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Direct interaction of Rab4 with syntaxin 4

JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第7期276卷 5265-5273页

作者： Li, L Omata, W Kojima, I Shibata, H Gunma Univ Inst Mol & Cellular Regulat Dept Cell Biol Maebashi Gumma 3718512 Japan

In the present study, we examined the possible interaction between Rab4 and syntaxin 4, both having been implicated in insulin-induced GLUT4 translocation. Rab4 and syntaxin 4 were coimmunoprecipitated from the lysates of electrically permeabilized rat adipocytes. The interaction between the two proteins was reduced by insulin treatment and increased by the addition of guanosine 5'-O-(3-thiotriphosphate) (GTP gammaS). An in vitro binding assay revealed that the bacterially expressed Rabi was bound to a glutathione S-transferase fusion protein containing the cytoplasmic domain of syntaxin 4 (GST-syntaxin 4-(1-273)) but not to syntaxin 1A or vesicle-associated membrane protein-2. The interaction between Rab4 and syntaxin 4 seemed to be regulated by the guanine nucleotide status of Rab4, because 1) GTP gammaS treatment of the cells significantly increased, but guanosine 5'-O-(2-thiodiphosphate) (GDP betaS) treatment decreased the amount of Rab4 pulled down with GST-syntaxin 4-(1-273) from the cell lysates;2) GTP gammaS loading on Rab4 caused a marked increase in the affinity of Rab4 to syntaxin 4 whereas GDP betaS loading had little effect;and 3) a GTPase-deficient mutant of Rab4 (Rab4(Q67L)), but not a GTP-binding-defective mutant (Rab4(S22N)), was bound to GST-syntaxin 4-(1-273). Although insulin stimulated [gamma-P-32]GTP binding to Rab4 in a time-dependent fashion, its effect on the Rab4 interaction with syntaxin 4 was apparently biphasic;an initial increase in Rab associated with syntaxin 4 was followed by a gradual dissociation of the GTPase from syntaxin 4. Finally, the binding of Rab4(Q67L) to GST-syntaxin 4-(1-273) was inhibited by munc-18c in a dose-dependent manner, indicating that GTP-loaded Rab4 binds to syntaxin 4 in the open conformation. These results suggest that 1) Rab4 interacts with syntaxin 4 in a direct and specific manner, and 2) the interaction is regulated by the guanine nucleotide status of Rab4 as well as by the conformational status of synta

关键词：脂细胞/药物作用脂细胞/代谢细胞区室化细胞培养的鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学鸟苷三磷酸/代谢胰岛素/药理学动力学膜蛋白质类/化学膜蛋白质类/代谢突变沉淀素试验蛋白质构象 Qa-SNARE蛋白质类大鼠 Sprague-Dawley 重组融合蛋白质类/代谢突触融合蛋白质1 硫代核苷酸类/药理学 rab4GTP结合蛋白质类/遗传学 rab4GTP结合蛋白质类/代谢动物大鼠

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The coenzyme B₁₂ analog 5′-deoxyadenosylcobinamide-GDP supports catalysis by methylmalonyl-CoA mutase in the absence of trans-ligand coordination

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第2期276卷 1015-1019页

作者： Chowdhury, S Thomas, MG Escalante-Semerena, JC Banerjee, R Univ Nebraska Dept Biochem Lincoln NE 68588 USA Univ Wisconsin Dept Bacteriol Madison WI 53706 USA

Methylmalonyl-CoA mutase is an 5'-adenosylcobalamin (AdoCbl)-dependent enzyme that catalyzes the rearrangement of methylmalonyl-CoA to succinyl-CoA The crystal structure of this protein revealed that binding of the cofactor is accompanied by a significant conformational change in which dimethylbenzimidazole, the lower axial ligand to cobalt in solution, is replaced by His(610) donated by the active site. The role of the lower axial ligand in the trillion fold labilization of the upper axial cobalt-carbon bond has been the subject of enduring debate in the model inorganic literature. In this study, we have used a cofactor analog, 5'deoxyadenosylcobinamide GDP (AdoCbi-GDP), which reconstitutes the enzyme in a "histidine-off' form and which allows us to evaluate the contribution of the lower axial ligand to catalysis, The k(cat) for the enzyme in the presence of AdoCbi-GDP is reduced by a factor of 4 compared with the native cofactor AdoCbl, The overall deuterium isotope effect in the presence of AdoCbi-GDP (V-D = 7.2 +/- 0.8) is comparable with that observed in the presence of AdoCbl (5.0 +/- 0.6) and indicates that the hydrogen transfer steps in this reaction are not significantly affected by the change in coordination state of the bound cofactor. These surprising results are in marked contrast to the effects ascribed to the corresponding lower axial histidine ligands in the cobalamin-dependent enzymes glutamate mutase and methionine synthase.

关键词：结合部位催化作用钴胺酰胺类/化学钴胺酰胺类/药理学氘电子自旋共振谱学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/化学鸟苷二磷酸/药理学组氨酸动力学配体甲基丙二酸单酰CoA变位酶/化学甲基丙二酸单酰CoA变位酶/代谢模型分子分子构象丙酸杆菌属/酶学重组蛋白质类/化学重组蛋白质类/代谢分光光度法

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Human neutrophil immunodeficiency syndrome is associated with an inhibitory Rac2 mutation

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第9期97卷 4654-4659页

作者： Ambruso, DR Knall, C Abell, AN Panepinto, J Kurkchubasche, A Thurman, G Gonzalez-Aller, C Hiester, A deBoer, M Harbeck, RJ Oyer, R Johnson, GL Roos, D Bonfils Blood Ctr Denver CO 80230 USA Univ Colorado Hlth Sci Ctr Dept Pediat Denver CO 80262 USA Univ Colorado Hlth Sci Ctr Dept Pharmacol Denver CO 80262 USA Rhode Isl Hosp Dept Pediat Hematol Oncol Providence RI 02903 USA Rhode Isl Hosp Dept Surg Providence RI 02903 USA Univ Amsterdam Acad Med Ctr Expt & Clin Immunol Lab NL-1105 AZ Amsterdam Netherlands Netherlands Blood Transfus Serv Cent Lab Amsterdam Netherlands Natl Jewish Med & Res Ctr Clin Labs Denver CO 80206 USA

A 5-week-old male infant presented with severe bacterial infections and poor wound healing, suggesting a neutrophil defect. Neutrophils from this patient exhibited decreased chemotaxis. polarization, azurophilic granule secretion, and superoxide anion (O-2(-)) production but had normal expression and up-regulation of CD11b. Rac2, which constitutes >96% of the Rac in neutrophils, is a member of the Rho family of GTPases that regulates the actin cytoskeleton and O-2(-) production. Western blot analysis of lysates from patient neutrophils demonstrated decreased levels of Rac2 protein. Addition of recombinant Rac to extracts of the patient neutrophils reconstituted O-2(-) production in an in vitro assay system. Molecular analysis identified a point mutation in one allele of the Rac2 gene resulting in the substitution of Asp57 by an Asn (RaC2(D57N)). Asp57 is invariant in all defined GTP-binding proteins. RaC2(D57N) binds GDP but not GTP and inhibits oxidase activation and O-2(-) production in vitro. These data represent the description of an inhibitory mutation in a member of the Rho family of GTPases associated with a human immunodeficiency syndrome.

关键词：抗原 CD/血液趋化性白细胞胞质溶胶/代谢鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/药理学免疫缺陷综合征/血液免疫缺陷综合征/遗传学免疫缺陷综合征/免疫学巨噬细胞1抗原/血液 NADPH氧化酶/血液 NADPH氧化酶/缺乏中性白细胞/生理学过氧化物酶/血液参考值超氧化物类/血液 racGTP结合蛋白质类/血液 racGTP结合蛋白质类/遗传学人类婴儿男(雄)性

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Histamine suppresses non-NMDA excitatory synaptic currents in rat supraoptic nucleus neurons

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JOURNAL OF NEUROPHYSIOLOGY 2000年第5期83卷 2616-2625页

作者： Li, ZH Hatton, GI Univ Calif Riverside Dept Neurosci Riverside CA 92521 USA

Whole cell patch-clamp recordings were obtained from supraoptic neurons to investigate the effects of histamine on excitatory postsynaptic currents evoked by electrical stimulation of areas around the posterior supraoptic nucleus. When cells were voltage-clamped at -70 mV, evoked excitatory postsynaptic currents had amplitudes of 88.4 +/- 9.6 pA and durations of 41.1 +/- 3.0 ms (mean +/- SE;n = 43). With twin stimulus pulses (20 Hz) used, paired-pulse facilitation ratios were 1.93 +/- 0.12. Bath application of 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX) abolished synaptic currents. Histamine at concentrations similar to 0.1-10 mu M reversibly suppressed excitatory postsynaptic currents in all supraoptic neurons tested. Within 2 min after application of (10 mu M) histamine, current amplitudes and durations decreased by 61.5 and 31.0%, respectively, with little change in the paired-pulse facilitation ratio. Dimaprit or imetit (H-2 or H-3 receptor agonists) did not reduce synaptic currents, whereas pyrilamine (H-1 receptor antagonist) blocked histamine-induced suppression of synaptic currents. When patch electrodes containing guanosine 5'-O-(2-thiodiphosphate) (GDP-beta-S) were used to record cells, histamine still suppressed current amplitudes by 49.1% and durations by 41.9%. Similarly, intracellular diffusion of bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) and H-7 did not abolish histamine-induced suppression of synaptic currents, either. Bath perifusion of 8-bromo-quanosine 3',5'- cyclic monophosphate reduced current amplitudes by 32.3% and durations by 27.9%. After bath perfusion of slices with N-omega-nitro-L-arginine methyl ester (L-NAME), histamine injection decreased current amplitudes only by 31.9%, much less than the inhibition rate in control (P < 0.01). In addition, histamine induced little change in current durations and paired-pulse facilitation ratios, representing a partial blockade of histamine effects on synaptic currents by L-NAME. In supr

关键词：动作电位/药物作用细胞培养的螯合剂/药理学剂量效应关系药物依他酸/类似物和衍生物依他酸/药理学电刺激酶抑制剂/药理学兴奋性突触后电位/药物作用鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学组胺/药理学组胺激动药/药理学组胺H1拮抗剂/药理学细胞内液/代谢 NG-硝基精氨酸甲酯/药理学神经元/细胞学神经元/药物作用神经元/代谢一氧化氮/代谢去甲肾上腺素/药理学膜片钳术信号传导/药物作用视上核/细胞学视上核/药物作用视上核/代谢硫代核苷酸类/药理学动物男(雄)性大鼠

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Slow synaptic inhibition mediated by metabotropic glutamate receptor activation of GIRK channels

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JOURNAL OF NEUROPHYSIOLOGY 2000年第5期84卷 2284-2290页

作者： Dutar, P Petrozzino, JJ Vu, HM Schmidt, MF Perkel, DJ Univ Penn Dept Neurosci Philadelphia PA 19104 USA

Glutamate is the predominant excitatory neurotransmitter in the vertebrate CNS. Ionotropic glutamate receptors mediate fast excitatory actions whereas metabotropic glutamate receptors (mGluRs) mediate a variety of slower effects. For example, mGluRs can mediate presynaptic inhibition, postsynaptic excitation, or, more rarely, postsynaptic inhibition. We previously described an unusually slow form of postsynaptic inhibition in one class of projection neuron in the song-control nucleus HVc of the songbird forebrain. These neurons, which participate in a circuit that is essential for vocal learning, exhibit an inhibitory postsynaptic potential (IPSP) that lasts several seconds. Only a portion of this slow IPSP is mediated by GABAB receptors. Since these cells are strongly hyperpolarized by agonists of mGluRs, we used intracellular recording from brain slices to investigate the mechanism of this hyperpolarization and to determine whether mGluRs contribute to the slow synaptic inhibition. We report that mGluRs hyperpolarize these HVc neurons by activating G protein-coupled, inwardly-rectifying potassium (GIRK) channels. MGluR antagonists blocked this response and the slow synaptic inhibition. Thus, glutamate can combine with GABA to mediate slow synaptic inhibition by activating GIRK channels in the CNS.

关键词：氨基酸类二羧酸/药理学巴氯芬/药理学螯合剂/药理学环亮氨酸/类似物和衍生物环亮氨酸/药理学依他酸/类似物和衍生物依他酸/药理学电生理学兴奋性氨基酸拮抗剂/药理学 G蛋白偶联内向整流钾通道 GABA激动剂/药理学鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学膜电位/药物作用膜电位/生理学神经抑制/生理学神经保护药/药理学钾通道/代谢钾通道内向整流受体亲代谢性谷氨酸盐/生理学鸣禽鸟突触/化学突触/生理学四乙基铵/药理学河豚毒素/药理学硫代核苷酸类/药理学动物男(雄)性

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G protein-mediated FMRFamidergic modulation of calcium influx in dissociated heart muscle cells from squid, Loligo forbesii

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第2期525卷 471-482页

作者： Chrachri, A Ödblom, M Williamson, R Marine Biol Assoc United Kingdom Lab Plymouth PL1 2PB Devon England Univ Plymouth Dept Biol Plymouth PL4 8AA Devon England

1. The actions of the neuropeptide FMRFamide (Phe-Met-Arg-Phe-NH2) on the L-type (I-Ca,I-L) and T-type (I-Ca,I-T) calcium currents were investigated in muscle cells dissociated from the heart of squid, Loligo forbseii. 2. The heart muscle cells could be divided into type I and type II cells, on the basis of morphological differences in the dissociated myocytes. FMRFamide induced a substantial block of the L-type calcium current seen in type I cells;this inhibition was rapid, reversible and dose dependent (IC50 = 0.1 mu M). FMRFamide induced an increase in the amplitude of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calcium current in either type of dissociated heart muscle cell, even at concentrations much higher than those found to affect the L-type calcium current. 3. Internal dialysis of isolated type I heart muscle cells With guanosine 5'-O-(3-thiotriphosphate (GTP gamma S, 100 mu M), a non-hydrolysable GTP analogue, mimicked the FMRFamide inhibition of the Ca2+ current and occluded any further FMRFamide-induced inhibition. Internal dialysis of these cells with guanosine 5'-O-(2-thiodiphosphate) (GDP beta S, 100 mu M) reduced the FMRFamide-induced inhibition of the peak Ca2+ current. The inhibitory effects of FMRFamide were abolished by pre-incubation of the cells with pertussis toxin (200 ng ml(-1)). 4. The activation kinetics of I-Ca,I-L were not affected by FMRFamide application, nor by internal perfusion with GTP gamma S, and the FMRFamide-induced reduction in I-Ca,I-L was not relieved by large depolarising prepulses. These data, indicate that FMRFamide can modulate I-Ca,I-L, but not I-Ca,I-T, in squid heart muscle cells, and that the underlying G protein pathway is dissimilar to that commonly associated with transmitter modulation of channel activity. 5. The FMRFamide-modulated increase in I-Ca,I-L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G protein pathway.

关键词：钙/代谢钙通道 L型/药物作用钙通道 L型/代谢钙通道 T型/药物作用钙通道 T型/代谢细胞分离十腕总目/细胞学十腕总目/代谢 FMRF酰胺/药理学 GTP结合蛋白质类/代谢鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学动力学膜电位心肌/细胞学心肌/代谢百白咳毒素硫代核苷酸类/药理学毒力因子鲍特菌属/药理学动物

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Heterotrimeric G-proteins of a filamentous fungus regulate cell wall composition and susceptibility to a plant PR-5 protein

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PLANT JOURNAL 2000年第1期22卷 61-69页

作者： Coca, MA Damsz, B Yun, DJ Hasegawa, PM Bressan, RA Narasimhan, ML Purdue Univ Ctr Plant Environm Stress Physiol W Lafayette IN 47907 USA

Membrane permeabilizing plant defensive proteins first encounter the fungal cell wall that can harbor specific components that facilitate or prevent access to the plasma membrane. However, signal transduction pathways controlling cell wall composition in filamentous fungi are largely unknown. We report here that the deposition of cell wall constituents that block the action of osmotin (PR-5), an antifungal plant defense protein, against Aspergillus nidulans requires the activity of a heterotrimeric G-protein mediated signaling pathway. The guanidine nucleotide GDP beta S, that locks G-proteins in a GDP bound inactive form, inhibits osmotin-induced conidial lysis. A dominant interfering mutation in FadA, the alpha-subunit of a heterotrimeric G-protein, confers resistance to osmotin, A deletion mutation in SfaD, the beta-subunit of a heterotrimeric G-protein also increases osmotin resistance. Aspergillus nidulans strains bearing these mutations also have increased tolerance to SDS, reduced cell wall porosity and increased chitin content in the cell wall.

关键词：构巢曲霉菌/药物作用构巢曲霉菌/遗传学构巢曲霉菌/代谢细胞壁/代谢真菌蛋白质类/拮抗剂和抑制剂真菌蛋白质类/遗传学真菌蛋白质类/代谢 GTP结合蛋白质类基因真菌鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学异源三聚体GTP结合蛋白质类/遗传学异源三聚体GTP结合蛋白质类/代谢突变植物蛋白质类/代谢植物蛋白质类/药理学植物有毒信号传导硫代核苷酸类/药理学烟草

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Modulation of pacemaker activity by salmon gonadotropin-releasing hormone (sGnRH) in terminal nerve (TN)-GnRH neurons

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JOURNAL OF NEUROPHYSIOLOGY 2000年第5期83卷 3196-3200页

作者： Abe, H Oka, Y Univ Tokyo Grad Sch Sci Misaki Marine Biol Stn Kanagawa 2380225 Japan

The terminal nerve (TN)-gonadotropin-releasing hormone (GnRH) neurons project widely in the brain instead of the pituitary and show endogenous pacemaker activity that is dependent on the physiological conditions of the animal. We suggest that the TN-GnRH system may act as a putative neuromodulator that is involved in the regulation of many long-lasting changes in the animal's behavior. In the present study, we find that the pacemaker activity of TN-GnRH neurons is modulated by salmon GnRH (sGnRH), which is the same molecular species of GnRH peptide produced by TN-GnRH neurons themselves. Bath application of sGnRH (2-200 nM) transiently decreased (early phase) and then subsequently increased (late phase) the frequency of pacemaker activity of TN-GnRH neurons in a dose-dependent manner. These biphasic changes of pacemaker activities were suppressed by intracellular application of guanosin 5'-0-(2-thiodi-phosphate) (GDP-P-S). The results suggest that G-protein coupled receptors are present on the cell surface and play a triggering role in modulating the frequency of pacemaker activities in TN-GnRH neurons. Because the TN-GnRH neurons make tight cell clusters with no intervening glial cells, it may be further suggested that GnRH released from GnRH neurons regulates the activities of their own (autocrine) and/or neighboring GnRH neurons (paracrine).

关键词：动作电位/药物作用动作电位/生理学麻醉药局部/药理学生物钟/药物作用生物钟/生理学脑/细胞学脑/药物作用脑/生理学细胞质/药物作用细胞质/代谢剂量效应关系药物鱼类/代谢促性腺素释放激素/拮抗剂和抑制剂促性腺素释放激素/代谢促性腺素释放激素/药理学鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学利多卡因/类似物和衍生物利多卡因/药理学膜电位神经元/药物作用神经元/代谢膜片钳术灌流反应时间/药物作用反应时间/生理学鲑钠通道阻滞剂硫代核苷酸类/药理学动物女(雌)性男(雄)性

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The role of Mg²⁺ cofactor in the guanine nucleotide exchange and GTP hydrolysis reactions of Rho family GTP-binding proteins

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第33期275卷 25299-25307页

作者： Zhang, BL Zhang, YQ Wang, ZX Zheng, Y Univ Tennessee Dept Biochem Memphis TN 38163 USA Acad Sinica Inst Biophys Beijing 100101 Peoples R China

The biological activities of Rho family GTPases are controlled by their guanine nucleotide binding states in cells. Here we have investigated the role of Mg2+ cofactor in the guanine nucleotide binding and hydrolysis processes of the Rho family members, Cdc42, Rad, and RhoA. Differing from Ras and Rab proteins, which require Mg2+ for GDP and GTP binding, the Rho GTPases bind the nucleotides in the presence or absence of Mg2+ similarly, with dissociation constants in the submicromolar concentration. The presence of Mg2+, however, resulted in a marked decrease in the intrinsic dissociation rates of the nucleotides. The catalytic activity of the guanine nucleotide exchange factors (GEFs) appeared to be negatively regulated by free Mg2+, and GEF binding to Rho GTPase resulted in a 10-fold decrease in affinity for Mg2+, suggesting that one role of GEF is to displace bound Mg2+ from the Rho proteins. The GDP dissociation rates of the GTPases could be further stimulated by GEF upon removal of bound Mg2+, indicating that the GEF-catalyzed nucleotide exchange involves a Mg2+-independent as well as a Mg2+-dependent mechanism. Although Mg2+ is not absolutely required for GTP hydrolysis by the Rho GTPases, the divalent ion apparently participates in the GTPase reaction, since the intrinsic GTP hydrolysis rates were enhanced 4-10-fold upon binding to Mg2+, and k(cat) values of the Rho GTPase-activating protein (RhoGAP)-catalyzed reactions were significantly increased when Mg2+ was present. Furthermore, the p50RhoGAP specificity for Cdc42 was lost in the absence of Mg2+ cofactor. These studies directly demonstrate a role of Mg2+ in regulating the kinetics of nucleotide binding and hydrolysis and in the GEF- and GAP-catalyzed reactions of Rho family GTPases, The results suggest that GEF facilitates nucleotide exchange by destabilizing both bound nucleotide and Mg2+, whereas RhoGAP utilizes the Mg2+ cofactor to achieve high catalytic efficiency and specificity.

关键词：剂量效应关系药物大肠杆菌/代谢鸟嘌呤核苷酸交换因子类/代谢鸟苷5'-O-(3-硫代三磷酸)/药理学鸟苷二磷酸/药理学鸟苷三磷酸/代谢水解作用动力学镁/代谢镁/生理学磷蛋白类/代谢蛋白质结合蛋白质丝氨酸苏氨酸激酶/代谢原癌基因蛋白质类/代谢重组蛋白质类/代谢光谱法荧光时间因素 cdc42GTP结合蛋白质/代谢 rac1GTP结合蛋白质/代谢 ρGTP结合蛋白质类/代谢 ρAGTP结合蛋白质/代谢人类

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Dendritic release of glutamate suppresses synaptic inhibition of pyramidal neurons in rat neocortex

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JOURNAL OF PHYSIOLOGY-LONDON 2000年第3期528卷 489-496页

作者： Zilberter, Y Karolinska Inst Dept Neurosci Div Neuroanat & Brain Dev S-17177 Stockholm Sweden

1. Dual whole-cell recordings were made in layer 2/3 of the rat neocortex in synaptically connected pyramidal cells and fast-spiking non-accommodating (FSN) interneurons. In 75% of cell pairs (n = 80), the cells formed reciprocal synaptic connections. 2. Trains of backpropagating action potentials in pyramidal cells induced Ca2+ transients in dendrites followed by inhibition of unitary IPSPs. IPSP depression was prevented by loading pyramidal cells with 5 mM BAPTA or EGTA. 3. IPSP depression was mimicked by the metabotropic glutamate receptor (mGluR) agonist ACPD and was prevented by a mixture of the mGluR antagonists CPCCOEt and EGLU. 4. IPSP depression was prevented by loading pyramidal cells with the antagonists of vesicular exocytosis botulinum toxin D (light chain) and GDP-beta -S. 5. It is concluded that Ca2+-dependent release of a retrograde messenger, most probably glutamate, from pyramidal cell dendrites suppresses the inhibition of pyramidal neurons via activation of mGluRs located in FSN interneuron nerve terminals.

关键词：动作电位/生理学肉毒毒素类/药理学钙/代谢环亮氨酸/类似物和衍生物环亮氨酸/药理学树突/代谢依他酸/类似物和衍生物依他酸/药理学电生理学谷氨酸/生理学鸟苷二磷酸/类似物和衍生物鸟苷二磷酸/药理学中间神经元/生理学新皮质/细胞学新皮质/生理学神经抑制/生理学锥体细胞/生理学大鼠 Wistar 受体亲代谢性谷氨酸盐/激动剂受体亲代谢性谷氨酸盐/拮抗剂和抑制剂突触/生理学突触传递/药物作用突触传递/生理学硫代核苷酸类/药理学动物大鼠

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