杨雄里
应用免疫组化、膜片钳、细胞内记录、钙成像等多学科技术,研究视网膜神经元回路的信号传递、调制的基础及其机制。
个性化签名
- 姓名:杨雄里
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学术头衔:
博士生导师, 中国科学院院士
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学科领域:
生理学
- 研究兴趣:应用免疫组化、膜片钳、细胞内记录、钙成像等多学科技术,研究视网膜神经元回路的信号传递、调制的基础及其机制。
杨雄里,1941年10月14日出生于上海。中国科学院院士(1991),发展中国家科学院(TWAS)院士(2006)。1963年上海科技大学生物系毕业。1963~2000年在中国科学院上海生理研究所工作, 1988-1999年任所长。复旦大学神经生物学研究所所长(2000~),脑科学研究院院长(2006~)。1980~82年在日本进修期间获学术博士学位。1985年~87年先后在美国哈佛大学、贝勒医学院从事合作研究。国际学术杂志“Progress in Neurobiology”编委(2000~),“Journal of Physiological Scineces”顾问编委(2000~),“辞海”副总主编(2000~),《中国科学》编委(1998~)。亚大地区生理学联合会(FAOPS)秘书长(2006~)。曾任《生理学报》主编(1988~2002),中国生理学会理事长(1998~2002)。《中国神经科学杂志》主编(1998~2004),国家重点基础研究规划(973项目)“脑功能和脑重大疾病的基础研究”首席科学家(1999~2004)。
长期从事神经科学研究,专注于视网膜神经机制的研究,已发表学术论文200余篇,专著五本,译著多部。研究工作得到科技部、教育部、中国科学院,自然科学基金委,上海市科委等基金资助。曾作为 Principal Investigator (PI)和Co-PI 分获美国国立健康研究院(NIH)和 “国际人类前沿科学计划组织(HFSPO)”研究基金资助。1988年国家人事部授予“国家级有突出贡献的中青年科技专家”称号,1989年、1996年分获中科院自然科学一等、二等奖。1991年当选为上海市十大科技精英之一。2001年获何梁何利科技进步奖。2006年获教育部自然科学一等奖,上海市自然科学一等奖。
主要研究方向:应用免疫组化、膜片钳、细胞内记录、钙成像等多学科技术,研究视网膜神经元回路的信号传递、调制的基础及其机制。
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杨雄里, JIU-LIN DU AND XIONG-LI YANG
,-0001,():
-1年11月30日
Subcellular localization and complements of GABAA and GABAC receptors on bullfrog retinal bipolar cells. J Neurophysiol 84: 666-676, 2000. γ-Aminobutyric acid (GABA) receptors on retinal bipolar cells (BCs) are highly relevant to spatial and temporal integration of visual signals in the outer and inner retina. In the present work, subcellular localization and complements of GABAA and GABAC receptors on BCs were investigated by whole cell recordings and local drug application via multi-barreled puff pipettes in the bullfrog retinal slice preparation. Four types of the BCs (types 1-4) were identified morphologically by injection of Lucifer yellow. According to the ramification levels of the axon terminals and the responses of these cells to glutamate (or kainate) applied at their dendrites, types 1 and 2 of BCs were supposed to be OFF type, whereas types 3 and 4 of BCs might be ON type. Bicuculline (BIC), a GABAA receptor antagonist, and imidazole-4-acetic acid (I4AA), a GABAC receptor antagonist, were used to distinguish GABA receptor-mediated responses. In all BCs tested, not only the axon terminals but also the dendrites showed high GABA sensitivity mediated by both GABAA and GABAC receptors. Subcellular localization and complements of GABAA and GABAC receptors at the dendrites and axon terminals were highly related to the dichotomy of OFF and ON BCs. In the case of OFF BCs, GABAA receptors were rather evenly distributed at the dendrites and axon terminals, but GABAC receptors were predominantly expressed at the axon terminals. Moreover, the relative contribution of GABAC receptors to the axon terminals was prevalent over that of GABAA receptors, while the situation was reversed at the dendrites. In the case of ON BCs, GABAA and GABAC receptors both preferred to be expressed at the axon terminals; relative contributions of these two GABA receptor subtypes to both the sites were comparable, while GABAC receptors were much less expressed than GABAA receptors. GABAA, but not GABAC receptors, were expressed clusteringly at axons of a population of BCs. In a minority of BCs, I4AA suppressed the GABAC responses at the dendrites, but not at the axon terminal, implying that the GABAC receptors at these two sites may be heterogeneous. Taken together, these results suggest that GABAA and GABAC receptors may play different roles in the outer and inner retina and the differential complements of the two receptors on OFF and ON BCs may be closely related to physiological functions of these cells.
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【期刊论文】GLYCINERGIC SYNAPTIC TRANSMISSION TO BULLFROG RETINAL BIPOLAR CELLS IS INPUT-SPECIFIC
杨雄里, J. L. DUa, b* and X. L. YANGa, b
Neuroscience Vol. 113, No.4, pp. 779-784, 2002,-0001,():
-1年11月30日
Glycinergic inhibitory postsynaptic currents (IPSCs) focally elicited at the dendrites and axon terminals were recorded from bipolar cells in the bullfrog retinal slice, using the whole-cell clamp technique. IPSCs driven by input from interplexiform cells at bipolar cell dendrites (ipc-IPSCs) had a much slower decay time constant (25.29
retinal slice preparation,, whole-cell recording,, peak-scaled non-stationary noise analysis,, glycine receptor,, single-channel conductance.,
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杨雄里, J. LIU, a, b, J.-W. ZHAO, J.-LDUa, AND X.-L. YANGa*
Neuroscience 132(2005)103-113,-0001,():
-1年11月30日
GABAB receptors at the cone terminals in bullfrog retina were characterized by immunocytochemical and whole-cell patch clamp techniques in retinal slice preparations. Somata, axons and synaptic terminals (pedicles) of cones were both GABAB receptor (GABABR) 1 and GABABR2 immunoreactive. Physiologically, barium/calcium currents of cones to voltage steps were significantly reduced in size when GABA was puffed to cone terminals in the presence of picrotoxin that is supposed to block both GABAA and GABAC receptors. Similar reduction in barium currents was obtained with puff application of baclofen to cone terminals. These results suggest the presence of functional GABAB receptors at the bullfrog cone terminals. Suppression of barium currents of cones by baclofen was dose-dependent. Moreover, barium currents of cones were potentiated by background illumination, as compared with those recorded in the dark. 6,7-Dinitroquinoxaline-2,3-dione, an antagonist of non-NMDA receptors that hyperpolarizes horizontal cells and reduces GABA release from these cells, and saclofen, a GABAB receptor antagonist, both potentiated barium currents of cones in the dark, thereby mimicking the effects of background illumination. It is suggested that changes in calcium influx into the cone synaptic terminals due to activation of GABAB receptors may provide a negative feedback mechanism for regulating signal transmission between cones and secondorder neurons in the retina by modifying the amount of glutamate released from the cones.
GABA,, calcium channel,, barium current,, transmitter release,, horizontal cell.,
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【期刊论文】Glycine modulates the center response of ON type rod-dominant bipolar cells in carp retina
杨雄里, Yin Shen, Ling Chen, Yong Ping, Xiong-Li Yang*
Brain Research Bulletin 67(2005)492-497,-0001,():
-1年11月30日
pots, which was reversed by co-application of 10μM strychnine. It was further found that illumination of the receptive field surround did not affect the depolarizing center response of RBCs. The above result therefore suggests that glycine modulates the center response of RBCs. Focal application of glycine to either dendrites or axon terminals of RBCs failed to induce any currents in both isolated cell and retinal slice preparations. On the other hand, glycine of 4mM increased the amplitude of the scotopic electroretinographic PIIIcomponent, which reflects the activity of rod photoreceptors. It seems likely that modulation by glycine of the RBC center response may be in part ascribed to a consequence of the potentiation of rod responses by glycine.
Glycine, Bipolar cell, Carp retina, Receptive field
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【期刊论文】Modulation by melatonin of glutamatergic synaptic transmission in the carp retina
杨雄里, Hai Huang, , Shu-Chen Lee and Xiong-Li Yang
J Physiol 569.3 (2005) pp 857-871,-0001,():
-1年11月30日
Melatonin is involved in a variety of physiological functions through activating specific receptors coupled to GTP-binding protein.Melatonin and its receptors are abundant in the retina. Here we showfor the first time that melatoninmodulates glutamatergic synaptic transmission fromcones to horizontal cells (HCs) in carp retina. Immunocytochemical data revealed the expression of the MT1 receptoroncarpHCs.Whole-cell recordings further showedthat melatonin ofphysiological concentrationspotentiatedglutamate-inducedcurrents fromisolatedcone-drivenHCs(H1cells) in a dose-dependent manner, by increasing the efficacy and apparent affinity of the glutamate receptor. The effects of melatonin were reversed by luzindole, but not by K 185, indicating the involvement of the MT1 receptor. Like melatonin, methylene blue (MB), a guanylate cyclase inhibitor, also potentiated the glutamate currents, but internal infusion of cGMP suppressed them. The effects of melatonin were not observed in cGMP-filled and MB-incubated HCs. These results suggest that the melatonin effects may be mediated by decreasing the intracellular concentration of cGMP. Consistent with these observations, melatonin depolarized the membrane potential of H1 cells and reduced their light responses, which could also be blocked by luzindole. These effects of melatonin persisted in the presence of the antagonists of receptors for dopamine, GABA and glycine, indicating a direct action of melatonin on H1 cells. Such modulation by melatonin of glutamatergic transmission from cones to HCs is thought to be in part responsible for circadian changes in light responsiveness of cone HCs in teleost retina.
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【期刊论文】Modulation by Brain Natriuretic Peptide of GABA Receptors on Rat Retinal ON-Type Bipolar Cells
杨雄里, Yong-Chun Yu, *, Li-Hui Cao, * and Xiong-Li Yang
The Journal of Neuroscience, January 11, 2006•26 (2): 696-707,-0001,():
-1年11月30日
Natriuretic peptides (NPs) may work as neuromodulators through their associated receptors [NP receptors (NPRs)]. By immunocytochemistry, we showed that NPR-A and NPR-B were expressed abundantly on both ON-type and OFF-type bipolar cells (BCs) in rat retina, including the dendrites, somata, and axon terminals. Whole-cell recordings made from isolated ON-type BCs further showed that brain natriuretic peptide (BNP) suppressedGABAA receptor-, but notGABAC receptor-, mediated currents of the BCs, which was blocked by the NPR-A antagonist anantin. The NPR-C agonist c-ANF [des(Gln18, Ser19, Gln20, Leu21, Gly22)ANF4 -23-NH2] did not suppress GABAA currents. The BNP effect on GABAA currents was abolished with preincubation with the pGC-A/B antagonist HS-142-1 but mimicked by application of 8-bromoguanosine-3',5'-cyclomonophosphate. These results suggest that elevated levels of intracellular cGMP caused by activation of NPR-A may mediate the BNP effect. Internal infusion of the cGMP-dependent protein kinase G (PKG) inhibitor KT5823 essentially blocked the BNP-induced reduction of GABAA currents. Moreover, calcium imaging showed that BNP caused a significant elevation of intracellular calcium that could be caused by increased calcium release from intracellular stores by PKG. The BNP effect was blocked by the ryanodine receptor modulators caffeine, ryanodine, and ruthenium red but not by the IP3 receptor antagonists heparin and xestospongin-C. Furthermore, the BNP effect was abolished after application of the blocker of endoplasmic reticulum Ca2+-ATPase thapsigargin and greatly reduced by the calmodulin inhibitorsW-7and calmidazolium.Wetherefore conclude that the increased calcium release from ryanodine-sensitive calcium stores byBNPmaybe responsible for the BNP-causedGABAA response suppression in ON-type BCs through stimulating calmodulin.
brain natriuretic peptide, GABA receptor, intracellular calcium, neuromodulation, bipolar cells, retina
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