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1.
为研究糖皮质激素对原代培养大鼠肾上腺嗜铬细胞(AMCC)受激动所致儿茶酚胺的快速作用,用HPLC-ED方法检测了乙酰胆碱(10^-5mol/L)烟碱(10^-5mol/L)毒蕈碱(10^-5mol/L)及55mmol/L的KCl在20min内所引起的儿茶酚胺量,地塞米松(Dex,10^-4mol/L及10^-5mol/L)及皮质酮(10^-5mol/L)可以抑制AMCC的儿茶酚分泌,10^-7mo  相似文献   

2.
以牛蛙离体椎旁神经节为标本,单个方波电刺激节前纤维,细胞内记录B细胞的动作电位,在正常情况下节前单个刺激,在B细胞发生一个动作单位,刺激与反应的关系是1∶1。灌流皮质醇(0.01μmol/L~1μmol/L)、皮质酮(1μmol/L)、孕酮(0.1μmol/L)、17β-雌二醇(0.001μmol/L)、醛固酮(0.001μmol/L)及胆固醇(0.1μmol/L),比较它们对神经节B细胞突触传递的快速作用。结果显示,皮质醇可使170个B细胞中的52个发生突触传递阻断,另外有4个细胞出现增强效应;皮质酮可使48个B细胞中的17个发生阻断;孕酮可使37个B细胞中的15个发生阻断;17β-雌二醇可使21个B细胞中的8个发生阻断;醛固酮对B细胞的突触传递无明显影响;胆固醇可使21个B细胞中6个产生增强效应。实验结果表明,皮质醇、皮质酮、孕酮及17β-雌二醇对牛蛙交感神经节部分B细胞突触传递具有快速阻断作用,尤以孕酮的作用最显著。盐皮质激素(醛固酮)对B细胞突触传递无明显影响,而胆固醇对B细胞突触传递有增强效应。  相似文献   

3.
为了研究脑缺血时兴奋性氨基酸与胆碱能神经的关系,采用双侧颈总动脉夹闭(CCAO)的脑缺血动物模型,用乙酰胆碱离子选择性微电极(ACh-ISMs)检测皮层ACh释放量,观察脑缺血再灌注时谷氨酸对大鼠皮层ACh释放量的影响。结果表明:10-1mol/LGlu对ACh-ISMs无干扰作用,在生理状态下不能显著地促进皮层ACh的释放,但可使脑缺血3min时皮层ACh释放量较未加Glu组增加58.1%(P<0.01),再灌注后皮层ACh活性恢复减慢。结果提示:Glu协同ACh释放的效应在脑缺血时明显放大,推测Glu和ACh可能在缺血性脑损伤中有放大的协同作用。  相似文献   

4.
在离体灌流的大鼠背根神经节(DRG)-脊髓标本上,用微电极进行了胞内记录。在157个神经元中,依神经纤维的传导速度将神经元分为A类和C类,其中A类75个,C类82个。当浴槽中滴加0.5×10-6mol/L的2-氯腺苷(CADO)后,66.7%(10/15)的C类细胞发生了去极化;而只有33.3%(4/12)的A类细胞发生了去极化,且其去极幅值及持续时间均小于C类细胞的效应。先加入2.5×10-6mol/L的8-苯茶碱(8—PT),再给予CADO,85.7%(6/7)的C类细胞的静息电位无变化,只有14.3%(1/7)的C类细胞出现了暂短的去极化效应。另外,给予CADO后,58.3%(7/12)的C类细胞动作电位幅值减少,有些细胞伴有膜的去极化;但A类细胞的动作电位幅度末见明显变化。结果表明:腺苷主要引起DRG中C类细胞去极化,并减小其动作电位。  相似文献   

5.
实验应用全细胞膜片钳技术在大鼠新鲜分离的背根神经节(DRG)神经元胞体膜上观察到P物质(SP)对NMDA和GABA激活电流有调制作用。单独给予SP(10-8~10-6mol/L)可在DRG神经元记录到一幅值较小的,浓度依赖性的无明显去敏感之内向电流。预加SP30s后,其对NMDA和GABA激活电流分别具有明显的增强和抑制作用,而且SP对NMDA和GABA激活电流的增强和抑制作用也是剂量依赖性的。如SP浓度为10-7mol/L时,可使NMDA激活电流较之对照增强46.3±7.2%(x±s,n=8);使GABA激活电流比对照减小38.9±7.8%(x±s,n=6).SP的此种调制作用可以在同一DRG神经元上观察到。  相似文献   

6.
为了研究脑缺血时兴奋性氨基酸与胆碱能神经的关系,采用双侧颈总动脉夹闭(CCAO)的脑缺血动物模型,用乙酰胆碱离子选择性微电极(ACh-ISMs)检测皮层ACh释放量,观察脑缺血再灌注时谷氨酸对六鼠皮层ACh释放量的影响。结果表明:10^-1molo/L Glu对ACh-ISMs无干扰作用,在生理状态下不能显著地促进皮层ACh的释放,但可使脑缺血3min时皮层ACh释放量较示加Glu组增加58.1%  相似文献   

7.
764—3对蛛网膜下腔出血后脑血管痉挛的防治   总被引:6,自引:0,他引:6  
764-3是从丹参中提取的一种单体,对缺血性脑损伤有保护作用。本工作用大鼠蛛网膜下腔出血(SAH)模型进一步观察SAH后脑血管痉挛(CVS)引起突触体功能、脑组织中丙二醛(MDA)超氧歧化酶(SOD)的变化以及764-3的影响。发现SAH后突触体钙摄取明显增加,脑组织中MDA浓度升高,皮层局部脑血流(r-CBF)下降。764-3可以抑制突触体的钙摄取和降低脑组织中MDA,改善r-CBF,使之在SA  相似文献   

8.
764-3对蛛网膜下腔出血后脑血管痉挛的防治   总被引:1,自引:0,他引:1  
764-3是从丹参中提取的一种单体,对缺血性脑损伤有保护作用。本工作用大鼠蛛网膜下腔出血(SAH)模型进一步观察SAH后脑血管痉挛(CVS)引起突触体功能、脑组织中丙二醛(MDA)超氧歧化酶(SOD)的变化以及764-3的影响。发现SAH后突触体钙摄取明显增加,脑组织中MDA浓度升高,皮层局部脑血流(r-CBF)下降。764-3可以抑制突触体的钙摄取和降低脑组织中MDA,改善r-CBF,使之在SAH80分钟后趋于恢复,764-3对CVS引起的脑损伤有保护作用。  相似文献   

9.
目的探讨精神分裂症可能的发病和衰退机理。方法利用日立835型快速氨基酸分析仪,测定和分析30例住院精神分裂症患者(急性15例,慢性15例)的血浆谷氨酸(Glu)、牛磺酸(Tau)、γ氨基丁酸(GABA)、甘氨酸(Gly)的含量变化,并与对照组(健康志愿者10例)比较。结果(1)血浆Glu和GABA含量患者组(83±24μmol/L,56±17μmol/L)显著低于对照组(126±57μmol/L,90±17μmol/L),而血浆Tau和Gly含量两组间差异无显著性;(2)慢性患者的血浆Glu和GABA含量(93±31μmol/L,66±22μmol/L)高于急性患者(69±19μmol/L,49±11μmol/L),存在随病程迁延而增高的趋势;(3)30例患者血浆GABA的含量与阴性症状(r=0.470,P<0.01)和社会功能缺陷(r=-0.567,P<0.01)的严重程度呈显著性相关。结论精神分裂症可能与Glu能和GABA能神经系统功能低下有关。中枢神经系统Glu和GABA严重的功能失调可能导致精神分裂症慢性衰退的结局。  相似文献   

10.
目的研究垂体腺苷酸环化酶激活肽(PACAP)对谷氨酸引起的海马神经元损伤的保护作用及其受体机制。方法海马神经元体外培养7d,给予谷氨酸。结果当谷氨酸是0.1~1.0mmol/L时,随着剂量的增加,神经元的存活率逐渐降低;10-9mol/L~10-13mol/L的PACAP,能减轻谷氨酸引起的海马神经元损伤;PACAPⅠ型受体特异性拮抗剂PACAP6-38能抑制PACAP减轻谷氨酸对海马神经元损伤作用。结论PACAP具有减轻谷氨酸引起的海马神经元损伤的作用,该作用是由PACAPⅠ型受体介导的。  相似文献   

11.
Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.  相似文献   

12.
Diagnostic Difficulties and Treatment Implications   总被引:1,自引:0,他引:1  
Robert J. Gumnit 《Epilepsia》1987,28(S3):S9-S13
Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.  相似文献   

13.
Cognitive Dysfunction Associated with Antiepileptic Drug Therapy   总被引:7,自引:5,他引:2  
Eileen P.G. Vining 《Epilepsia》1987,28(S2):S18-S22
Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.  相似文献   

14.
B. J. Wilder 《Epilepsia》1987,28(S2):S1-S7
Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.  相似文献   

15.
Hepatic Considerations in the Use of Antiepileptic Drugs   总被引:5,自引:4,他引:1  
Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.  相似文献   

16.
Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.  相似文献   

17.
Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.  相似文献   

18.
Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.  相似文献   

19.
Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity   总被引:5,自引:1,他引:4  
G. Trube  R. Netzer 《Epilepsia》1994,35(S5):S62-S67
Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.  相似文献   

20.
Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.  相似文献   

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