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Reciprocal communication systems between astrocytes and neurones

PROGRESS IN NEUROBIOLOGY 2000年第6期62卷 561-581页

作者： Carmignoto, G Univ Padua Dept Expt Biomed Sci I-35121 Padua Italy Univ Padua CNR Ctr Study Biomembranes I-35121 Padua Italy

Over the past decade, a growing body of evidence has emerged on the existence in the brain of a close bidirectional communication system between neurones and astrocytes. This article reviews recent advances in understanding the rules governing these interactions and describes putative, novel functions attributable to astrocytes in neuronal transmission. Astrocytes can respond to the neurotransmitter released from active synaptic terminals, with cytosolic Ca2+ oscillations whose frequency is under the dynamic control of neuronal activity. In response to these neuronal signals, astrocytes can signal back to neurones by releasing various neurone active compounds, such as the excitatory neurotransmitter glutamate. Interestingly, there is accumulating evidence that glutamate is released via a Ca2+-dependent mechanism which may share common properties with neurotransmitter exocytosis in neurones. This bidirectional communication system between neurones and astrocytes may lead to profound changes in neuronal excitability and synaptic transmission. While there clearly is an enormous amount of experimental and theoretical work yet to figure out, a coherent view is now emerging which incorporates the astrocyte, with the presynaptic terminal and the postsynaptic target neurone, as a possible third functional element of the synapse. (C) 2000 Published by Elsevier Science Ltd.

关键词：星形细胞/细胞学星形细胞/代谢钙通道/代谢钙信号/生理学细胞间通讯/生理学细胞培养的谷氨酸/代谢配体长时程增强/生理学神经元/细胞学神经元/代谢受体谷氨酸/代谢信号传导/生理学动物人类

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Hebbian modification of a hippocampal population pattern in the rat

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第1期521卷 159-167页

作者： King, C Henze, DA Leinekugel, X Buzsáki, G Rutgers State Univ Ctr Mol & Behav Neurosci Newark NJ 07102 USA

1. The study of the physiological role of long-term potentiation (LTP) is often hampered by the challenge of finding a physiological event that can be used to assess synaptic strength. We explored the possibility of utilising a naturally occurring event, the hippocampal sharp wave (SPW), for the assessment of synaptic strength and the induction of LTP in vivo. 2. We used two methods in which hippocampal cells were either recorded intracellularly or extracellularly in vivo. In both cases, a linear association between the magnitude of the SPW and cellular responsiveness was observed. 3. LTP was induced by depolarising cells during SPWs by either direct intracellular current injection or extracellular microstimulation adjacent to the cell body. Both of these approaches led to an increase in the slope of the linear association between SPWs and cellular responsiveness. 4. This change was achieved without a rise in overall cell excitability, implying that the synapses providing input to CA1 cells during sharp waves had undergone potentiation. 5. Our findings show that the Hebbian pairing of cellular activation with spontaneous, naturally occurring synaptic events is capable of inducing LTP.

关键词：海马/细胞学海马/生理学长时程增强/生理学膜电位记忆/生理学神经元可塑性/生理学锥体细胞/生理学大鼠 Sprague-Dawley 突触/生理学动物大鼠

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Effects of adenosine receptors on the synaptic and EPSP-spike components of long-term potentiation and depotentiation in the guinea-pig hippocampus

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期521卷 451-466页

作者： Fujii, S Kuroda, Y Ito, K Kaneko, K Kato, H Yamagata Univ Sch Med Dept Physiol Yamagata 99023 Japan Tokyo Metropolitan Inst Neurosci Dept Mol & Cellular Neurobiol Fuchu Tokyo 183 Japan

1. Long-term potentiation (LTP) of synaptic efficacy comprises two components: a synaptic component consisting of increased field excitatory postsynaptic potentials (EPSPs), and a component consisting of a larger population spike amplitude for a given EPSP size (E-S potentiation). In hippocampal CA1 neurons, delivery of three weak bursts (5 pulses at 100 Hz, 20 min intervals) induced LTP in both the EPSP and E-S components. In the same cells, reversal of LTP (depotentiation, DP) in the field EPSP and the E-S component was achieved by delivering three trains of low-frequency stimuli (LFS;200 pulses at 1 Hz, 20 min intervals). 2. The effects of adenosine A(1) and A(2) receptor antagonists on the synaptic and E-S components of LTP and DP in CA1 neurons were studied by perfusing guinea-pig hippocampal slices with either 8-cyclopentyltheophylline (8-CPT) or CP-66713. 3. When bursts or LFS were applied to CA1 inputs in the presence of the A(1) receptor antagonist 8-CPT, the field EPSP was enhanced in LTP and attenuated in DP, while the E-S relationship was not significantly affected in either LTP or DP. 4. When similar experiments were performed using the A(2) receptor antagonist CP-66713, the field EPSP was blocked in LTP, but. facilitated in DP, while E-S potentiation was enhanced during both LTP and DP. 5. The results show that A(1) and A(2) adenosine receptors modulate both the synaptic and E-S components: of the induction and reversal of LTP. Based on these results, we discuss the key issue of the contribution of these receptors to the dynamics of neuronal plasticity modification in hippocampal CA1 neurons.

关键词：动作电位/药物作用动作电位/生理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学海马/化学海马/生理学长时程增强/生理学神经元可塑性/生理学器官培养技术吡嗪类/药理学受体肾上腺素能α1/生理学受体肾上腺素能α2/生理学突触传递/药物作用突触传递/生理学茶碱/类似物和衍生物茶碱/药理学动物豚鼠男(雄)性

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Presynaptic long-term depression at a central glutamatergic synapse: a role for CaMKII

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NATURE NEUROSCIENCE 1998年第5期1卷 378-383页

作者： Margrie, TW Rostas, JAP Sah, P Univ Newcastle Fac Med & Hlth Sci Neurosci Grp Callaghan NSW 2308 Australia Univ Newcastle Fac Med & Hlth Sci Disciplines Med Biochem & Human Physiol Callaghan NSW 2308 Australia

CaMKII is a calcium-activated kinase that is abundant in neurons and has been strongly implicated in memory and learning. Here we show that low-frequency stimulation of glutamatergic afferents in hippocampal slices from juvenile domestic chicks results in long-term depression of synaptic transmission. This reduction does not require activation of NMDA or metabotropic glutamate receptors and does not require a rise in postsynaptic calcium. However, buffering presynaptic calcium prevents the reduction of the excitatory postsynaptic potential or current that is induced by low-frequency stimulation. in addition, application of the calmodulin antagonist calmidazolium, or the specific CaMKII antagonist KN-93, completely blocks long-term depression. These findings demonstrate a newsy discovered form of long-term synaptic depression in the avian hippocampus.

关键词：动物新生/生理学脑/生理学鸡电刺激谷氨酰胺/生理学海马/生理学长时程增强/生理学突触前末梢/生理学突触/生理学突触传递/生理学动物

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Long-term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第1期518卷 109-119页

作者： Caillard, O Ben-Ari, Y Gaiarsa, JL Hop Port Royal INSERM U29 Inst Natl Sante & Rech Med F-75014 Paris France

1. The plasticity of GABAergic synapses was investigated in neonatal rat hippocampal slices obtained between postnatal days 3 and 6 using intracellular recording techniques. Ionotropic glutamate receptor antagonists were present throughout the experiments to isolate GABA, receptor-mediated postsynaptic potentials (GABA(A) PSPs) or currents (GABA(A) PSCs). 2. Repetitive depolarizing pulses (20 pulses, 0.5 s duration, at 0.1 Hz, each pulse generating 4-6 action potentials) induced a long-term potentiation in the slope and amplitude of the evoked GABA(A) PSPs and GABA(A) PSCs. 3. Long-term potentiation was prevented by intracellular injection of the calcium chelator BAPTA (50 mu M), or when the voltage-dependent calcium channels blockers Ni2+ (50 mu M) and nimodipine(10 mu M) were bath applied. 4. Repetitive depolarizing pulses induced a persistent (over 1 h) increase in the frequency of spontaneous GABA(A) PSCs. 5. Repetitive depolarizing pulses induced a lung-lasting increase in the frequency of miniature GABA(A) PSCs, without altering their amplitude or decay-time constant. 6. It is concluded that the postsynaptic activation of voltage-dependent calcium channels leads to a long-term potentiation of GABAergic synaptic transmission in neonatal rat hippocampus. This form of plasticity is expressed as an increase in the probability of GABA release or in the number of functional synapses, rather than as an upregulation of postsynaptic GABA(A) receptor numbers or conductance at functional synapses.

关键词：动物新生/生理学螯合剂/药理学依他酸/类似物和衍生物依他酸/药理学电刺激 GABA-A受体拮抗剂海马/生理学长时程增强/生理学膜电位/生理学膜片钳术大鼠 Wistar 突触传递/生理学 γ氨基丁酸/生理学动物男(雄)性大鼠

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Photolytically released nitric oxide produces a delayed but persistent suppression of LTP in area CA1 of the rat hippocampal slice

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期515卷 453-462页

作者： Murphy, KPSJ Bliss, TVP Univ Cambridge Dept Pharmacol Cambridge CB2 1QJ England Natl Inst Med Res Div Neurophysiol London NW7 1AA England

1. We have used flash photolysis of a caged form of nitric oxide (NO), potassium pentachloronitrosylruthenate (K2Ru(NO)Cl-5), to apply known concentrations of NO, with a high degree of temporal resolution, to hippocampal slices prepared from juvenile male rats maintained in an interface recording chamber, 2. Photolytically released NO (1-4.5 mu M) from bath applied caged NO reduced the magnitude of long-term potentiation (LTP) in a concentration-dependent manner. This effect was abolished in the presence of the NO scavenger haemoglobin. NO had no effect on preestablished LTP. 3. Exposure to photolytically released NO had no effect on normal fast synaptic transmission, but did result in depression of N-methyl-D-aspartate (NMDA) receptor-mediated transmission recorded using extracellular electrodes. The onset of NO-induced depression was relatively slow, taking >40 s to manifest itself, and several minutes to achieve maximum depression (t(1/2) approximate to 70 s). NO-induced depression persisted for more than 2 h after photolysis, The time courses of the action of NO on NMDA receptor-mediated responses and its action on the induction of LTP were similar. 4. These results suggest that released NO may play a role in determining the subsequent threshold for the induction of LTP at Schaffer-commissural synapses through a reduction in the efficacy of NMDA receptor function when repeated conditioning trains are used.

关键词：电生理学血红蛋白类/药理学海马/生理学长时程增强/生理学一氧化氮/拮抗剂和抑制剂一氧化氮/生理学光解大鼠 Sprague-Dawley 受体 N-甲基-D-天冬氨酸/生理学突触传递/生理学时间因素动物男(雄)性大鼠

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Ca²⁺/calmodulin-kinase II enhances channel conductance of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate type glutamate receptors

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第6期96卷 3269-3274页

作者： Derkach, V Barria, A Soderling, TR Oregon Hlth Sci Univ Vollum Inst Portland OR 97201 USA

The ability of central glutamatergic synapses to change their strength in response to the intensity of synaptic input, which occurs, for example, in long-term potentiation (LTP), is thought to provide a cellular basis for memory formation and learning. LTP in the CA1 field of the hippocampus requires activation of Ca2+/calmodulin-kinase II (CaM-KII), which phosphorylates Ser-831 in the GluR1 sub unit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate glutamate receptor (AMPA-R), and this activation/phosphorylation is thought to be a postsynaptic mechanism in LTP, In this study, we have identified a molecular mechanism by which CaM-KII potentiates AMPA-Rs. Coexpression in HEK-293 cells of activated CaM-KII with GluR1 did not affect the glutamate affinity of the receptor, the kinetics of desensitization and recovery, channel rectification, open probability, or gating, Single-channel recordings identified multiple conductance states for GluR1, and coexpression with CaM-KII or a mutation of Ser-831 to Asp increased the contribution of the higher conductance states. These results indicate that CaM-KII can mediate plasticity at glutamatergic synapses by increasing single-channel conductance of existing functional AR;IPA-Rs or by recruiting new high-conductance-state AMPA-Rs.

关键词：钙-钙调素依赖性蛋白激酶2型钙-钙调素依赖性蛋白激酶类/生理学细胞系离子通道/生理学长时程增强/生理学神经元可塑性/生理学磷酰化受体 AMPA/生理学信号传导/生理学人类

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Long-term potentiation of excitatory inputs to brain reward areas by nicotine

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NEURON 2000年第2期27卷 349-357页

作者： Mansvelder, HD McGehee, DS Univ Chicago Dept Anesthesia & Crit Care Whitman Lab Chicago IL 60637 USA

Nicotine reinforces smoking behavior by activating nicotinic acetylcholine receptors (nAChRs) in the mid-brain dopaminergic (DA) reward centers, including the ventral tegmental area (VTA). Although nicotine induces prolonged excitation of the VTA in vivo, the nAChRs on the DA neurons desensitize in seconds. Here, we show that activation of nAChRs on presynaptic terminals in the VTA enhances glutamatergic inputs to DA neurons. Under conditions where the released glutamate can activate NMDA receptors, long-term potentiation (LTP) of the excitatory inputs is induced. Both the short- and the long-term effects of nicotine required activation of presynaptic alpha 7 subunit-containing nAChRs. These results can explain the long-term excitation of brain reward areas induced by a brief nicotine exposure. They also show that nicotine alters synaptic function through mechanisms that are linked to learning and memory.

关键词：多巴胺/代谢剂量效应关系药物电刺激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/生理学尼古丁/药理学烟碱激动剂/药理学膜片钳术突触前末梢/药物作用突触前末梢/代谢喹恶啉类/药理学大鼠 Sprague-Dawley 受体烟碱/代谢突触传递/药物作用突触传递/生理学腹侧被盖区/药物作用 γ氨基丁酸/代谢动物大鼠

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Linking Hebb's coincidence-detection to memory formation

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CURRENT OPINION IN NEUROBIOLOGY 2000年第2期10卷 266-273页

作者： Tsien, JZ Princeton Univ Dept Mol Biol Princeton NJ 08544 USA

The theoretical foundations of learning and memory were laid by Donald Hebb 50 years ago. Recent genetic experiments that enhanced coincidence-detection of the NMDA receptor (a molecular master-switch in implementing Hebb's rule) and that led to better learning and memory in adult animals have substantially validated Hebb's rule in memory formation in the brain.

关键词：行为动物/生理学学习/生理学长时程增强/遗传学长时程增强/生理学记忆/生理学小鼠基因敲除小鼠神经学突变型模型神经学神经元可塑性/生理学受体 N-甲基-D-天冬氨酸/生理学时间知觉/生理学动物小鼠

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2-deoxyglucose-induced long-term potentiation of monosynaptic IPSPs in CA1 hippocampal neurons

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JOURNAL OF NEUROPHYSIOLOGY 2000年第2期83卷 879-887页

作者： Krnjevic, K Zhao, YT McGill Univ Anaesthesia Res Dept Montreal PQ H3G 1Y6 Canada

In previous experiments on excitatory synaptic transmission in CA1, temporary (10-20 min) replacement of glucose with 10 mM 2-deoxyglucose (2-DG) consistently caused a marked and very sustained potentiation (2-DG LTP). To find out whether 2-DG has a similar effect on inhibitory synapses, we recorded pharmacologically isolated mononosynaptic inhibitory postsynaptic potentials (IPSPs;under current clamp) and inhibitory postsynaptic currents (IPSCs;under voltage clamp);2-DG was applied both in the presence and the absence of antagonists of N-methyl-D-aspartate (NMDA). In spite of sharply varied results (some neurons showing large potentiation, lasting for >1 h, and many little or none), overall there was a significant and similar potentiation of IPSP conductance, both for the early (at approximate to 30 ms) and later (at approximate to 140 ms) components of IPSPs or IPSCs: by 35.1 +/- 10.25% (mean +/- SE;for n = 24, P = 0.0023) and 36.5 +/- 16.3% (for n = 19, P = 0.038), respectively. The similar potentiation of the early and late IPSP points to a presynaptic mechanism of LTP. Overall, the LTP was statistically significant only when 2-DG was applied in the absence of glutamate antagonists. Tetanic stimulations (in presence or absence of glutamate antagonists) only depressed IPSPs (by half). In conclusion, although smaller and more variable, 2-DG-induced LTP of inhibitory synapses appears to be broadly similar to the 2-DG-induced LTP of excitatory postsynaptic potentials previously observed in CA1.

关键词： 2-氨基-5-膦酰基戊酸盐/药理学抗代谢药/药理学脱氧葡萄糖/药理学兴奋性氨基酸拮抗剂/药理学海马/细胞学海马/生理学长时程增强/药物作用长时程增强/生理学微电极神经抑制/药物作用神经抑制/生理学膜片钳术锥体细胞/化学锥体细胞/药物作用锥体细胞/生理学喹恶啉类/药理学大鼠 Sprague-Dawley 受体 N-甲基-D-天冬氨酸/生理学动物男(雄)性小鼠大鼠

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