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Two dynamic processes for the induction of long-term potentiation in hippocampal CA1 neurons

BIOLOGICAL CYBERNETICS 2000年第3期82卷 189-195页

作者： Aihara, T Tsukada, M Matsuda, H Tamagawa Univ Dept Informat Commun Engn Tokyo 194 Japan

This work sets out to investigate fast and slow dynamic processes and how they effect the induction of long-term potentiation (LTP). Functionally, the fast process will work as a time window to take a spatial coincidence among various inputs pi-ejected to the hippocampus, and the slow process will work as a temporal integrator of a sequence of dynamic events. Firstly, the two factors were studied using a "burst" stimulus and a "long-interval patterns" stimulus. Secondly, we propose that, for the induction of LTP, there are two dynamic processes, fast and slow, which are productively activated by bursts and long-interval patterns. The model parameters, a time constant of short dynamics and one of long dynamics, were determined by fitting the values obtained from model simulation to the experimental data. A molecular factor or cellular factors with these two time constants are likely to be induced in LTP induction.

关键词：动作电位钙/代谢电刺激兴奋性突触后电位/生理学谷氨酸/代谢海马/细胞学海马/生理学离子通道闸门/生理学最小二乘法分析长时程增强/生理学模型神经学神经元/细胞学神经元/生理学锥体细胞/生理学受体 N-甲基-D-天冬氨酸/生理学突触传递/生理学动物豚鼠

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A transient, neuron-wide form of CREB-mediated long-term facilitation can be stabilized at specific synapses by local protein synthesis

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CELL 1999年第2期99卷 221-237页

作者： Casadio, A Martin, KC Giustetto, M Zhu, HX Chen, M Bartsch, D Bailey, CH Kandel, ER Columbia Univ Coll Phys & Surg Howard Hughes Med Inst New York NY 10032 USA Columbia Univ Coll Phys & Surg Ctr Neurobiol & Behav New York NY 10032 USA

In a culture system where a bifurcated Aplysia sensory neuron makes synapses with two motor neurons, repeated application of serotonin (5-HT) to one synapse produces a CREB-mediated, synapse-specific, longterm facilitation, which can be captured at the opposite synapse by a single pulse of 5-HT. Repeated pulses of 5-HT applied to the cell body of the sensory neuron produce a CREB-dependent, cell-wide facilitation, which, unlike synapse-specific facilitation, is not associated with growth and does not persist beyond 48 hr. Persistent facilitation and synapse-specific growth can be induced by a single pulse of 5-HT applied to a peripheral synapse. Thus, the short-term process initiated by a single pulse of 5-HT serves not only to produce transient facilitation, but also to mark and stabilize any synapse of the neuron for long-term facilitation by means of a covalent mark and rapamycin-sensitive local protein synthesis.

关键词：海螺/生理学细胞培养的 cAMP反应元件结合蛋白质/代谢更生霉素/药理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学基因表达调控/药物作用长时程增强/药物作用长时程增强/生理学记忆/生理学运动神经元/药物作用运动神经元/生理学神经组织蛋白质类/生物合成神经组织蛋白质类/遗传学神经元传入/药物作用神经元传入/生理学蛋白质生物合成血清素/药理学血清素/生理学西罗莫司/药理学突触/药物作用突触/生理学动物

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Dehydroepiandrosterone sulfate (DHEAS) counteracts decremental effects of corticosterone on dentate gyrus LTP. Implications for depression

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BRAIN RESEARCH BULLETIN 2000年第3期52卷 229-234页

作者： Kaminska, M Harris, J Gijsbers, K Dubrovsky, B McGill Univ Sch Med Neurophysiol Lab Montreal PQ H3G 1X9 Canada Univ Stirling Dept Psychol Stirling FK9 4LA Scotland

It is well-established that levels of corticosterone sufficient to occupy Type II glucocorticoid receptors produce a decrement in long-term potentiation (LTP) in the dentate gyrus of the hippocampus in rats. In the present series of experiments we investigate the interaction of corticosterone and the neurosteroid dehydroepiandrosterone sulfate (DHEAS) on LTP in the rat dentate gyrus. In confirmation of previous studies, we found that corticosterone (2 mg/kg) had decremental effects on LTP. However, simultaneous injection of corticosterone and DHEAS (30 mg/kg) elicited excitatory post-synaptic potentials and population spikes that were not significantly different from those observed in control animals. The results are discussed in terms of the interaction of the two hormones, the agonist effects of DHEAS on sigma receptors, and their relation with the antidepressant effects of DHEA.

关键词：动作电位/药物作用动作电位/生理学消炎药/药理学皮质酮/药理学硫酸脱氢表雄酮/药理学齿状回/生理学抑郁/病理生理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学长时程增强/药物作用长时程增强/生理学大鼠 Sprague-Dawley 动物男(雄)性大鼠

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Kainate receptors are involved in synaptic plasticity

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NATURE 1999年第6759期402卷 297-301页

作者： Bortolotto, ZA Clarke, VRJ Delany, CM Parry, MC Smolders, I Vignes, M Ho, KH Miu, P Brinton, BT Fantaske, R Ogden, A Gates, M Ornstein, PL Lodge, D Bleakman, D Collingridge, GL Univ Bristol Sch Med Dept Anat MRC Ctr Synapt Plast Bristol BS8 1TD Avon England Free Univ Brussels Inst Pharmaceut Dept Pharmaceut Chem & Drug Anal B-1090 Brussels Belgium Univ Montpellier 2 Lab Plasticite Cerebrale CNRS F-34095 Montpellier France Allelix Biopharmaceut Mississauga ON L4V 1V7 Canada Eli Lilly & Co Lilly Corp Ctr Indianapolis IN 46285 USA

The ability of synapses to modify their synaptic strength in response to activity is a fundamental property of the nervous system and may be an essential component of learning and memory(1). There are three classes of ionotropic glutamate receptor, namely NMDA (N-methyl-D-aspartate), AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid) and kainate receptors(2);critical roles in synaptic plasticity have been identified for two of these. Thus, at many synapses in the brain, transient activation of NMDA receptors leads to a persistent modification in the strength of synaptic transmission mediated by AMPA receptors(3,4). Here, to determine whether kainate receptors(5-7) are involved in synaptic plasticity, we have used a new antagonist, LY382884 ((3S, 4aR, 6S, 8aR)-6-( (4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydroisoquinoline-3-carboxylic acid), which antagonizes kainate receptors at concentrations that do not affect AMPA or NMDA receptors. We find that LY382884 is a selective antagonist at neuronal kainate receptors containing the GluR5 subunit. it has no effect on long-term potentiation (LTP) that is dependent on NMDA receptors but prevents the induction of mossy fibre LTP, which is independent of NMDA receptors. Thus, kainate receptors can act as the induction trigger for longterm changes in synaptic transmission.

关键词：细胞系兴奋性氨基酸拮抗剂/药理学兴奋性突触后电位海马/生理学异喹啉类/药理学犬尿烯酸/药理学长时程增强/药物作用长时程增强/生理学苔藓纤维海马/生理学大鼠 Sprague-Dawley 受体 AMPA/药物作用受体 AMPA/代谢受体红藻氨酸/拮抗剂和抑制剂受体红藻氨酸/生理学受体 N-甲基-D-天冬氨酸/药物作用受体 N-甲基-D-天冬氨酸/代谢突触/生理学突触膜/代谢突触传递动物人类大鼠

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Multiple forms of LTP in hippocampal CA3 neurons use a common postsynaptic mechanism

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NATURE NEUROSCIENCE 1999年第7期2卷 625-633页

作者： Yeckel, MF Kapur, A Johnston, D Baylor Coll Med Div Neurosci Houston TX 77030 USA

We investigated long-term potentiation (LTP) at mossy fiber synapses on CA3 pyramidal neurons in the hippocampus. Using Ca2+ imaging techniques, we show here that when postsynaptic Ca2+ was sufficiently buffered so that [Ca2+](i) did not rise during synaptic stimulation, the induction of mossy fiber LTP was prevented. In addition, induction of mossy fiber LTP was suppressed by postsynaptic injection of a peptide inhibitor of cAMP-dependent protein kinase. Finally, when ionotropic glutamate receptors were blocked, LTP depended on the postsynaptic release of Ca2+ from internal stores triggered by activation of metabotropic glutamate receptors. These results support the conclusion that mossy fiber LTP and LTP at other hippocampal synapses share a common induction mechanism involving an initial rise in postsynaptic [Ca2+].

关键词：轴突/生理学钙/代谢螯合剂/药理学依他酸/药理学电刺激兴奋性突触后电位/生理学海马/生理学长时程增强/生理学神经纤维/生理学膜片钳术锥体细胞/生理学大鼠 Sprague-Dawley 时间因素动物大鼠

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Calcium-stimulated adenylyl cyclase activity is critical for hippocampus-dependent long-term memory and late phase LTP

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NEURON 1999年第4期23卷 787-798页

作者： Wong, ST Athos, J Figueroa, XA Pineda, VV Schaefer, ML Chavkin, CC Muglia, LJ Storm, DR Univ Washington Sch Med Dept Pharmacol Seattle WA 98195 USA Washington Univ Sch Med Dept Pediat St Louis MO 63130 USA Washington Univ Sch Med Dept Mol Biol & Pharmacol St Louis MO 63130 USA

It is hypothesized that Ca2+ stimulation of calmodulin (CaM)-activated adenylyl cyclases (AC1 or AC8) generates cAMP signals critical for late phase LTP (L-LTP) and long-term memory (LTM). However, mice lacking either AC1 or AC8 exhibit normal L-LTP and LTM. Here, we report that mice lacking both enzymes (DKO) do not exhibit L-LTP or LTM. To determine if these defects are due to a loss of cAMP increases in the hippocampus, DKO mice were unilaterally cannulated to deliver forskolin. Administration of forskolin to area CA1 before training restored normal LTM. We conclude that Ca2+-stimulated adenylyl cyclase activity is essential for L-LTP and LTM and that AC1 or AC8 can produce the necessary cAMP signal.

关键词：回避学习/生理学脑/药物作用脑/酶学钙/生理学钙调蛋白/生理学提示电生理学恐惧/生理学恐惧/心理学海马/药物作用海马/酶学海马/生理学免疫组织化学长时程增强/药物作用长时程增强/生理学记忆/药物作用记忆/生理学小鼠基因敲除显微镜检查共焦动物小鼠

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Synaptic transmission and hippocampal long-term potentiation in transgenic mice expressing FAD-linked presenilin 1

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NEUROBIOLOGY OF DISEASE 1999年第1期6卷 56-62页

作者： Parent, A Linden, DJ Sisodia, SS Borchelt, DR Univ Chicago Dept Pharmacol & Physiol Sci Chicago IL 60637 USA Johns Hopkins Univ Sch Med Dept Neurosci Baltimore MD 21205 USA Johns Hopkins Univ Sch Med Dept Pathol Baltimore MD 21205 USA NINDS Epilepsy Res Branch Bethesda MD 20892 USA

Mutations in two related genes, presenilin 1 acid presenilin 2 (PS1 and PSZ), cause a subset of early-onset familial Alzheimer's disease (FAD). PS1 is expressed in a variety of neuronal and peripheral tissues, including neuronal populations known to be at risk in Alzheimer's disease such as CA1 hippocampal neurons. To examine whether FAD-linked mutations in PS1 directly influence the physiology of learning and memory, we measured the field excitatory postsynaptic potential (fEPSP) at the Schaffer collateral-CA1 synapse in hippocampal slices. Basal synaptic transmission and long-term potentiation (LTP) were examined in neurons of transgenic mice expressing wild-type human PS1 (WtTg) and FAD-linked A246E PS1 variant (MTg) and in neurons of nontransgenic littermates (NTg). Several measures of basal synaptic transmission were unaltered in WtTg and MTg compared to NTg mice, including maximum fEPSP slope, maximum fEPSP amplitude, maximum fiber volley amplitude, and the function relating fiber volley amplitude to fEPSP slope, an index of basal synaptic strength. In addition, paired-pulse facilitation was not changed. However, upon theta burst stimulation or high-frequency stimulation, input-specific LTP in MTg animals had a larger initial amplitude and was more persistent than that in WtTg or NTg animals. These data suggest that the FAD-linked A246E variant of PS1 leads to higher degree of LTP induction in mice. (C) 1999 Academic Press.

关键词：动作电位/生理学阿尔茨海默病/遗传学阿尔茨海默病/病理生理学认知/生理学兴奋性突触后电位/生理学基因表达/生理学海马/生理学长时程增强/生理学膜蛋白质类/遗传学小鼠转基因神经元可塑性/生理学早老素1 突触传递/生理学动物人类小鼠

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LTP promotes formation of multiple spine synapses between a single axon terminal and a dendrite

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NATURE 1999年第6760期402卷 421-425页

作者： Toni, N Buchs, PA Nikonenko, I Bron, CR Muller, D Univ Geneva CMU CH-1211 Geneva 4 Switzerland Univ Bern Inst Anat CH-3000 Bern Switzerland

Structural remodelling of synapses(1-4) and formation of new synaptic contacts(5-8) has been postulated as a possible mechanism underlying the late phase of long-term potentiation (LTP), a form of plasticity which is involved in learning and memory(9). Here we use electron microscopy to analyse the morphology of synapses activated by high-frequency stimulation and identified by accumulated calcium in dendritic spines. LTP induction resulted in a sequence of morphological changes consisting of a transient remodelling of the postsynaptic membrane followed by a marked increase in the proportion of axon terminals contacting two or more dendritic spines. Three-dimensional reconstruction revealed that these spines arose from the same dendrite. As pharmacological blockade of LTP prevented these morphological changes, we conclude that LTP is associated with the formation of new, mature and probably functional synapses contacting the same presynaptic terminal and thereby duplicating activated synapses.

关键词：轴突/生理学轴突/超微结构钙/代谢树突/生理学树突/超微结构海马/生理学海马/超微结构长时程增强/生理学器官培养技术突触/生理学突触/超微结构时间因素

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Protein tyrosine kinase is required for the induction of long-term potentiation in the rat hippocampus

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第3期520卷 783-796页

作者： Huang, CC Hsu, KS Natl Cheng Kung Univ Coll Med Dept Pharmacol Tainan 70101 Taiwan

1. Protein tyrosine phosphorylation is thought to play an important rob in the regulation of neuronal function. Previous work has shown that protein tyrosine kinase (PTK) inhibitors can inhibit the induction of long-term potentiation (LTP), a candidate synaptic mechanism involved in memory formation. However, how PTK activity might contribute to LTP induction remains elusive. To understand the role of PTK. pathways in the development of LTP better, a set of studies was implemented in area CA1. of rat hippocampal slices using both intra- and extracellular recordings. We show here that bath application or injection into postsynaptic cells of the PTK inhibitors genistein and lavendustin A blocked the induction of LTP produced by high-frequency tetanic stimulation. 2. Application of lavendustin A 10 min before or 3 min after induction effectively blocked LTP. However, application at 10 or 30 min after induction had no detectable effect on potentiation. 3. PTK inhibitor pretreatment did not affect the long-lasting enhancement of synaptic response produced by phorbol 12,13-dibutyrate (PDBu), forskolin plus 3-isobutyl-L-methyl-xanthine (IBMX), or tetraethylammonium (TEA). In contrast, PTK inhibitors significantly blocked postanoxic LTP. 4. EPQ(pY)EEIPIA, an activator of Src family PTKs, produced a gradual and robust increase in the synaptic response and occluded LTP. 5. These results suggest that Src family kinases are potential candidates for the PTKs contributing to the molecular mechanism of LTP induction at Schaffer collateral-CA1 synapses.

关键词： 1-甲基-3-异丁基黄嘌呤/药理学缺氧/病理生理学电刺激酶抑制剂/药理学兴奋性突触后电位/药物作用福司柯林/药理学海马/生理学长时程增强/药物作用长时程增强/生理学酚类/药理学佛波醇12 13-二丁酸盐/药理学磷酸二酯酶抑制剂/药理学蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/生理学大鼠 Sprague-Dawley 受体 AMPA/生理学受体 N-甲基-D-天冬氨酸/生理学四乙基铵/药理学 src族激酶类/生理学动物男(雄)性大鼠

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Role of AMPA receptor cycling in synaptic transmission and plasticity

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NEURON 1999年第3期24卷 649-658页

作者： Lüscher, C Xia, HH Beattie, EC Carroll, RC von Zastrow, M Malenka, RC Nicoll, RA Univ Calif San Francisco Dept Cellular & Mol Pharmacol San Francisco CA 94143 USA Univ Calif San Francisco Dept Physiol San Francisco CA 94143 USA Univ Calif San Francisco Dept Psychiat San Francisco CA 94143 USA

Compounds known to disrupt exocytosis or endocytosis were introduced into CA1 pyramidal cells while monitoring excitatory postsynaptic currents (EPSCs). Disrupting exocytosis or the interaction of GluR2 with NSF caused a gradual reduction in the AMPAR EPSC, while inhibition of endocytosis caused a gradual increase in the AMPAR EPSC. These manipulations had no effect on the NMDAR EPSC but prevented the subsequent induction of LTD. These results suggest that AMPARs, but not NMDARs, cycle into and out of the synaptic membrane at a rapid rate and that certain forms of synaptic plasticity may utilize this dynamic process.

关键词：载体蛋白质类/生理学胞吞作用/生理学胞吐作用/生理学长时程增强/生理学 N-乙基顺丁烯二酰亚胺-敏感蛋白质类神经元可塑性/生理学大鼠 Sprague-Dawley 受体 AMPA/生理学突触/生理学突触传递/生理学膜泡运输蛋白质类动物大鼠

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