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Wind-up of spinal cord neurones and pain sensation: much ado about something?

PROGRESS IN NEUROBIOLOGY 2000年第2期61卷 169-203页

作者： Herrero, JF Laird, JMA Lopez-Garcia, JA Univ Alcala de Henares Dept Fisiol Madrid 28871 Spain

Wind-up is a frequency-dependent increase in the excitability of spinal cord neurones, evoked by electrical stimulation of afferent C-fibres. Although it has been studied over the past thirty years, there are still uncertainties about its physiological meaning. Glutamate (NMDA) and tachykinin NK1 receptors are required to generate wind-up and therefore a positive modulation between these two receptor types has been suggested by some authors. However, most drugs capable of reducing the excitability of spinal cord neurones, including opioids and NSAIDs, can also reduce or even abolish wind-up. Thus, other theories involving synaptic efficacy, potassium channels, calcium channels, etc, have also been proposed for the generation of this phenomenon. Whatever the mechanisms involved in its generation, wind-up has been interpreted as a system for the amplification in the spinal cord of the nociceptive message that arrives from peripheral nociceptors connected to C-fibres. This probably reflects the physiological system activated in the spinal cord after an intense or persistent barrage of afferent nociceptive impulses. On the other hand, wind-up, central sensitisation and hyperalgesia are not the same phenomena, although they may share common properties. Wind-up can be an important tool to study the processing of nociceptive information in the spinal cord, and the central effects of drugs that modulate the nociceptive system. This paper reviews the physiological and pharmacological data on wind-up of spinal cord neurones, and the perceptual correlates of wind-up in human subjects, in the context of its possible relation to the triggering of hyperalgesic stales, and also the multiple factors which contribute to the generation of wind-up. (C) 2000 Elsevier Science Ltd. All rights reserved.

关键词：传入通路/生理学镇痛药/药理学麻醉药局部/药理学消炎药非甾类/药理学痛觉过敏/病理生理学炎症离子转运/药物作用模型神经学吗啡/药理学神经纤维/药物作用神经纤维/生理学神经组织蛋白质类/药物作用神经组织蛋白质类/生理学神经痛/病理生理学神经元可塑性/药物作用神经元可塑性/生理学神经元传入/药物作用神经元传入/生理学神经肽类/生理学疼痛感受器/生理学疼痛/药物疗法疼痛/病理生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/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/生理学受体神经激肽1/药物作用受体神经激肽1/生理学反射/生理学脊髓/细胞学脊髓/病理生理学 P物质/生理学突触传递/药物作用内脏/神经支配动物猫人类

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G-protein-independent signaling by G-protein-coupled receptors

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TRENDS IN NEUROSCIENCES 2000年第10期23卷 469-475页

作者： Heuss, C Gerber, U Univ Zurich Brain Res Inst CH-8057 Zurich Switzerland

Two classes of receptors transduce neurotransmitter signals: ionotropic receptors and heptahelical metabotropic receptors. Whereas the ionotropic receptors are structurally associated with a membrane channel, a mediating mechanism is necessary to functionally link metabotropic receptors with their respective effecters. According to the accepted paradigm, the first step in the metabotropic transduction process requires the activation of heterotrimeric G-proteins, An increasing number of observations, however, point to a novel mechanism through which neurotransmitters can initiate biochemical signals and modulate neuronal excitability, According to this mechanism metabotropic receptors induce responses by activating transduction systems that do not involve G-proteins.

关键词：基因表达调控异源三聚体GTP结合蛋白质类/生理学无脊椎动物/生理学 MAP激酶信号系统/药物作用模型神经学神经组织蛋白质类/生理学神经递质药/药理学受体蛋白质酪氨酸激酶类/生理学受体生长因子/生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学受体神经递质/分类受体神经递质/药物作用受体神经递质/生理学信号传导/药物作用信号传导/生理学突触传递/药物作用突触传递/生理学转录激活脊椎动物/生理学 src族激酶类/生理学动物人类

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GABAergic mIPSCs in rat cerebellar Purkinje cells are modulated by TrkB and mGluR1-mediated stimulation of Src

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期524卷 677-684页

作者： Boxall, AR Max Planck Inst Biophys Chem Arbeitsgrp Zellulare Neurobiol AG142 D-37077 Gottingen Germany

1. Whilst protein tyrosine kinase (PTK) activity can modulate expressed GABA(A) receptors in cell culture, the physiological consequences on synaptic GABA(A) receptors are unknown. This was examined using whole-cell recording of bicuculline-sensitive mIPSCs in Purkinje cells (PCs) in cerebellar slices. 2. Postsynaptic application of a peptide activator of the non-receptor PTK Src (Src-peptide) enhanced mIPSC amplitudes by 39% in the presence of brain-derived neurotrophic factor (BDNF) only;neurotrophin-3 (NT-3) was ineffective in this regard. Thus Src and TrkB (the receptor for BDNF) can physiologically interact to modulate synaptic GABA(A) receptors. 3. In the presence of BDNF, pharmacological activation of metabotrophic glutamate receptor subtype 1 (mGluR1) by (S)-3,5-dihydrophenylglycine (3,5-DHPG) also lead to a 32% enhancement of mIPSCs. This enhancement was blocked by intracellular dialysis of PCs with PP1, a selective inhibitor of Src. 4. It is concluded that, whilst GABA, receptors are not constitutively regulated by endogenous PTK activity in PCs, co-activation of TrkB by BDNF and Src by mGluR1 is required to modulate GABAergic synapses in PCs.

关键词：荷包牡丹碱/药理学脑源性神经营养因子/药理学酶抑制剂/药理学诱发电位/药物作用诱发电位/生理学兴奋性氨基酸拮抗剂/药理学 GABA拮抗剂/药理学甘氨酸/类似物和衍生物甘氨酸/药理学神经抑制/药物作用神经抑制/生理学寡肽类/代谢器官培养技术酚类/药理学浦肯野细胞/化学浦肯野细胞/代谢受体 trkB/生理学受体 GABA-A/生理学受体亲代谢性谷氨酸盐/生理学雷琐辛类/药理学星状孢子素/药理学突触/化学突触/酶学钒酸盐类/药理学 γ氨基丁酸/生理学动物大鼠

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Group I metabotropic glutamate receptors mediate an inward current in rat substantia nigra dopamine neurons that is independent from calcium mobilization

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JOURNAL OF NEUROPHYSIOLOGY 1999年第4期82卷 1974-1981页

作者： Guatteo, E Mercuri, NB Bernardi, G Knöpfel, T IRCCS S Lucia Expt Neurol Lab I-00179 Rome Italy Univ Roma Tor Vergata Neurol Clin I-00179 Rome Italy Brain Sci Inst Wako Saitama 3510198 Japan

Metabotropic glutamate receptors modulate neuronal excitability via a multitude of mechanisms, and they have been implicated in the pathogenesis of neurodegenerative processes. Here we investigated the responses mediated by group I metabotropic glutamate receptors (mGluRs) in dopamine neurons of the rat substantia nigra pars compacta, using whole cell patch-clamp recordings in combination with microfluorometric measurements of [Ca2+](i) and [Na+](i). The selective group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (3,5-DHPG) was bath-applied (20 mu M, 30 s to 2 min) or applied locally by means of short-lasting (2-4 s) pressure pulses, delivered through an agonist-containing pipette positioned close to the cell body of the neuron. 3,5-DHPG evoked an inward current characterized by a transient and a sustained component, the latter of which was uncovered only with long-lasting agonist applications. The fast component coincided with a transient elevation of [Ca2+](i), whereas the total current was associated with a rise in [Na+](i). These responses were not affected either by the superfusion of ionotropic excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-2-amino-5-phosphono-pentanoic acid (D-APV), nor by the sodium channel blocker tetrodotoxin (TTX). (S)-alpha-methyl-4-carboxyphenylglycine (S-MCPG) and the more selective mGluR1 antagonist 7(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate (CPCCOEt) depressed both 3,5-DKPG-induced inward current components and, although less effectively, the associated [Ca2+], elevations. On repeated agonist applications the inward current and the calcium transients both desensitized. The time constant of recovery from desensitization differed significantly between these two responses, being 67.4 +/- 4.4 s for the inward current and 28.6 +/- 2.7 s for the calcium response. Bathing the tissue in a calcium-free/EGTA medium or adding thapsigargin (1 mu M) to the extracellular medium prevented the generati

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/药理学钙/代谢钙/药理学色酮类/药理学环亮氨酸/类似物和衍生物环亮氨酸/药理学依他酸/药理学兴奋性氨基酸拮抗剂/药理学甘氨酸/类似物和衍生物甘氨酸/药理学显微镜检查荧光神经元/细胞学神经元/药物作用神经元/生理学膜片钳术受体亲代谢性谷氨酸盐/激动剂受体亲代谢性谷氨酸盐/拮抗剂和抑制剂受体亲代谢性谷氨酸盐/生理学雷琐辛类/药理学黑质/生理学河豚毒素/药理学毒胡萝卜内酯/药理学动物大鼠

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Physiological evidence for ionotropic and metabotropic glutamate receptors in rat taste cells

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JOURNAL OF NEUROPHYSIOLOGY 1999年第5期82卷 2061-2069页

作者： Lin, WH Kinnamon, SC Colorado State Univ Dept Anat & Neurobiol Ft Collins CO 80523 USA Univ Colorado Hlth Sci Ctr Rocky Mt Taste & Smell Ctr Denver CO 80262 USA

Monosodium glutamate (MSG) elicits a unique taste in humans called umami. Recent molecular studies suggest that glutamate receptors similar to those in brain are present in taste cells, but their precise role in taste transduction remains to be elucidated. We used giga-seal whole cell recording to examine the effects of MSG and glutamate receptor agonists on membrane properties of taste cells from rat fungiform papillae. MSG (1 mM) induced three subsets of responses in cells voltage-clamped at -80 mV: a decrease in holding current (subset I), an increase in holding current (subset II), and a biphasic response consisting of an increase, followed by a decrease in holding current (subset III). Most subset II glutamate responses were mimicked by the ionotropic glutamate receptor (iGluR) agonist N-methyl-D-aspartate (NMDA). The current was potentiated by glycine and was suppressed by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5). The group III metabotropic glutamate receptor (mGluR) agonist L-2-amino-4-phosphonobutyric acid (L-Ap4) usually mimicked the subset I glutamate response. This hyperpolarizing response was suppressed by the mGluR antagonist (RS)-alpha-cyclopropyl-4-phosphonophenyl-glycine (CPPG) and by 8-bromo-cAMP, suggesting a role for cAMP in the transduction pathway. In a small subset of taste cells, L-AP4 elicited an increase in holding current, resulting in taste cell depolarization under current clamp. Taken together, our results suggest that NMDA-like receptors and at least two types of group III mGluRs are present in taste receptor cells, and these may be coactivated by MSG. Further studies are required to determine which receptors are located on the apical membrane and how they contribute to the umami taste.

关键词： 2-氨基-5-膦酰基戊酸盐/药理学 8-溴环腺苷一磷酸/药理学兴奋性氨基酸激动剂/药理学兴奋性氨基酸拮抗剂/药理学甘氨酸/类似物和衍生物甘氨酸/药理学膜电位/药物作用膜电位/生理学 N-甲基天冬氨酸/药理学膜片钳术大鼠 Sprague-Dawley 受体谷氨酸/药物作用受体谷氨酸/生理学受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学味蕾/生理学动物男(雄)性大鼠

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Role for rapid dendritic protein synthesis in hippocampal mGluR-dependent long-term depression

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SCIENCE 2000年第5469期288卷 1254-1256页

作者： Huber, KM Kayser, MS Bear, MF Brown Univ Howard Hughes Med Inst Providence RI 02912 USA Brown Univ Dept Neurosci Providence RI 02912 USA

A hippocampal pyramidal neuron receives more than 10(4) excitatory glutamatergic synapses. Many of these synapses contain the molecular machinery for messenger RNA translation, suggesting that the protein complement (and thus function) of each synapse can be regulated on the basis of activity. Here, Local postsynaptic protein synthesis, triggered by synaptic activation of metabotropic glutamate receptors, was found to modify synaptic transmission within minutes.

关键词：氨基酸类/药理学茴香霉素/药理学树突/药物作用树突/代谢电刺激兴奋性氨基酸拮抗剂/药理学海马/代谢海马/生理学甲氧基羟基苯乙二醇/类似物和衍生物甲氧基羟基苯乙二醇/药理学神经组织蛋白质类/拮抗剂和抑制剂神经组织蛋白质类/生物合成神经组织蛋白质类/遗传学神经抑制/药物作用神经抑制/生理学蛋白质生物合成/药物作用蛋白质合成抑制药/药理学 RNA 信使/代谢受体亲代谢性谷氨酸盐/生理学突触传递/药物作用突触传递/生理学呫吨类/药理学动物大鼠

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Metabotropic glutamate receptor modulation of glutamate responses in the suprachiasmatic nucleus

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JOURNAL OF NEUROPHYSIOLOGY 1999年第3期81卷 1308-1317页

作者： Haak, LL Stanford Univ Dept Biol Sci Program Neurosci Stanford CA 94305 USA

Glutamate is the primary excitatory transmitter in the suprachiasmatic nucleus (SCN). Ionotropic glutamate receptors (iGluRs) mediate transduction of light information from the retina to the SCN, an important circadian clock phase shifting pathway. Metabotropic glutamate receptors (mGluRs) may play a significant modulatory role. mGluR modulation of SCN responses to glutamate was investigated with fura-2 calcium imaging in SCN exp]ant cultures. SCN neurons showed reproducible calcium responses to glutamate, kainate, and N-methyl-D-aspartate (NMDA). Although the type I/II mGluR agonists L-CCG-I and t-ACPD did not evoke calcium responses, they did inhibit kainate- and NMDA-evoked calcium rises. This interaction was insensitive to pertussis toxin Protein kinase A (PKA) activation by 8-bromo-cAMP significantly reduced iGluR inhibition by mGluR agonists. The inhibitory effect of mGluRs was enhanced by activating protein kinase C (PKC) and significantly reduced in the presence of the PKC inhibitor H7. Previous reports show that L-type calcium channels can be modulated by PKC and PKA. In SCN cells, about one-half of the calcium rise evoked by kainate or NMDA was blocked by the L-type calcium channel antagonist nimodipine. Calcium rises evoked by K+ were used to test whether mGluR inhibition of iGluR calcium rises involved calcium channel modulation. These calcium rises were primarily attributable to activation of voltage-activated calcium channels. PKC activation inhibited K+-evoked calcium rises, but PKC inhibition did nest affect L-CCG-I inhibition of these rises. In contrast, 8Br-cAMP had no effect alone but blocked L-CCG-I inhibition. Taken together, these results suggest that activation of mGluRs, likely type II, modulates glutamate-evoked calcium responses in SCN neurons. mGluR inhibition of iGluR calcium rises can be differentially influenced by PKC or PKA activation. Regulation of glutamate-mediated calcium influx could occur at L-type calcium channels, K+ channels,

关键词：环AMP依赖性蛋白激酶Ⅱ型环AMP依赖性蛋白激酶类/代谢 GTP结合蛋白质类/生理学谷氨酸/生理学免疫组织化学神经组织蛋白质类/生理学神经元/生理学蛋白激酶C/代谢大鼠 Sprague-Dawley 受体亲代谢性谷氨酸盐/生理学第二信使系统/生理学信号传导/生理学上交叉核/细胞学上交叉核/生理学动物大鼠

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Regulation of locomotor activity by metabotropic glutamate receptors in the nucleus accumbens and ventral tegmental area

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 406-414页

作者： Swanson, CJ Kalivas, PW Med Univ S Carolina Dept Physiol & Neurosci Charleston SC 29425 USA

Glutamatergic innervation of the ventral tegmental area (VTA) and the nucleus accumbens (NA) regulates locomotor activity. The present study was designed to evaluate the involvement of metabotropic glutamate receptors (mGluRs) in motor activity. Agonists selective for each of the three subgroups of mGluRs were microinjected into the VTA or NA, and motor activity was monitored. The group I agonist (S)-3,5-dihydroxyphenylglycine elicited a dose-dependent elevation in motor activity after microinjection into either the VTA or NA. The effect in the NA was blocked by the mGluR1-specific antagonist 7-(hydroxyimino) cyclopropa[b]chromen-1a-carboxylate ethyl ester. The group II agonist (2S,2',3')-2-(2',3'-dicarboxycyclopropyl) glycine also elicited a short-duration motor activation after microinjection into either structure. The dose response in the VTA was biphasic, and the coadministration of the group II/III-specific antagonist (RS)-alpha-methyl-4-phosphonophenylglycine partially blocked motor activation in both the NA and VTA. Although the group III agonist L-(+)-2-amino-4-phosphonobutyric acid produced a relatively modest behavioral stimulation after microinjection into the NA, it was without effect in the VTA. These data indicate a role for mGluR subgroups in the regulation of motor activity in the VTA and NA.

关键词：行为动物/药物作用色酮类/药理学环丙烷类/药理学剂量效应关系药物兴奋性氨基酸拮抗剂/药理学甘氨酸/类似物和衍生物甘氨酸/药理学甲氧基羟基苯乙二醇/类似物和衍生物甲氧基羟基苯乙二醇/药理学微量注射运动活动/生理学伏核/生理学大鼠 Sprague-Dawley 受体亲代谢性谷氨酸盐/拮抗剂和抑制剂受体亲代谢性谷氨酸盐/生理学立体定位技术时间因素腹侧被盖区/生理学录像动物男(雄)性大鼠

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Group I mGluR agonist DHPG facilitates the induction of LTP in rat prelimbic cortex in vitro

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JOURNAL OF NEUROPHYSIOLOGY 1999年第4期82卷 1927-1933页

作者： Morris, SH Knevett, S Lerner, EG Bindman, LJ Univ London Univ Coll Dept Physiol London WC1E 6BT England

Long-term potentiation (LTP) of synaptic transmission is a favored neural model for learning and memory. In isolated slices of rat prelimbic col tex, glutamatergic activation of metabotropic receptors (mGluRs) is required for the production of LTP at synapses on layer V neurons. Group I mGluRs are found in neocortex, and in prelimbic cortex they have been located on layer V neurons. We have now investigated whether application of the selective group I mGluR agonist, (S)-3,5-dihydroxyphenylglycine (DHPG) facilitates the induction of LTP. We recorded field potentials in layer V in response to test shocks applied to layer II and measured the population spike peak amplitude and slope. Intracellular recording was used to examine the correspondence between excitatory postsynaptic potentials (EPSPs) and action potentials with components of the field potential, and to further investigate the action of DHPG. Repetitive bursts of stimulation at theta frequencies (TBS) did not consistently alter the magnitude or slope of the population spike (mean response 105 +/- 4%, mean +/- SE of control at 30 min after TBS ended, n = 9 slices, no significant difference). When DHPG was added to the bathing medium for 10 min during continued test stimulation, the slope and amplitude of the population spike were significantly reduced, but 30 min after wash out of the DHPG, they recovered (mean response 89 +/- 10% of control, n = 6 slices, no significant difference). However, when TBS was administered in conjunction with bath application of DHPG, LTP of the population spike was induced (mean response 147 +/- 12% of control at 30 min after TBS ended, P = 0.004, paired t-test, n = 9 slices). We conclude that co-application of DHPG with TBS facilitates the induction of LTP of the population spike, which supports a role for group I mGluRs in the activity-dependent induction of LTP in the prelimbic cortex.

关键词：兴奋性突触后电位/药物作用兴奋性突触后电位/生理学额叶/药物作用额叶/生理学长时程增强/药物作用甲氧基羟基苯乙二醇/类似物和衍生物甲氧基羟基苯乙二醇/药理学神经元/药物作用神经元/生理学大鼠 Sprague-Dawley 受体亲代谢性谷氨酸盐/药物作用受体亲代谢性谷氨酸盐/生理学突触/药物作用突触/生理学动物男(雄)性大鼠

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Cocaine and kindling alter the sensitivity of group II and III metabotropic glutamate receptors in the central amygdala

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JOURNAL OF NEUROPHYSIOLOGY 2000年第2期84卷 759-770页

作者： Neugebauer, V Zinebi, F Russell, R Gallagher, JP Shinnick-Gallagher, P Univ Texas Med Branch Dept Pharmacol & Toxicol Galveston TX 77555 USA

G-protein-coupled metabotropic glutamate receptors (mGluRs) are being implicated in various forms of neuroplasticity and CNS disorders. This study examined whether the sensitivities of mGluR agonists are modulated in a distinct fashion in different models of synaptic plasticity, specifically, kindling and chronic cocaine treatment. The influence of kindling and chronic cocaine exposure in vivo was examined in vitro on the modulation of synaptic transmission by group II and III metabotropic glutamate receptors using whole cell voltage-clamp recordings of central amygdala (CeA) neurons. Synaptic transmission was evoked by electrical stimulation of the basolateral amygdala (BLA) and ventral amygdaloid pathway (VAP) afferents in brain slices from control rats and from rats treated with cocaine or exposed to three to five stage-five kindled seizures. This study shows that after chemical stimulation with chronic cocaine exposure or after electrical stimulation with kindling the receptor sensitivities for mGluR agonists are altered in opposite ways. In slices from control rats, group II agonists, (2S,1'S,2'S)-2-(carboxycyclopropyl)glycine (LCCG1) and (1)-2-aminobicyclo[3.1.0]hexane-2,6-dicarboxylic acid (LY354740), depressed neurotransmission more potently at the BLA-CeA than at the VAP-CeA synapse while group III agonist, L(+)-2-amino-4-phosphonobutyrate (LAP4), depressed neurotransmission more potently at the VAP-CeA synapse than at the BLA-CeA. These agonist actions were not seen (were absent) in amygdala neurons from chronic cocaine-treated animals. In contrast, after kindling, concentration response relationships for LCCG1 and LAP4 were shifted to the left, suggesting that sensitivity to these agonists is increased. Except at high concentrations, LCCG1, LY354740, and LAP4 neither induced membrane currents nor changed current-voltage relationships. Loss of mGluR inhibition with chronic cocaine treatment may contribute to counter-adaptive changes including anxiety and d

关键词： 6-氰-7-硝基喹喔啉-2 3-二酮/药理学氨基酸类二羧酸/药理学杏仁核/化学杏仁核/药物作用杏仁核/生理学细胞膜/药物作用细胞膜/生理学色酮类/药理学可卡因/药理学可卡因相关性障碍/药物疗法可卡因相关性障碍/病理生理学多巴胺摄取抑制剂/药理学兴奋性氨基酸激动剂/药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/药理学点燃效应神经病学/生理学膜片钳术次膦酸类/药理学丙醇胺类/药理学吡啶类/药理学大鼠 Sprague-Dawley 受体亲代谢性谷氨酸盐/生理学突触/药物作用突触/生理学突触传递/药物作用突触传递/生理学动物男(雄)性大鼠

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