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Blockade of hippocampal long-term potentiation by sustained tetanic stimulation near the recording site

JOURNAL OF NEUROPHYSIOLOGY 1999年第2期81卷 940-944页

作者： Kauer, JA Duke Univ Med Ctr Dept Neurobiol Durham NC 27710 USA

Specific patterns of electrical stimulation trigger several forms of synaptic plasticity in hippocampal pyramidal cells, including a long-term potentiation (LTP) of excitatory synaptic transmission. I investigated the effect of commonly used stimulation protocols at different distances from the recording site. Sustained electrical stimulation (100 Hz, 1 s) delivered close to the recording site prevented LTP induction;the same stimulation from a second electrode placed farther away subsequently produced LTP at the same recording site. Strong stimulation near the recording site could also interfere with LTP triggered from a distal site. In contrast to sustained high-frequency stimulation, intermittent stimulation (theta burst pattern) delivered close to the recording site produced normal LTP. These data support the hypothesis that strong stimulation releases a factor that acts locally to prevent LTP.

关键词：电刺激电极兴奋性突触后电位/生理学海马/生理学长时程增强/生理学大鼠 Sprague-Dawley 时间因素动物男(雄)性大鼠

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The concept of long term potentiation of transmission at synapses

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PROGRESS IN NEUROBIOLOGY 2000年第2期60卷 109-137页

作者： Bennett, MR Univ Sydney Biomed Res Inst Neurobiol Lab Sydney NSW 2006 Australia Univ Sydney Dept Physiol Sydney NSW 2006 Australia

The phenomenon of long term potentiation (LTP) of synaptic transmission, whereby a series of conditioning trains of impulses potentiate the size of synaptic potentials for periods in excess of hours, was discovered in the mammalian hippocampus by Lomo [1966, Acta Physiol. Scand. 68(Suppl. 277);128] and subsequently characterized by Bliss and Lomo (1970, J. Physiol. 207, 61P). The search for the underlying mechanisms of LTP makes for fascinating reading. The induction of associative LTP was shown by Collingridge er al. (1982, J. Physiol. 334, 33-46) to be dependent on the presence of N-methyl-D-aspartate receptors, following the discovery of these receptors by Watkins and Evans (1981, A. Rev. Pharmac. Toxic. 21, 165-204). There has, however, been continuing controversy as to whether the maintenance phase of LTP over periods of hours may be attributed to an increase in the amount of transmitter released or to an increase in the number of glutamate receptors or both. There is more agreement on the important role or protein kinases in the maintenance phase of LTP. The role of LTP in memory is just now being elucidated. (C) 1999 Elsevier Science Ltd. All rights reserved.

关键词：长时程增强/生理学神经元/生理学突触传递/生理学动物人类

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LTP mechanisms: from silence to four-lane traffic

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CURRENT OPINION IN NEUROBIOLOGY 2000年第3期10卷 352-357页

作者： Malinow, R Mainen, ZF Hayashi, Y Cold Spring Harbor Lab Cold Spring Harbor NY 11724 USA

Brief periods of strong neuronal activity induce long-lasting changes in synaptic function. This synaptic plasticity is thought to play important roles in learning and memory. One example - long-term potentation in the CA1 region of the hippocampus - has been studied extensively, and conflicting views regarding the underlying mechanisms have emerged. Recent findings, regarding basic properties of synaptic transmission, appear to reconcile these diverging views.

关键词：海马/细胞学海马/生理学长时程增强/生理学神经元/生理学突触/生理学动物

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Effect of adrenaline on the post-tetanic potentiation in mouse skeletal muscle

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JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY 2000年第3期21卷 247-254页

作者： Decostre, V Gillis, JM Gailly, P Univ Catholique Louvain Dept Physiol B-1200 Brussels Belgium

We report the influence of adrenergic stimulation on the amplitude and time course of post-tetanic potentiation of twitch contraction. This was complemented by measurements of the peak of [Ca2+](i) transients in twitches and of the level of myosin light chain 2 (LC2) phosphorylation, before, 20 and 300 s after the conditioning tetanus. Soon after the tetanus, twitch potentiation and increases of LC2 phosphorylation and of [Ca2+](i) peak were similar in control conditions and in the presence of adrenaline. In control conditions, twitch potentiation, LC2 phosphorylation and [Ca2+](i) peak returned to, or close to, pre-tetanic values in 300 s. On the contrary, in the presence of adrenaline, twitch potentiation and LC2 phosphorylation were partially or fully maintained respectively, while the increase of [Ca2+](i) peak was not. This situation allowed us to analyse the relative contributions of elevated LC2 phosphorylation and [Ca2+](i) peak in the twitch post-tetanic potentiation phenomenon. Moreover, it was shown that the increase of LC2 phosphorylation (up to 0.5 mol P/mol LC2) affected neither the kinetic parameters of the twitch nor the maximal velocity of shortening. It is proposed that the maintenance of LC2 phosphorylation in the presence of adrenaline results from the inhibition of myosin light chain phosphatase. This could be achieved through the production of the active, phosphorylated form of the inhibitor-1, an endogenous inhibitor, which binds to the catalytic sub-units common to class 1 protein phosphatases.

关键词：钙/生理学电刺激长时程增强/生理学小鼠近交C57BL 肌收缩/生理学肌骨骼/神经支配肌骨骼/生理学肌球蛋白轻链/生理学磷酰化动物小鼠

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Structural synaptic modifications associated with hippocampal LTP and behavioral learning

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CEREBRAL CORTEX 2000年第10期10卷 952-962页

作者： Geinisman, Y Northwestern Univ Sch Med Dept Cell & Mol Biol Chicago IL 60611 USA

An important problem in the neurobiology of memory is whether cellular mechanisms of learning and memory include the formation of new synapses or the remodeling of existing ones. To elucidate this problem, numerous studies have examined alterations in the number and structure of synapses following behavioral learning and hippocampal lone-term potentiation (LTP), which is viewed as a synaptic model of memory The data reported in the literature and obtained in this laboratory are analyzed here to evaluate what kind of structural modification is likely to account for synaptic plasticity associated with learning and memory. It has been demonstrated that LTP induction elicits the formation of additional synapses between activated axon terminals and newly emerging dendritic spines. Similarly, some forms of learning have been shown to increase the number of synapses. Although many ultrastructural studies examining the effect of LTP or learning failed to find a change in total synapse number, this population measure might not detect an increase in a small proportion of synapses established by activated terminals. LTP and learning have also been shown to induce a remodeling of synapses. This process is proposed to involve the transformation of certain synaptic subtypes into more efficacious ones, including the conversion of 'silent' synapses into functional synapses. It appears, therefore, that cellular mechanisms of learning and memory are likely to include both synaptogenesis and synapse remodeling.

关键词：行为/生理学海马/生理学海马/超微结构学习/生理学长时程增强/生理学受体 N-甲基-D-天冬氨酸/生理学突触/生理学突触/超微结构动物

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Voltage-sensitive calcium currents are acutely increased by nerve growth factor in PC12 cells

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JOURNAL OF NEUROPHYSIOLOGY 1999年第6期82卷 2847-2852页

作者： Jia, M Li, MX Liu, XW Jiang, H Nelson, PG Guroff, G NICHHD Dev Neurobiol Lab NIH Bethesda MD 20892 USA NICHHD Growth Factors Sect NIH Bethesda MD 20892 USA Henry Ford Hlth Sci Ctr William T Gossett Neurol Labs Detroit MI 48202 USA John D Dingell Vet Adm Med Ctr Detroit MI 48201 USA

Whole cell calcium currents were recorded from PC12 cells with the perforated patch technique. Currents were evoked by step depolarization from a holding potential of -90 mV. Nerve growth factor (NGF) increased calcium currents through L-type calcium channels by >75% within 3-5 min. This increase was inhibited by K-252a, by nifedipine, and by inhibition or down-regulation of kinase C. Brain-derived neurotrophic factor (BDNF) also increased calcium current, but to a smaller extent. Thus increases in calcium current can be linked to activation of either the high- or the low-affinity nerve growth factor receptor. Increases in presynaptic calcium uptake appear to be a crucial element in the short-term actions of the neurotrophins on neurotransmitter release leading to long-term potentiation. Also, the control of calcium uptake is likely to be an important factor in the long-term actions of the neurotrophins on neuronal survival and neuronal protection. The present data indicate that the PC12 cell may be a useful model for studying the effect of the neurotrophins on calcium uptake.

关键词：脑源性神经营养因子/代谢钙/代谢钙通道 L型/药物作用长时程增强/生理学神经生长因子类/代谢神经生长因子类/药理学 PC12细胞蛋白激酶C/代谢 RNA 信使/生物合成 RNA 信使/遗传学逆转录聚合酶链反应突触/生理学动物大鼠

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Blocking the NGF-TrkA interaction rescues the developmental loss of LTP in the rat visual cortex: Role of the cholinergic system

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NEURON 2000年第1期25卷 165-175页

作者： Pesavento, E Margotti, E Righi, M Cattaneo, A Domenici, L Scuola Int Super Studi Avanzati Program Neurosci I-34014 Trieste Italy CNR Ist Neurofisiol I-56127 Pisa Italy

Although nerve growth factor (NGF) is a crucial factor in the activity-dependent development and plasticity of visual cortex, its role in synaptic efficacy changes is largely undefined. We demonstrate that the maintenance phase of long-term potentiation (LTP) is blocked by local application of exogenous NGF in rat visual cortex at an early stage of postnatal development. Long-term depression (LTD) and bidirectional plasticity are unaffected. At later postnatal ages, blockade of either endogenous NGF by immunoadhesin (TrkA-IgG) or TrkA receptors by monoclonal antibody rescues LTP. Muscarinic receptor activation/inhibition suggests that LTP dependence on NGF is mediated by the cholinergic system. These results indicate that NGF regulates synaptic strength in well-characterized cortical circuitries.

关键词：抗体单克隆/药理学抗体特异性阿托品/药理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学免疫球蛋白G/药理学长时程增强/药物作用长时程增强/生理学赖氨酸/类似物和衍生物赖氨酸/药代动力学毒蕈碱拮抗剂/药理学神经生长因子/免疫学神经生长因子/代谢神经生长因子/药理学神经元可塑性/药物作用神经元可塑性/生理学神经元/化学神经元/细胞学神经元/代谢 PC12细胞大鼠 Wistar 受体 trkA/拮抗剂和抑制剂受体 trkA/免疫学受体 trkA/代谢受体胆碱能/生理学视皮质/细胞学视皮质/生长和发育视皮质/代谢动物大鼠

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Enrichment induces structural changes and recovery from nonspatial memory deficits in CA1 NMDAR1-knockout mice

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NATURE NEUROSCIENCE 2000年第3期3卷 238-244页

作者： Rampon, C Tang, YP Goodhouse, J Shimizu, E Kyin, M Tsien, JZ Princeton Univ Dept Mol Biol Princeton NJ 08540 USA

We produced CA1-specific NMDA receptor 1 subunit-knockout (CA1-KO) mice to determine the NMDA receptor dependence of nonspatial memory formation and of experience-induced structural plasticity in the CA1 region. CA1-KO mice were profoundly impaired in object recognition, olfactory discrimination and contextual fear memories. Surprisingly, these deficits could be rescued by enriching experience. Using stereological electron microscopy, we found that enrichment induced an increase of the synapse density in the CA1 region in knockouts as well as control littermates. Therefore, our data indicate that CA1 NMDA receptor activity is critical in hippocampus-dependent nonspatial memory, but is not essential for experience-induced synaptic structural changes.

关键词：条件反射(心理学)/生理学提示树突/生理学树突/超微结构电休克探究行为/生理学恐惧/生理学偏食/生理学长时程增强/生理学记忆/生理学记忆障碍/遗传学记忆障碍/病理生理学小鼠基因敲除模式识别视觉/生理学锥体细胞/细胞学锥体细胞/生长和发育锥体细胞/生理学锥体细胞/超微结构受体 N-甲基-D-天冬氨酸/缺乏受体 N-甲基-D-天冬氨酸/遗传学受体 N-甲基-D-天冬氨酸/生理学嗅觉/生理学空间知觉/生理学突触/生理学突触/超微结构动物女(雌)性男(雄)性小鼠

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Response of hippocampal synapses to natural stimulation patterns

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NEURON 1999年第1期22卷 157-166页

作者： Dobrunz, LE Stevens, CF Salk Inst Biol Studies Howard Hughes Med Inst Mol Neurobiol Lab La Jolla CA 92037 USA

We have studied the synaptic responses in hippocampal slices to stimulus patterns derived from in vivo recordings of place cell firing in a behaving rodent. We find that synaptic strength is strongly modulated during the presentation of these natural stimulus trains, varying 2-fold or more because of short-term plasticity. This modulation of synaptic strength is precise and deterministic, because the pattern of synaptic response amplitudes is nearly identical from one presentation of the train to the next. The mechanism of synaptic modulation is primarily a change in release probability rather than a change in the size of the elementary postsynaptic response. In addition, natural stimulus trains are effective in inducing long-term potentiation (LTP). We conclude that short-term synaptic plasticity-facilitation, augmentation, and depression-plays a prominent role in normal synaptic function.

关键词：动作电位/生理学海马/生理学长时程增强/生理学神经元/生理学物理刺激大鼠 Long-Evans 突触/生理学温度动物大鼠

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Use-dependent AMPA receptor block in mice lacking GluR2 suggests postsynaptic site for LTP expression

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NATURE NEUROSCIENCE 1998年第7期1卷 579-586页

作者： Mainen, ZF Jia, ZP Roder, J Malinow, R Cold Spring Harbor Lab Cold Spring Harbor NY 11724 USA Mt Sinai Hosp Res Inst Toronto ON M5G 1X5 Canada

The mechanisms responsible for enhanced transmission during long-term potentiation (LTP) at CA1 hippocampal synapses remain elusive. Several popular models for LTP expression propose an increase in 'use' of existing synaptic elements, such as increased probability of transmitter release or increased opening of postsynaptic receptors. To test these models directly, we studied a GluR2 knockout mouse in which AMPA receptor transmission is rendered sensitive to a use-dependent block by polyamine compounds. This method can detect increases during manipulations affecting transmitter release or AMPA receptor channel open time and probability, but shows no such changes during LTP. Our results indicate that the recruitment of new AMPA receptors and/or an increase in the conductance of these receptors is responsible for the expression of CA1 LTP.

关键词：动作电位/生理学兴奋性突触后电位/生理学长时程增强/生理学小鼠基因敲除/遗传学小鼠基因敲除/代谢小鼠基因敲除/生理学聚胺类/药理学受体 AMPA/拮抗剂和抑制剂受体 AMPA/遗传学受体 AMPA/生理学突触/生理学突触传递/生理学动物小鼠

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