两栖类交感神经节的突触传递

两栖类交感神经节广泛地用于神经生物学研究，包括突触和膜生物物理学研究。交感神经节细胞体积大，细胞的形状简单，无树突，突触位于细胞体上，神经节结构简单，但同时又具中间神经元，在体外易于长时间存活。两栖动物交感神经节表现出多种突触后电位，包括快兴奋性突触后电位（ｆＥＰＳＰ），慢抑制性突触后电位（ｓＩＰＳＰ），慢兴奋性突触后电位（ｓＥＰＳＰ），晚期慢兴奋性突触后电位，同时还表现多种突触塑性，说明该神经节     

氯氰菊酯与辛硫磷混用对美洲大蠊中枢神经的电生理影响

研究了氯氰菊酯与辛硫磷以１∶１０比例混用对美洲大蠊中枢神经兴奋性突触后电位（ＥＰＳＰｓ）的影响．混用对ＥＰＳＰｓ的兴奋程度均高于辛硫磷单用，特别是顺式氯氰菊酯加辛硫磷，ＥＰＳＰｓ开始兴奋的时间大为缩短，仅需１．３ｍｉｎ，振幅幅值增加１１０％．认为，两类杀虫剂混用增效的原因之一是提高了对靶标酶———乙酰胆碱酯酶（ＡＣｈＥ）的抑制．     

氯氰菊酯与辛硫磷混用对美洲大蠊中枢神经的？…

研究了氯氰菊酯与辛硫磷以１：１０比例混用对美洲大蠊中枢神经兴奋性突触后电位一（ＥＰＳＰＳ）的影响,混用对ＥＰＳＰＳ的兴奋程度均高于辛硫磷单用,特别是顺式氯氰菊酯加辛硫磷,ＥＰＳＰＳ开始兴奋的时间大为缩短,仅需１．３ｍｉｎ,振幅幅值增加１１０％,认为,两类杀虫剂混用增效的原因之一是提高了对靶标酶－－乙酰胆碱酯酶（ＡＣｈＥ）的抑制。     

人胎颈交感节肽能神经元的免疫细胞化学的研究

取１６例２４～３２周龄的死亡人胎作材料，用免疫细胞化学方法，于光镜下观察到颈上神经节（简称颈上节）和星状神经节（简称星状节）中存在含血管活性肠肽（ＶＩＰ）神经元和纤维，含生长抑素（ＳＯＭ）神经元和纤雏以及含Ｐ物质（ＳＰ）纤维，但未发现含ＳＰ神经元。二节中的含ＶＩＰ神经元和含ＳＯＭ神经元形状多种，免疫反应染色深浅不等，颈上节以大、中型细胞为主，而星状节以中、小型细胞居多。上述神经元类型和分布未有明显的胎龄变化。结果揭示颈交感神经节中，含ＶＩＰ和含ＳＯＭ神经元在出生前已经发育。ＶＩＰ、ＳＯＭ和ＳＰ３种神经肽在胎儿期已作为神经传导物或神经调节物而发挥功能。     

Depolarization Induced by Substance P on Rat Stellate Ganglion Neurons

应用细胞内生物电记录技术，观察神经肽Ｐ物质（ＳＰ）对大鼠星状神经节细胞的影响。ＳＰ在１μｍｏｌ～１０μｍｏｌ或更高的浓度范围内，供试３５个细胞，有２８个细胞发生膜除极反应。用低钙（０．２５ｍｍ）或用含河豚毒素（ＴＴＸ，１μｍｏｌ）克氏液灌流神经节，不影响ＳＰ引起的除极反应的幅度和时程。ＳＰ引起除极反应的同时常伴有膜电阻增大。当膜电位增大时，除极化反应幅度变小，反转电位为－８０ｍＶ至－１００ｍＶ。研究表明，ＳＰ对部分星状神经节细胞具有兴奋作用，使通过这些细胞的信息传递增强；ＳＰ对细胞膜的除极作用是由于其引起细胞膜钾导降低所致。     

P物质对大鼠星状神经节细胞的影响

应用细胞内生物电记录方法，观察神经肽Ｐ物质（ＳＰ）对大鼠星状神经节能细胞的影响，用灌流或用加压向细胞周围施加ＳＰ可使部分细胞发生膜除极反应，用低钙或用含河豚毒素克氏液灌流神经节，并不影响ＳＰ引起的除极反应的幅度和时程。ＳＰ引起除极反应的同时常伴有膜电阻增大，当膜电位增大时，除极化反应幅度变小，反转电位为－８０ｍＶ至－１００ｍＶ，研究表明，ＳＰ对部分星状神经节细胞具有直接兴奋作用，并且ＳＰ对细胞膜的     

用昆虫谷氨酸电位检测磷酰胺酯化合物的活性

采用电生理细胞内微电极记录果蝇３龄幼虫神经－肌肉接点的兴奋性接点电位（ｅｘｃｉｔａｔｏｒｙ ｊｕｎｃｔｉｏｎａｌ ｐｏｔｅｎ－ｔｉａｌｓ，ＥＪＰ），观察加药前后ＥＪＰ幅值的 变化以及电位是否被阻断及阻断时间，实验结果初步表明：１８种磷酰胺酯ＢＰＯＮ系列均可阻断ＥＪＰ，但它们的阻断时间相关很大，从７．２５ｍｉｎ到４３．００ｍｉｎ。这些化合物对谷氨酸电位的作用可分为三种：１．电位逐渐被阻断；２．电位先     

一种具有刺激红系细胞集落生成的螺旋藻（Spirulina platensis）蛋白

从螺旋藻体中通过ＤＥＡＥ纤维素层析、硫酸铵分部沉淀和葡聚糖Ｇ７５凝胶过滤得到一种具有离体情况下刺激红系细胞集落生成的功能蛋白质．ＳＤＳ—ＰＡＧＥ测分子量为１５０００道尔顿，等电点为４．８，含有藻蓝胆素．该蛋白命名为螺旋藻１５０００蛋白（Ｓｐｉｒｕｌｉａｐｌａｔｅｎｓｉｓ１５０００，ＳＰ—１５０００）．     

SPE电极上Pt单组分及Pt—Au双组分还原态CO2阳极剥离 …

采用循环伏安法,对ＳＰＥ Ｐｔ电极以及ＳＰＥ Ａｕ－Ｐｔ电极上还原态ＣＯ２的电化学氧化行为研究表明,此类电极的电化学特性与光滑Ｐｔ电极一致：ＣＯ２在氢原子吸附电位区０￣２５０ｍＶ（ｖｓ．ＲＨＥ）处,可与电极上化学吸附的氢反应,生成还原态的ＣＯ２,通过线性扫描,还原态ＣＯ２即发生一不可逆电化学氧化过程（阳极剥离）。在ＳＰＥ Ｐｔ系列及ＳＰＥ Ａｕ－Ｐｔ系列上ＣＯ２的电化学行为表明,当ＳＰＥ Ｐｔ系列     

4—氨基吡啶对大鼠海马CA1区神经元突触可塑性的影响

论文采用离体脑片和膜片箝技术，观察了4－氨基吡啶（4－aminopridine,4-AP)对海马薛氏侧枝（Schaffer fibers)-CA1突触通路活动的影响，研究结果证明4－AP可以提高海马CA1区突触传递的效率，延长兴奋性突触后电位（EPSPs)反应的潜伏期，并对长时程压抑（LTD）的幅度有抑制作用。     

Hyperpolarization following activation of K+ channels by excitatory postsynaptic potentials

We have postulated that an excitatory postsynaptic potential (e.p.s.p.) may open voltage-sensitive K+ ('M') channels, in an appropriate depolarizing range, and that this could alter the e.p.s.p. waveform. Consequently, the fast e.p.s.p. in neurones of sympathetic ganglia, elicited by a nicotinic action of acetylcholine (ACh), could be followed by a hyperpolarization, produced by the opening of M channels during the depolarizing e.p.s.p. and their subsequent slow closure (time constant-150 mg). This introduces the concept that transmitter-induced p.s.ps may trigger voltage-sensitive conductances other than those initiating action potentials, and that in the present case this could produce a true post-e.p.s.p. hyperpolarization. (Some hyperpolarizations other than inhibitory postsynaptic potentials (i.p.s.ps) have been reported to follow e.p.s.ps.) We show here that this is so.     

Muscarinic inhibitory transmission in mammalian sympathetic ganglia mediated by increased potassium conductance

Slow muscarinic inhibition may be a powerful influence on membrane properties in the peripheral and central nervous system. But the location of the muscarinic receptors in sympathetic ganglia, either on interneurones or on the postganglionic membrane, and the underlying mechanism of the inhibitory response, remains controversial. In mammalian sympathetic ganglia synaptic activation of muscarinic receptors located on inhibitory interneurones was thought to release catecholamines leading to a membrane hyperpolarization called the slow inhibitory postsynaptic potential, or s.-i.p.s.p.. However, the s.-i.p.s.p. in parasympathetic ganglia and in amphibian sympathetic ganglia is due to direct monosynaptic activation of muscarinic receptors, accompanied by an increased potassium conductance (but see ref. 11), and is not mediated by catecholamines. The situation is less clear in mammalian sympathetic ganglia and monosynaptic s.-i.p.s.ps observed in other ganglia could be exceptions to the hypothesis. We showed earlier that the s.-i.p.s.p. in rabbit superior cervical ganglia is not affected by catecholamine antagonists. We now show that the s.-i.p.s.p. in a mammalian sympathetic ganglion is due to the monosynaptic activation of muscarinic receptors, probably by an increase in potassium conductance.     

Peptidergic transmitters in synaptic boutons of sympathetic ganglia

In sympathetic ganglia of the bullfrog, a slow synaptic potential lasting for minutes--the late slow excitatory postsynaptic potential (e.p.s.p.)--was discovered. This slow response, unlike other previously known synaptic potentials in the autonomic nervous system, is not mediated by acetylcholine or monoamines. Similar non-cholinergic, non-adrenergic slow synaptic potentials have since been found in several other vertebrate autonomic ganglia. We found that the late slow e.p.s.p. is probably mediated by a peptide that is identical to, or closely resembles, mammalian luteinizing hormone releasing hormone (LHRH), because (1) when applied directly to sympathetic neurones, LHRH and its agonists elicit a slow depolarization, associated with similar changes in membrane conductance and excitability as those occurring during the late slow e.p.s.p. Furthermore, both peptide-induced and nerve-evoked responses are blocked by antagonists of LHRH; and (2) radioimmunoassays indicate that a chain of sympathetic ganglia contains 100-800 pg of a LHRH-like peptide. Its distribution among spinal nerves, the great reduction of this substance following denervation, and its release from ganglia following isotonic KCl treatment or nerve stimulation suggest that the LHRH-like material is contained in preganglionic nerve fibres. Here we report that immunohistochemical staining of sympathetic ganglia shows that LHRH-like immunoreactivity is indeed present in synaptic boutons. We also show that the two types of ganglion cells (B cells and C cells) receive strikingly different patterns of peptidergic innervation.     

Presynaptic induction of heterosynaptic associative plasticity in the mammalian brain

The induction of associative synaptic plasticity in the mammalian central nervous system classically depends on coincident presynaptic and postsynaptic activity. According to this principle, associative homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission can be induced only if synaptic release occurs during postsynaptic depolarization. In contrast, heterosynaptic plasticity in mammals is considered to rely on activity-independent, non-associative processes. Here we describe a novel mechanism underlying the induction of associative LTP in the lateral amygdala (LA). Simultaneous activation of converging cortical and thalamic afferents specifically induced associative, N-methyl-D-aspartate (NMDA)-receptor-dependent LTP at cortical, but not at thalamic, inputs. Surprisingly, the induction of associative LTP at cortical inputs was completely independent of postsynaptic activity, including depolarization, postsynaptic NMDA receptor activation or an increase in postsynaptic Ca2+ concentration, and did not require network activity. LTP expression was mediated by a persistent increase in the presynaptic probability of release at cortical afferents. Our study shows the presynaptic induction and expression of heterosynaptic and associative synaptic plasticity on simultaneous activity of converging afferents. Our data indicate that input specificity of associative LTP can be determined exclusively by presynaptic properties.     

Long-term potentiation of electrotonic coupling at mixed synapses

Long-term potentiation of chemical synapses is closely related to memory and learning. Studies of this process have concentrated on chemically mediated excitatory synapses. By contrast, activity-dependent modification of gap junctions, which also widely exist in higher structures such as hippocampus and neocortex, has not been described. Here we report that at mixed synapses between sensory afferents and an identified reticulospinal neuron, the electrotonic coupling potential can be potentiated, as well as the chemically mediated excitatory postsynaptic potential, for a prolonged time period using a stimulation paradigm like that which produces long-term potentiation in hippocampus. The effect on coupling is due to an increase in gap-junctional conductance. Our data indicate that the potentiation of both synaptic components requires an increase in intracellular calcium, involves activation of NMDA (N-methyl-D-aspartate) receptors, and is specific to the tetanized pathway.     

A new cellular mechanism for coupling inputs arriving at different cortical layers

Pyramidal neurons in layer 5 of the neocortex of the brain extend their axons and dendrites into all layers. They are also unusual in having both an axonal and a dendritic zone for the initiation of action potentials. Distal dendritic inputs, which normally appear greatly attenuated at the axon, must cross a high threshold at the dendritic initiation zone to evoke calcium action potentials but can then generate bursts of axonal action potentials. Here we show that a single back-propagating sodium action potential generated in the axon facilitates the initiation of these calcium action potentials when it coincides with distal dendritic input within a time window of several milliseconds. Inhibitory dendritic input can selectively block the initiation of dendritic calcium action potentials, preventing bursts of axonal action potentials. Thus, excitatory and inhibitory postsynaptic potentials arising in the distal dendrites can exert significantly greater control over action potential initiation in the axon than would be expected from their electrotonically isolated locations. The coincidence of a single back-propagating action potential with a subthreshold distal excitatory postsynaptic potential to evoke a burst of axonal action potentials represents a new mechanism by which the main cortical output neurons can associate inputs arriving at different cortical layers.     

Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells.

Persistent changes in synaptic efficacy are thought to underlie the formation of learning and memory in the brain. High-frequency activation of an afferent excitatory fibre system can induce long-term potentiation, and conjunctive activation of two distinct excitatory synaptic inputs to the cerebellar Purkinje cells can lead to long-term depression of the synaptic activity of one of the inputs. Here we report a new form of neural plasticity in which activation of an excitatory synaptic input can induce a potentiation of inhibitory synaptic signals to the same cell. In cerebellar Purkinje cells stimulation of the excitatory climbing fibre synapses is followed by a long-lasting (up to 75 min) potentiation of gamma-aminobutyric acid A (GABAA) receptor-mediated inhibitory postsynaptic currents (i.p.s.cs), a phenomenon that we term rebound potentiation. Using whole-cell patch-clamp recordings in combination with fluorometric video imaging of intracellular calcium ion concentration, we find that a climbing fibre-induced transient increase in postsynaptic calcium concentration triggers the induction of rebound potentiation. Because the response of Purkinje cells to bath-applied exogenous GABA is also potentiated after climbing fibre-stimulation with a time course similar to that of the rebound potentiation of i.p.s.cs, we conclude that the potentiation is caused by a calcium-dependent upregulation of postsynaptic GABAA receptor function. We propose that rebound potentiation is a mechanism by which in vivo block of climbing fibre activity induces an increase in excitability in Purkinje cells. Moreover, rebound potentiation of i.p.s.cs is a cellular mechanism which, in addition to the long-term depression of parallel fibre synaptic activity, may have an important role for motor learning in the cerebellum.     

Curare has a voltage-dependent blocking action on the glutamate synapse.

The skeletal muscle of members of Orthoptera and Diptera receives an innervation which is probably glutaminergic. Recent study of the ventral muscle fibres in the larvae of the beetle, Tenebrio molitor, has revealed that the transmitter action can be mimicked by the iontophoretic application of L-glutamate to the junctional sites at which the extracellular excitatory postsynaptic potentials (e.p.s.ps) could be recorded (D.Y. and H.W., unpublished observation). Contrary to the evidence favouring glutamate as a transmitter of junctional excitation in insects, some investigators have found that curare (+)tubocrarine, TC), a classic acetylcholine (ACh) antagonist, suppresses the neurally evoked muscle potentials in the fly Sacophaga, and Tenebrio. Here, we have analysed the action of curare on the neuromuscular junction of Tenebrio larvae and found that curare blocked the glutaminergic transmission by antagonising the transmitter at the postsynaptic site.     

炸药殉爆实验和数值模拟

为解决炸药殉爆实验可以给出炸药殉爆条件,但不能得到炸药爆炸过程细节的问题,进行了固黑铝(GHL)炸药殉爆实验,通过观测残留炸药和见证板变形,判断被发炸药爆炸情况. 并采用非线性有限元计算方法对炸药殉爆实验进行了数值模拟计算. 计算模型中主要考虑了主发炸药爆炸冲击波在空气中的传播及其对被发炸药的冲击起爆. 用欧拉法描述主发炸药及周围空气介质,用拉格朗日法描述被发炸药和见证板. 通过数值模拟计算,分析了炸药殉爆过程中,被发炸药爆轰波的成长历程. 结果表明:被发炸药起爆点位于药柱下端,爆轰波先向下传播,使底部炸药先爆炸,然后转为向上传播起爆整个炸药柱;炸药底端压力不高,远低于炸药C-J爆压,对见证板的破坏作用较小.     

Autistic-like behaviours and hyperactivity in mice lacking ProSAP1/Shank2

Autism spectrum disorders comprise a range of neurodevelopmental disorders characterized by deficits in social interaction and communication, and by repetitive behaviour. Mutations in synaptic proteins such as neuroligins, neurexins, GKAPs/SAPAPs and ProSAPs/Shanks were identified in patients with autism spectrum disorder, but the causative mechanisms remain largely unknown. ProSAPs/Shanks build large homo- and heteromeric protein complexes at excitatory synapses and organize the complex protein machinery of the postsynaptic density in a laminar fashion. Here we demonstrate that genetic deletion of ProSAP1/Shank2 results in an early, brain-region-specific upregulation of ionotropic glutamate receptors at the synapse and increased levels of ProSAP2/Shank3. Moreover, ProSAP1/Shank2(-/-) mutants exhibit fewer dendritic spines and show reduced basal synaptic transmission, a reduced frequency of miniature excitatory postsynaptic currents and enhanced N-methyl-d-aspartate receptor-mediated excitatory currents at the physiological level. Mutants are extremely hyperactive and display profound autistic-like behavioural alterations including repetitive grooming as well as abnormalities in vocal and social behaviours. By comparing the data on ProSAP1/Shank2(-/-) mutants with ProSAP2/Shank3αβ(-/-) mice, we show that different abnormalities in synaptic glutamate receptor expression can cause alterations in social interactions and communication. Accordingly, we propose that appropriate therapies for autism spectrum disorders are to be carefully matched to the underlying synaptopathic phenotype.