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Effects of GABA receptor antagonist on trigeminal caudalis nociceptive neurons in normal and neonatally capsaicin-treated rats

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JOURNAL OF NEUROPHYSIOLOGY 1999年第5期82卷 2154-2162页

作者： Chiang, CY Kwan, CL Ku, JW Sessle, BJ Univ Toronto Fac Dent Toronto ON M5G 1G6 Canada

We have recently demonstrated that significant increases in cutaneous mechanoreceptive field (RF) size and spontaneous activity occur in nociceptive neurons of trigeminal subnucleus caudalis (Vc, the medullary dorsal horn) of adult rats depleted of C-fiber afferents by neonatal treatment with capsaicin. These neuronal changes in capsaicin-treated (CAP) rats are suggestive of central neuroplasticity and involve N-methyl-D-aspartic acid (NMDA) receptor mechanisms. The present study examined whether the GABA(A) receptor antagonist bicuculline (BIC) or the GABA(B) receptor antagonist 2-hydroxysaclofen (SAC) can influence the RF properties and activity of Ve nociceptive neurons classified as either nociceptive-specific or wide-dynamic range in CAP adult rats or in neonatally vehicle-treated (CON) rats. C-fiber depletion was confirmed in the CAP rats by a significant decrease in plasma extravasation of Evans blue dye in a skin area receiving topical application of mustard oil, a small-fiber excitant and inflammatory irritant As previously reported, marked increases in cutaneous RF size and spontaneous activity occurred in Vc nociceptive neurons of adult CAP rats, compared with CON rats. GABA(A) receptor blockade by BIC (i.t.) in CON rats produced a significant increase in spontaneous activity and in pinch RF size and tactile RF size (or appearance of a tactile area in the RF of nociceptive-specific neurons), as well as a significant lowering of the mechanical threshold and a significant enhancement of responses to pinch stimuli applied to the RF. In CAP rats, GABA(B) receptor blockade also produced significant changes similar to those documented in CON rats, except for a paradoxical and significant decrease in pinch RF size and no noticeable changes in responses to pinch stimuli. GABA(A) receptor blockade by SAC (i.t.) did not produce any significant changes in Vc nociceptive neurons in either CON or CAP rats. These results suggest that GABA(A) receptor-mediated inhibitio

关键词：动物新生巴氯芬/类似物和衍生物巴氯芬/药理学荷包牡丹碱/类似物和衍生物荷包牡丹碱/药理学脑图辣椒辣素/投药和剂量辣椒辣素/药理学功能偏侧化 GABA拮抗剂/药理学 GABA-A受体拮抗剂延髓/药物作用延髓/生理学微量注射神经元可塑性/药物作用神经元可塑性/生理学神经元/药物作用神经元/生理学疼痛感受器/药物作用疼痛感受器/生理学疼痛/病理生理学物理刺激大鼠 Sprague-Dawley 触觉三叉神经/药物作用三叉神经/生理学三叉神经/病理生理学动物男(雄)性大鼠

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

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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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Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3-CA1 synapses

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NATURE NEUROSCIENCE 2000年第11期3卷 1107-1112页

作者： Bolshakov, VY Carboni, L Cobb, MH Siegelbaum, SA Belardetti, F Columbia Univ Howard Hughes Med Inst Ctr Neurobiol & Behav Dept Pharmacol New York NY 10032 USA Harvard Univ Sch Med McLean Hosp Dept Psychiat Belmont MA 02478 USA Glaxo Wellcome Med Res Ctr Dept Biol I-37135 Verona Italy Univ Texas SW Med Ctr Dept Pharmacol Dallas TX 75235 USA

Although the function of the p42/p44 mitogen-activated protein (MAP) kinase pathway in longterm potentiation at hippocampal CA3-CA1 synapses has been well described, relatively little is known about the importance of the p38 MAP kinase pathway in synaptic plasticity. Here we show that the p38 MAP kinase pathway, a parallel signaling cascade activated by distinct upstream kinases, mediates the induction of metabotropic glutamate receptor-dependent long-term depression at CA3-CA1 synapses. Thus, two parallel MAP kinase pathways contribute to opposing forms of long-term plasticity at a central synapse.

关键词：电刺激酶抑制剂/药理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学海马/细胞学海马/药物作用海马/生理学 MAP激酶信号系统/药物作用 MAP激酶信号系统/生理学丝裂原活化蛋白激酶1/生理学丝裂原激活蛋白激酶类/生理学神经元可塑性/药物作用神经元可塑性/生理学大鼠 Sprague-Dawley 信号传导突触/药物作用突触/生理学 p38丝裂原活化蛋白激酶类动物大鼠

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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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Neurite growth inhibitors restrict plasticity and functional recovery following corticospinal tract lesions

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NATURE NEUROSCIENCE 1998年第2期1卷 124-131页

作者： Thallmair, M Metz, GAS Z'Graggen, WJ Raineteau, O Kartje, GL Schwab, ME Univ Zurich Brain Res Inst CH-8029 Zurich Switzerland Swiss Fed Inst Technol CH-8029 Zurich Switzerland

Anatomical plasticity and functional recovery after lesions of the rodent corticospinal tract (CST) decrease postnatally in parallel with myelin formation. Myelin-associated neurite growth inhibitory proteins prevent regenerative fiber growth, but whether they also prevent reactive sprouting of unlesioned fibers is less clear. Here we show that after unilateral CST lesion in the adult rat brainstem, both intact and lesioned tracts show topographically appropriate sprouting after treatment with a monoclonal antibody that neutralizes these inhibitory proteins. Antibody-treated animals showed full recovery in motor and sensory tests, whereas untreated lesioned rats exhibited persistent severe deficits. Neutralization of myelin-associated neurite growth inhibitors thus restores in adults the structural plasticity and functional recovery normally found only at perinatal ages.

关键词：抗体单克隆/药理学中枢神经系统疾病/病理生理学生长抑制物/生理学运动活动/药物作用髓鞘/生理学神经再生/生理学神经突/生理学神经元可塑性/药物作用神经元可塑性/生理学锥体束/药物作用锥体束/病理生理学大鼠近交Lew 感觉/药物作用突触传递/药物作用动物大鼠

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Diverse roles of intracellular cAMP in early synaptic modifications in the rat visual cortex

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期522卷 417-426页

作者： Yoshimura, H Kato, N Kyoto Univ Grad Sch Med Dept Integrat Brain Sci Kyoto 6068501 Japan Kansai Med Univ Dept Physiol Moriguchi Osaka 5708506 Japan

1. The effects of increasing intracellular cAMP concentration were studied using photolysis of caged-cAMP in layer II/III neurons recorded intracellularly in visual cortex slices. The recorded neurons exhibited either after-hyperpolarization (AHP) or after-depolarization (ADP) in response to depolarizing current injection. Depending on which afterpotential appeared, the effects of photolysis differed. 2. In ADP-generating neurons, photolysis of caged-cAMP induced long-lasting depression of postsynaptic potentials (PSPs) evoked by grey matter (GM) stimulation, without altering the size of the ADP. In AHP-generating neurons, photolysis induced long-lasting potentiation of GM-evoked PSPs, with the size of the AHP reduced in the same time course. White matter (WM)-evoked PXPs showed no change. 3. Extracellular application of bromo-cAMP depressed both GM- and WM-evoked PSPs in ADP- and AHP-generating neurons. This depression may be due to presynaptic effects of cAMP, since photolysis-evoked postsynaptic increase in cAMP concentration net er induced depression of PSPs in AHP-generating neurons. This depression was reversible but continued until bromo-cAMP was washed out, while ADP and AHP in the postsynaptic neurons were depressed only temporarily and returned to the pre-application level even in the continued presence of bromo-cAMP. 4. Bromo-cAMP was applied following photolysis of caged-cAMP. In the neurons in which the photolysis potentiated GM-evoked PSPs this potentiation was cancelled out by bromo-cAMP (depotentiation). In the other neurons, PSPs were depressed only reversibly. 5. Thus, It postsynaptic increase in cAMP concentration exerts more diverse effects on synaptic plasticity than thus far reported, depending on the difference in neuronal intrinsic excitability and probably on how much, or the way in which, cAMP concentration is increased.

关键词： 8-溴环腺苷一磷酸/药理学培养技术环AMP/类似物和衍生物环AMP/代谢环AMP/药理学电刺激兴奋性突触后电位/药物作用细胞内液/代谢长时程增强/药物作用神经元可塑性/药物作用神经元/细胞学神经元/药物作用神经元/代谢膜片钳术光解大鼠 Wistar 突触/代谢视皮质/细胞学视皮质/代谢动物大鼠

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Rho GTPases regulate distinct aspects of dendritic arbor growth in Xenopus central neurons in vivo

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NATURE NEUROSCIENCE 2000年第3期3卷 217-225页

作者： Li, Z Van Aelst, L Cline, HT Cold Spring Harbor Lab Cold Spring Harbor NY 11724 USA SUNY Stony Brook Dept Neurobiol & Behav Stony Brook NY 11794 USA

The development and structural plasticity of dendritic arbors are governed by several factors, including synaptic activity, neurotrophins and other growth-regulating molecules. The signal transduction pathways leading to dendritic structural changes are unknown, but likely include cytoskeleton regulatory components. To test whether GTPases regulate dendritic arbor development, we collected time-lapse images of single optic tectal neurons in albino Xenopus tadpoles expressing dominant negative or constitutively active forms of Rac, Cdc42 or RhoA. Analysis of images collected at two-hour intervals over eight hours indicated that enhanced Rac activity selectively increased branch additions and retractions, as did Cdc42 to a lesser extent. Activation of endogenous RhoA decreased branch extension without affecting branch additions and retractions, whereas dominant-negative RhoA increased branch extension. Finally, we provide data suggesting that RhoA mediates the promotion of normal dendritic arbor development by NMDA receptor activation.

关键词： 2-氨基-5-膦酰基戊酸盐/药理学肌动蛋白类/代谢细胞大小/药物作用细胞骨架/药物作用细胞骨架/代谢树突/药物作用树突/酶学树突/生理学树突/超微结构酶激活/遗传学基因显性/遗传学幼虫/细胞学幼虫/药物作用突变/遗传学神经元可塑性/药物作用受体 N-甲基-D-天冬氨酸/拮抗剂和抑制剂受体 N-甲基-D-天冬氨酸/生理学重组融合蛋白质类/遗传学重组融合蛋白质类/代谢信号传导/药物作用痘苗病毒/遗传学爪蟾光滑 cdc42GTP结合蛋白质/遗传学 cdc42GTP结合蛋白质/代谢 racGTP结合蛋白质类/遗传学 racGTP结合蛋白质类/代谢 ρGTP结合蛋白质类/遗传学 ρGTP结合蛋白质类/代谢 ρAGTP结合蛋白质/遗传学 ρAGTP结合蛋白质/代谢动物人类

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Distinct temporal profiles of activity-dependent calcium increase in pyramidal neurons of the rat visual cortex

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JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期519卷 467-479页

作者： Kato, N Tanaka, T Yamamoto, K Isomura, Y Kyoto Univ Grad Sch Med Dept Integrat Brain Sci Kyoto 6068501 Japan

1. Using fluo-3-based fluorometry, we studied variation in depolarization-induced calcium increases in the proximal dendrites or soma of pyramidal neurons in layer II/III of the rat visual cortex. 2. Depolarization for all durations tested (0.1-2 s;0.5 nA) evoked a train of action potentials and a small increase in calcium signal (mean 26%) which peaked within I s of the onset of depolarization. With depolarization for longer than Is, this small increase was often followed by a larger increase (73%). This later phase of calcium increase occurred without sudden changes in action potential firing. 3. Application of ryanodine, which suppresses intracellular calcium release, abolished the second phase without affecting the early phase in a use-dependent manner. Meanwhile, no major changes were observed in the pattern of action potential firing. 4. In calcium-free medium, both the early and late phases were almost undetectable, although action potential firing was still evoked by injection of depolarizing currents. Since the late phase depended on intracellular calcium release, this effect of calcium-free medium on the late phase is likely to be indirect through an influence on the early phase. 5. This two-phase profile was observed with somatic depolarization or with antidromic action potentials induced by tetanization. Neocortical pyramidal neurons can thus recruit calcium from different sources, even without chemical sensitization, generating temporally diverse profiles of intracellular calcium signal in response to action potential firing. 6. Such variety in the mechanisms of calcium increase may be relevant to the role of calcium as a versatile second messenger for various types of synaptic plasticity.

关键词：苯胺化合物钙/代谢钙信号/药物作用钙信号/生理学电刺激兴奋性突触后电位/药物作用兴奋性突触后电位/生理学荧光染料 Fura-2 神经元可塑性/药物作用神经元可塑性/生理学膜片钳术光度测定法锥体细胞/药物作用锥体细胞/代谢锥体细胞/生理学大鼠 Wistar 时间因素视皮质/细胞学视皮质/代谢视皮质/生理学呫吨类动物大鼠

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A selective role of calcineurin Aα in synaptic depotentiation in hippocampus

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第8期96卷 4650-4655页

作者： Zhuo, M Zhang, W Son, H Mansuy, I Sobel, RA Seidman, J Kandel, ER Columbia Univ Howard Hughes Med Inst New York NY 10032 USA Columbia Univ Ctr Neurobiol & Behav New York NY 10032 USA Harvard Univ Sch Med Dept Genet Boston MA 02115 USA Harvard Univ Sch Med Dept Pathol Boston MA 02115 USA Stanford Univ Sch Med Dept Pathol Stanford CA 94305 USA

Pharmacological studies have suggested that long-term potentiation (LTP) and long-term depression (LTD) and depotentiation, three forms of synaptic plasticity in the hippocampus, require the activity of the phosphatase calcineurin, At least two different isoforms of calcineurin are found in the central nervous system. To investigate whether all of these forms of synaptic plasticity require the same isoforms of calcineurin, we have examined LTD, depotentiation, and LTP in mice lacking the predominant calcineurin isoform in the central nervous system, A alpha(-/-) mice. Depotentiation was abolished completely whereas neither LTD nor LTP were affected. These studies provide genetic evidence that the A alpha isoform of calcineurin is important for the reversal of LTP in the hippocampus and indicate that depotentiation and LTD operate through somewhat different molecular mechanisms.

关键词：脑/细胞学脑/生理学钙神经素/缺乏钙神经素/遗传学钙神经素/生理学环孢菌素/药理学二聚作用海马/细胞学海马/生理学同工酶类/缺乏同工酶类/遗传学同工酶类/生理学长时程增强/生理学小鼠基因敲除神经元可塑性/药物作用神经元可塑性/生理学突触/生理学动物小鼠

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An evaluation of the synapse specificity of long-term depression induced in rat cerebellar slices

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期527卷 563-577页

作者： Reynolds, T Hartell, NA Aston Univ Inst Pharmaceut Sci Div Life & Hlth Sci Birmingham B4 7ET W Midlands England

1. Whole-cell excitatory postsynaptic currents (EFSCs) were recorded from single Purkinje cells (PCs) in rat cerebellar slices in response to alternate activation of two separate sets of parallel fibres (PF1 and PF2). Pairing the stimulation of one input (PF1) with PC depolarisation at 1 Hz for 5 min produced varied effects, including a long-term depression (LTD) of subsequent responses, a medium-term potentiation, or no change relative to baseline levels (n = 14). In all but two cases PF2 responses mirrored those in PF1, in both direction and magnitude even though this second pathway was not specifically activated during pairing. 2. Increasing the stimulus strength to evoke larger amplitude EPSCs (> 1000 pA) dramatically increased the proportion of cells that underwent LTD in both PF1 and PF2. LTD in both pathways was postsynaptic calcium dependent. PC depolarisation alone (n = 7) or PF1 stimulation paired with PC hyperpolarisation (n = 6) failed to induce LTD at either site. 3. Pairing PF1 stimulation with climbing fibre (CB) activation at 1 Hz for 5 min produced LTD in the majority of cells regardless of the strength of PF stimulation. LTD under these conditions was not, however, input specific, even at the lowest stimulus strengths. 4. With EPSCs greater than 1000 pA in amplitude, depression was apparent in both pathways even when the duration of PF, pairing with depolarisation was limited to 1 min. Full expression of LTD in PF2 required stimulation of this pathway to be resumed within a distinct temporal window of conjunctive pairing with PF1. Introducing a delay of 20 min before resumption of PF2 activation preserved the input specificity of synaptic depression. 5. We conclude that pairing either PC depolarisation or CF activation with stimulation of a discrete set of PFs produces LTD that spreads to adjacent synapses on the same PC.

关键词：小脑/细胞学小脑/药物作用小脑/生理学抑制化学性电刺激电生理学兴奋性突触后电位/药物作用兴奋性突触后电位/生理学荧光染料膜电位/生理学神经纤维/药物作用神经元可塑性/药物作用神经元可塑性/生理学膜片钳术浦肯野细胞/药物作用浦肯野细胞/生理学大鼠 Wistar 突触/药物作用突触/生理学动物男(雄)性大鼠

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