduced turnover, and reduce release of acetylcholine from striatal slices in vitro. Depleting 5-HT by inhibiting synthesis or by destroying the neurons containing 5-HT potentiates acetylcholine release, and increases acetylcholine turnover in the cerebral cortex and hippocampus. Selective antagonists for the 5-HT3 receptor subtypes which seem to have effects on mood and activity may exert their effect through the regulation of acetylcholine release in the cortex and limbic system. Radioligand binding studies show a high density of 5-HT3 receptors in the cholinergic-rich entorhinal cortex and we provide evidence that a reduction in cortical cholinergic function can be effected in vitro by 5-HT3 receptors.     

电刺激大鼠mPFC对听皮层神经元听反应的影响

实验在40只成年SD大鼠上进行,使用常规电生理学方法,观察了电刺激大鼠内侧额叶前皮质(medial prefrontal cortex, mPFC)对听皮层神经元听反应的影响.在122个神经元上观察了电刺激mPFC对听反应的影响.对其中93个神经元作了详细分析发现,有73个神经元的听反应受到易化（39个,41.9%）或抑制（34个,36.6%）.刺激mPFC对听反应的影响存在最佳刺激间隔,大多数神经元（51个,69%）在10~15 ms之间.结果提示,大鼠mPFC可对听皮层神经元的听反应调制,这种调制可能是通过多级神经元环路实现的.     

Transitional function of DG to CA3 in the hippocampus

Using single cell channel model, the transmission features of CA3-DG network in the hippocampus are investigated. The influence of the stimulation on discharge pattern of pyramidal neurons is analyzed, which shows that it starts with period spiking discharges, followed by period-doubling bifurcation to chaos, and period 3 discharge evolving into chaos, and ultimately a period of bursting discharges. By the synaptic model, the CA3-DG network model is constructed, which analyzes the summation of postsynaptic currents in the network, the influence of postsynaptic current on discharge rhythm as well as the mechanism of bursting discharges. The strong capacity of spatiotemporal encoding in the network indicates the features of CA3 network during the information transmission process in the hippocampus. The modeling result with time delay of the synaptic transmission is in accordance with the experimental phenomena of action potential in the hippocampus.