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浙江大学学报（医学版） 2015年第5期44卷 546-552页

作者：谢雯孟凯贾红张莉西安交通大学医学部基础医学院生理学与病理生理学系

目的：研究蛋白合成抑制剂在成年大鼠海马CA1区长时程增强和去强化中的作用。方法：实验采用海马脑组织切片细胞外场电位记录技术，记录海马CA1区突触后场电位，在长时程增强诱导前和诱导后分别给予蛋白合成抑制剂．探讨其在海马脑片CA... 详细信息

目的：研究蛋白合成抑制剂在成年大鼠海马CA1区长时程增强和去强化中的作用。方法：实验采用海马脑组织切片细胞外场电位记录技术，记录海马CA1区突触后场电位，在长时程增强诱导前和诱导后分别给予蛋白合成抑制剂．探讨其在海马脑片CA1区长时程增强和去强化中的作用。结果：对海马脑片CA1区长时程增强诱导后2h给予两组高强度双脉冲低频刺激（HI—PP-LFS），引起长时程增强去强化，其翻转率是59．81％；对海马脑组织切片CA1区长时程增强诱导刺激前给予茴香霉素和放线菌酮，可明显减小长时程增强的幅度，与对照组差异具有统计学意义（P〈0．05）。在此条件下HI—PP-LFS可以使长时程增强去强化至基线水平；对海马脑组织切片CA1区长时程增强诱导90min后给予茴香霉素和放线茵酮，HI—PP-LFS仍然诱导了去强化，长时程增强的翻转率与对照组差异无统计学意义（P〉0．05）。结论：对海马脑片组织切片Cal区长时程增强诱导前给予蛋白合成抑制剂可明显减弱长时程增强，并且这种情况下HI-PP-LFs可以翻转长时程增强至基线水平；在长时程增强诱导后给予蛋白合成抑制剂对长时程增强的维持及翻转均没有影响。

关键词：长时程增强/药物作用大鼠,Sprague—Dawley 海马蛋白质合成抑制药/药理学

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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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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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Lipopolysaccharide inhibits long term potentiation in the rat dentate gyrus by activating caspase-1

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26252-26258页

作者： Vereker, E Campbell, V Roche, E McEntee, E Lynch, MA Univ Dublin Trinity Coll Dept Physiol Dublin 2 Ireland

Lipopolysaccharide, a component of the cell wall of Gram-negative bacteria, may be responsible for at least some of the pathophysiological sequelae of bacterial infections, probably by inducing an increase in interleukin-1 beta (IL-1 beta) concentration. We report that intraperitoneal injection of lipopolysaccharide increased hippocampal caspase-1 activity and IL-1 beta concentration;these changes were associated with increased activity of the stress-activated kinase c-Jun NH2-terminal kinase, decreased glutamate release, and impaired long term potentiation. The degenerative changes in hippocampus and entorhinal cortical neurones were consistent with apoptosis because translocation of cyto chrome c and poly(ADP-ribose) polymerase cleavage were increased. Inhibition of caspase-1 blocked these changes, suggesting that IL-1 beta mediated the lipopolysaccharide-induced changes.

关键词：半胱氨酸天冬氨酸蛋白酶1/代谢培养技术细胞色素c组/代谢齿状回/药物作用齿状回/酶学酶激活海马/药物作用海马/代谢白细胞介素1/代谢 JNK丝裂原活化蛋白激酶类脂多糖类/药理学长时程增强/药物作用丝裂原激活蛋白激酶类/代谢磷酰化大鼠 Wistar 动物男(雄)性大鼠

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Prenatal exposure to a low concentration of carbon monoxide disrupts hippocampal long-term potentiation in rat offspring

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期294卷 728-734页

作者： Mereu, G Cammalleri, M Fa, M Francesconi, W Saba, P Tattoli, M Trabace, L Vaccari, A Cuomo, V Univ Bari Sch Med Dept Pharmacol & Human Physiol Policlin Piazza Giulio Cesare 11 I-70124 Bari Italy

The aim of the present study was to investigate whether functional changes at CA3-CA1 synapses in the hippocampus could underlie learning and memory deficits produced in rat offspring by a prenatal exposure model simulating the carbon monoxide (CO) exposure observed in human cigarette smokers. Electrophysiological endpoints, including long-term potentiation, were examined in 15- to 30-day-old male rats whose mothers were exposed, from day 0 to day 20 of gestation, to 150 ppm of CO resulting in blood levels of carboxyhemoglobin comparable to those found in human cigarette smokers. Evoked field excitatory postsynaptic potentials were measured in the stratum radiatum in hippocampal slices. Results show that before tetanus, input/output functions, presynaptic volley, and paired-pulse facilitation were not affected in CO-exposed offspring, indicating that basal synaptic excitability and terminal Ca2+ influx were not influenced by prenatal exposure to this gas. Conversely, evoked field excitatory postsynaptic potentials potentiation in response to tetanization was reduced by about 23% and decayed rapidly to baseline values in slices from CO-exposed animals. No changes between and within groups were observed in paired-pulse facilitation after tetanus. The selective impairment of long-term potentiation expression exhibited by CO-exposed rats was paralleled by a significant decrease in heme-oxygenase 2 and neuronal nitric-oxide synthase in the hippocampus. No changes in either enzymatic activity were found in frontal cortex and cerebellum. These electrophysiological and biochemical alterations might account for cognitive deficits previously observed in rats exposed prenatally to CO. Our findings could have clinical implications for the offspring of mothers who smoke during pregnancy.

关键词：一氧化碳/毒性碳氧血红蛋白/代谢小脑/药物作用小脑/酶学兴奋性突触后电位/药物作用额叶/药物作用额叶/酶学血红素氧化酶(脱环)/代谢长时程增强/药物作用一氧化氮合酶/代谢一氧化氮合酶Ⅰ型产前暴露迟发效应锥体细胞/药物作用锥体细胞/酶学锥体细胞/生理学大鼠 Wistar 突触传递/药物作用动物女(雌)性男(雄)性妊娠大鼠

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Acetylcholine-mediated modulation of striatal function

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TRENDS IN NEUROSCIENCES 2000年第3期23卷 120-126页

作者： Calabresi, P Centonze, D Gubellini, P Pisani, A Bernardi, G Univ Roma Tor Vergata Dipartimento Neurosci Neurol Clin Rome Italy CNR Ist Med Sperimentale I-00137 Rome Italy Osped S Lucia IRCCS Rome Italy

Striatal spiny neurones serve as a major anatomical locus for the relay of cortical information now through the basal ganglia. These projection neurones also represent the main synaptic target of cholinergic interneurones,whose physiological role in striatal activity still remains largely enigmatic. The striatal cholinergic system has been implicated in the pathophysiology of movement disorders such as Parkinson's disease, but the cellular mechanisms underlying cholinergic-neurone function are still unknown. On the basis of in vitro electrophysiological evidence,obtained from a rat corticostriatal-slice preparation, we propose that endogenous ACh exerts a complex modulation of striatal synaptic transmission, which produces both short-term and long-term effects. ACh-mediated mechanisms might be of crucial importance in processing the cortical inputs to the striatum.

关键词：乙酰胆碱/代谢乙酰胆碱/药理学细胞培养的纹状体/解剖学和组织学纹状体/药物作用纹状体/代谢兴奋性氨基酸类/生物合成中间神经元/细胞学中间神经元/代谢长时程增强/药物作用长时程增强/生理学 N-甲基天冬氨酸/代谢神经网/代谢受体毒蕈碱/代谢突触传递/药物作用突触传递/生理学 γ氨基丁酸/生物合成动物人类大鼠

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Mechanisms of use-dependent plasticity in the human motor cortex

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第7期97卷 3661-3665页

作者： Bütefisch, CM Davis, BC Wise, SP Sawaki, L Kopylev, L Classen, J Cohen, LG NINDS Human Cort Physiol Sect NIH Bethesda MD 20892 USA NIMH Lab Syst Neurosci NIH Bethesda MD 20892 USA NINDS Biometry & Field Studies Branch NIH Bethesda MD 20892 USA Univ Rostock Neurol Klin D-18055 Rostock Germany

Practicing movements results in improvement in performance and in plasticity of the motor cortex. To identify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated with drugs that influence synaptic plasticity. Use-dependent plasticity was reduced substantially by dextromethorphan (an N-methyl-D-aspartate receptor blocker) and by lorazepam [a gamma-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identify N-methyl-D-aspartate receptor activation and GABAergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex and point to similarities in the mechanisms underlying this form of plasticity and long-term potentiation.

关键词：右美沙芬/药理学诱发电位/药物作用长时程增强/药物作用劳拉西泮/药理学运动皮质/药物作用运动皮质/生理学 N-甲基天冬氨酸/药理学三嗪类/药理学人类

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Visual input induces long-term potentiation of developing retinotectal synapses

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NATURE NEUROSCIENCE 2000年第7期3卷 708-715页

作者： Zhang, LI Tao, HW Poo, M Univ Calif San Diego Dept Biol La Jolla CA 92093 USA

Early visual experience is essential in the refinement of developing neural connections. In vivo whole-cell recording from the tectum of Xenopus tadpoles showed that repetitive dimming-light stimulation applied to the contralateral eye resulted in persistent enhancement of glutamatergic inputs, but not GABAergic or glycinergic inputs, on tectal neurons. This enhancement can be attributed to potentiation of retinotectal synapses. It required spiking of postsynaptic tectal cells as well as activation of NMDA receptors, and effectively occluded long-term potentiation (LTP) of retinotectal synapses induced by direct electrical stimulation of retinal ganglion cells. Thus, LTP-like synaptic modification can be induced by natural visual inputs and may be part of the underlying mechanism for the activity-dependent refinement of developing connections.

关键词： 2-氨基-5-膦酰基戊酸盐/药理学 6-氰-7-硝基喹喔啉-2 3-二酮/药理学荷包牡丹碱/类似物和衍生物荷包牡丹碱/药理学二羧酸类/药理学光长时程增强/药物作用长时程增强/生理学神经元/药物作用神经元/生理学神经递质摄取抑制药/药理学光刺激吡咯烷类/药理学视网膜/生理学突触/药物作用突触/生理学视通路/生理学视知觉/生理学爪蟾属动物

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Inhibitory control of LTP and LTD: Stability of synapse strength

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JOURNAL OF NEUROPHYSIOLOGY 1999年第4期81卷 1559-1566页

作者： Steele, PM Mauk, MD Univ Texas Sch Med Dept Neurobiol & Anat Houston TX 77030 USA Univ Texas Sch Med WM Keck Ctr Neurobiol Learning & Memory Houston TX 77030 USA

Although much is known about the induction of synaptic plasticity, the persistence of memories suggests the importance of understanding factors that maintain synaptic strength and prevent unwanted synaptic changes. Here we present evidence that recurrent inhibitory connections in the CA1 region of hippocampus may contribute to this task by modulating the relative ability to induce long-term potentiation and depression (LTP and LTD). Bath application of the gamma-aminobutyric acid (GABA) type A agonist muscimol to hippocampal slices increased the range of frequencies that produce LTD, whereas in the presence of the GABA type A antagonist picrotoxin LTD was induced only at very low stimulation frequencies (0.25-0.5 Hz). Because one source of GABAergic input to CAI pyramidal cells is via recurrent inhibition, we tested the prediction that elevated postsynaptic spike activity would increase feedback GABA inhibition and favor the induction of LTD. By using an induction stimulation of 8 Hz, which alone produced no net change in synaptic strength, we found that stimulation presented during antidromic activation of pyramidal cell spikes induced LTD. This effect was blocked by picrotoxin. The influence of recurrent inhibition on LTP and LTD displays properties that may decrease the potential for self-reinforcing, runaway changes in synapse strength. A mechanism of this sort may help maintain patterns of synaptic strengths despite the ongoing opportunities for plasticity produced by synapse activation.

关键词： 2-氨基-5-膦酰基戊酸盐/药理学动作电位/药物作用动作电位/生理学电刺激电生理学兴奋性氨基酸拮抗剂/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 GABA拮抗剂/药理学长时程增强/药物作用长时程增强/生理学神经抑制/生理学神经元可塑性/生理学印防己毒素/药理学锥体细胞/化学锥体细胞/药物作用锥体细胞/生理学大鼠 Sprague-Dawley 受体 GABA-A/生理学受体 N-甲基-D-天冬氨酸/生理学突触/化学突触/药物作用突触/生理学 γ氨基丁酸/生理学动物大鼠

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Estradiol modulates long-term synaptic depression in female rat hippocampus

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JOURNAL OF NEUROPHYSIOLOGY 2000年第4期84卷 1800-1808页

作者： Zamani, MR Desmond, NL Levy, WB Univ Virginia Hlth Syst Dept Neurol Surg Charlottesville VA 22908 USA

Fluctuating estradiol levels in the adult, female rat modify the anatomical and functional organization of the hippocampal CA1 region. When systemic levels of estradiol are low, e.g., on estrus or in ovariectomized (OVX) rats, long-term synaptic potentiation is difficult to induce in vivo. However, little is known about the role of this ovarian hormone in long-term synaptic depression. Using multiple conditioning paradigms, we assess the magnitude of long-term depression (LTD) at CA3-CA1 synapses in vitro from adult, ovariectomized rats as a function of systemic estradiol replacement. In hippocampal slices from control OVX rats with low levels of estradiol, a low-frequency (2 Hz), asynchronous conditioning stimulation protocol does not produce LTD at 1 h postconditioning. However, this same protocol induces robust LTD in slices from estradiol-treated OVX rats. When the conditioning frequency is increased to 4 Hz, slices from both groups of rats show robust LTD in vitro. At an even higher conditioning frequency (10 Hz), the 2-Hz-based observations are reversed;no consistent changes in synaptic transmission are observed in slices from estradiol-treated OVX rats, but those from control rats (OVX 1 oil) show robust LTD. Thus estradiol reduces the frequency threshold for LTD induction at the CA3-CA1 synapses. Further, regardless of the conditioning frequency employed, where robust LTD is seen, its induction depends on normally functioning N-methyl-D-aspartate (NMDA) receptors during conditioning. The shift in conditioning frequency needed to elicit LTD is consistent with a decrease in NMDA receptor activation with decreasing estradiol levels.

关键词：条件反射(心理学) 辨别阈/药物作用电刺激/方法雌二醇/血液雌二醇/药理学海马/生理学长时程增强/药物作用卵巢切除术大鼠 Sprague-Dawley 受体 N-甲基-D-天冬氨酸/生理学芝麻油/药理学性征突触/生理学时间因素动物女(雌)性男(雄)性大鼠

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