【转贴】nature paper by Poo 同一时间在Nature主刊上面有三篇文章发表
这个帖子发布于 20 年零 183 天前，其中的信息可能已发生改变或有所发展。
横跨不同领域，横跨中国和美国
一个是他LP做通讯作者（以前的学生），
一个是他在大陆培养的学生做通讯作者
还有一个是他自己做通讯作者
发信人: demoner (得失之间), 信区: Biology
标 题: nature paper by Poo and Dan.
发信站: Unknown Space - 未名空间 (Wed Mar 9 17:07:27 2005), 转信
灌一篇nature不难，难的是每年都灌，每个月都灌nature...
为什么Poo可以数十年如一日，坚持不懈，而且驰骋在不同的领域？
以前是他自己做correspondence，他的学生Dan做第一作者，
现在是Dan做correspondence....
Poo真是了不起的人。
第一篇
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v434/n7030/full/nature03366_fs.html
Nature 434, 221 - 225 (10 March 2005); doi:10.1038/nature03366
Spike-timing-dependent synaptic plasticity depends on dendritic location
ROBERT C. FROEMKE, MU-MING POO & YANG DAN
Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720-3200, USA
Correspondence and requests for materials should be addressed to Y.D. (ydan@berkeley.edu).
In the neocortex, each neuron receives thousands of synaptic inputs distributed across an extensive dendritic tree. Although postsynaptic processing of each input is known to depend on its dendritic location1-8, it is unclear whether activity-dependent synaptic modification is also location-dependent. Here we report that both the magnitude and the temporal specificity of spike-timing-dependent synaptic modification9-17 vary along the apical dendrite of rat cortical layer 2/3 pyramidal neurons. At the distal dendrite, the magnitude of long-term potentiation is smaller, and the window of pre-/postsynaptic spike interval for long-term depression (LTD) is broader. The spike-timing window for LTD correlates with the window of action potential-induced suppression of ***A (N-methyl-D-aspartate) receptors; this correlation applies to both their dendritic location-dependence and pharmacological properties. Presynaptic stimulation with partial blockade of ***A receptors induced LTD and occluded further induction of spike-timing-dependent LTD, suggesting that ***A receptor suppression underlies LTD induction. Computer simulation studies showed that the dendritic inhomogeneity of spike-timing-dependent synaptic modification leads to differential input selection at distal and proximal dendrites according to the temporal characteristics of presynaptic spike trains. Such location-dependent tuning of inputs, together with the dendritic heterogeneity of postsynaptic processing, could enhance the computational capacity of cortical pyramidal neurons.
第二篇
Gordon Wang好像是他们实验室的研究生/本科生，记不清楚了。。
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/vaop/ncurrent/full/nature03478_fs.html
Nature AOP, published online 9 March 2005; doi:10.1038/nature03478
Requirement of TRPC channels in netrin-1-induced chemotropic turning of
nerve growth cones
GORDON X. WANG AND MU-MING POO
Ion channels formed by the TRP (transient receptor potential) superfamily
of proteins act as sensors for temperature, osmolarity, mechanical stress
and taste1, 2. The growth cones of developing axons are responsible for
sensing extracellular guidance factors, many of which trigger Ca2+ influx
at the growth cone3, 4; however, the identity of the ion channels involved
remains to be clarified. Here, we report that TRP-like channel activity
exists in the growth cones of cultured Xenopus neurons and can be modulated
by exposure to netrin-1 and brain-derived neurotrophic factor, two chemoattractants
for axon guidance. Whole-cell recording from growth cones showed that
netrin-1 induced a membrane depolarization, part of which remained after
all major voltage-dependent channels were blocked. Furthermore, the membrane
depolarization was sensitive to blockers of TRP channels. Pharmacological
blockade of putative TRP currents or downregulation of Xenopus TRP-1 (
xTRPC1) expression with a specific morpholino oligonucleotide abolished
the growth-cone turning and Ca2+ elevation induced by a netrin-1 gradient
. Thus, TRPC currents reflect early events in the growth cone's detection
of some extracellular guidance signals, resulting in membrane depolarization
and cytoplasmic Ca2+ elevation that mediates the turning of growth cones
第三篇
袁小兵是Poo在上海一手培养的新人，这篇文章大概为了体现“本土nature”
所以连Poo的名字都没有留。。。大家完全可以想象Poo在背后的努力。
再次对Poo表示敬仰。。
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/vaop/ncurrent/full/nature03477_fs.html
Nature AOP, published online 9 March 2005; doi:10.1038/nature03477
Essential role of TRPC channels in the guidance of nerve growth cones by brain-derived neurotrophic factor
YAN LI1,2,*, YI-CHANG JIA1,2,*, KAI CUI1,2,*, NING LI1,2, ZAI-YU ZHENG1,2, YI-ZHENG WANG1 & XIAO-BING YUAN1
1 Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2 Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
* These authors contributed equally to this work
Correspondence and requests for materials should be addressed to X.-b.Y. (yuanxb@ion.ac.cn) or Y.-z.W. (yzwang@ion.ac.cn).
Brain-derived neurotrophic factor (BDNF) is known to promote neuronal survival and differentiation1 and to guide axon extension both in vitro2, 3 and in vivo4. The BDNF-induced chemo-attraction of axonal growth cones requires Ca2+ signalling3, but how Ca2+ is regulated by BDNF at the growth cone remains largely unclear. Extracellular application of BDNF triggers membrane currents resembling those through TRPC (transient receptor potential canonical) channels in rat pontine neurons5 and in Xenopus spinal neurons6. Here, we report that in cultured cerebellar granule cells, TRPC channels contribute to the BDNF-induced elevation of Ca2+ at the growth cone and are required for BDNF-induced chemo-attractive turning. Several members of the TRPC family are highly expressed in these neurons, and both Ca2+ elevation and growth-cone turning induced by BDNF are abolished by pharmacological inhibition of TRPC channels, overexpression of a dominant-negative form of TRPC3 or TRPC6, or downregulation of TRPC3 expression via short interfering RNA. Thus, TRPC channel activity is essential for nerve-growth-cone guidance by BDNF.
一个是他LP做通讯作者（以前的学生），
一个是他在大陆培养的学生做通讯作者
还有一个是他自己做通讯作者
发信人: demoner (得失之间), 信区: Biology
标 题: nature paper by Poo and Dan.
发信站: Unknown Space - 未名空间 (Wed Mar 9 17:07:27 2005), 转信
灌一篇nature不难，难的是每年都灌，每个月都灌nature...
为什么Poo可以数十年如一日，坚持不懈，而且驰骋在不同的领域？
以前是他自己做correspondence，他的学生Dan做第一作者，
现在是Dan做correspondence....
Poo真是了不起的人。
第一篇
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/v434/n7030/full/nature03366_fs.html
Nature 434, 221 - 225 (10 March 2005); doi:10.1038/nature03366
Spike-timing-dependent synaptic plasticity depends on dendritic location
ROBERT C. FROEMKE, MU-MING POO & YANG DAN
Department of Molecular and Cell Biology and Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720-3200, USA
Correspondence and requests for materials should be addressed to Y.D. (ydan@berkeley.edu).
In the neocortex, each neuron receives thousands of synaptic inputs distributed across an extensive dendritic tree. Although postsynaptic processing of each input is known to depend on its dendritic location1-8, it is unclear whether activity-dependent synaptic modification is also location-dependent. Here we report that both the magnitude and the temporal specificity of spike-timing-dependent synaptic modification9-17 vary along the apical dendrite of rat cortical layer 2/3 pyramidal neurons. At the distal dendrite, the magnitude of long-term potentiation is smaller, and the window of pre-/postsynaptic spike interval for long-term depression (LTD) is broader. The spike-timing window for LTD correlates with the window of action potential-induced suppression of ***A (N-methyl-D-aspartate) receptors; this correlation applies to both their dendritic location-dependence and pharmacological properties. Presynaptic stimulation with partial blockade of ***A receptors induced LTD and occluded further induction of spike-timing-dependent LTD, suggesting that ***A receptor suppression underlies LTD induction. Computer simulation studies showed that the dendritic inhomogeneity of spike-timing-dependent synaptic modification leads to differential input selection at distal and proximal dendrites according to the temporal characteristics of presynaptic spike trains. Such location-dependent tuning of inputs, together with the dendritic heterogeneity of postsynaptic processing, could enhance the computational capacity of cortical pyramidal neurons.
第二篇
Gordon Wang好像是他们实验室的研究生/本科生，记不清楚了。。
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/vaop/ncurrent/full/nature03478_fs.html
Nature AOP, published online 9 March 2005; doi:10.1038/nature03478
Requirement of TRPC channels in netrin-1-induced chemotropic turning of
nerve growth cones
GORDON X. WANG AND MU-MING POO
Ion channels formed by the TRP (transient receptor potential) superfamily
of proteins act as sensors for temperature, osmolarity, mechanical stress
and taste1, 2. The growth cones of developing axons are responsible for
sensing extracellular guidance factors, many of which trigger Ca2+ influx
at the growth cone3, 4; however, the identity of the ion channels involved
remains to be clarified. Here, we report that TRP-like channel activity
exists in the growth cones of cultured Xenopus neurons and can be modulated
by exposure to netrin-1 and brain-derived neurotrophic factor, two chemoattractants
for axon guidance. Whole-cell recording from growth cones showed that
netrin-1 induced a membrane depolarization, part of which remained after
all major voltage-dependent channels were blocked. Furthermore, the membrane
depolarization was sensitive to blockers of TRP channels. Pharmacological
blockade of putative TRP currents or downregulation of Xenopus TRP-1 (
xTRPC1) expression with a specific morpholino oligonucleotide abolished
the growth-cone turning and Ca2+ elevation induced by a netrin-1 gradient
. Thus, TRPC currents reflect early events in the growth cone's detection
of some extracellular guidance signals, resulting in membrane depolarization
and cytoplasmic Ca2+ elevation that mediates the turning of growth cones
第三篇
袁小兵是Poo在上海一手培养的新人，这篇文章大概为了体现“本土nature”
所以连Poo的名字都没有留。。。大家完全可以想象Poo在背后的努力。
再次对Poo表示敬仰。。
http://www.nature.com/cgi-taf/DynaPage.taf?file=/nature/journal/vaop/ncurrent/full/nature03477_fs.html
Nature AOP, published online 9 March 2005; doi:10.1038/nature03477
Essential role of TRPC channels in the guidance of nerve growth cones by brain-derived neurotrophic factor
YAN LI1,2,*, YI-CHANG JIA1,2,*, KAI CUI1,2,*, NING LI1,2, ZAI-YU ZHENG1,2, YI-ZHENG WANG1 & XIAO-BING YUAN1
1 Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2 Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China
* These authors contributed equally to this work
Correspondence and requests for materials should be addressed to X.-b.Y. (yuanxb@ion.ac.cn) or Y.-z.W. (yzwang@ion.ac.cn).
Brain-derived neurotrophic factor (BDNF) is known to promote neuronal survival and differentiation1 and to guide axon extension both in vitro2, 3 and in vivo4. The BDNF-induced chemo-attraction of axonal growth cones requires Ca2+ signalling3, but how Ca2+ is regulated by BDNF at the growth cone remains largely unclear. Extracellular application of BDNF triggers membrane currents resembling those through TRPC (transient receptor potential canonical) channels in rat pontine neurons5 and in Xenopus spinal neurons6. Here, we report that in cultured cerebellar granule cells, TRPC channels contribute to the BDNF-induced elevation of Ca2+ at the growth cone and are required for BDNF-induced chemo-attractive turning. Several members of the TRPC family are highly expressed in these neurons, and both Ca2+ elevation and growth-cone turning induced by BDNF are abolished by pharmacological inhibition of TRPC channels, overexpression of a dominant-negative form of TRPC3 or TRPC6, or downregulation of TRPC3 expression via short interfering RNA. Thus, TRPC channel activity is essential for nerve-growth-cone guidance by BDNF.
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