| 查看: 159 | 回复: 0 | ||
| 当前主题已经存档。 | ||
[资源]
英文学术论文投稿---如何写给杂志社两篇例文
|
||
|
Sample Text Dear Editor, We would like to submit the enclosed manuscript entitled "GDNF Acutely Modulates Neuronal Excitability and A-type Potassium Channels in Midbrain Dopaminergic Neurons", which we wish to be considered for publication in Nature Neuroscience. GDNF has long been thought to be a potent neurotrophic factor for the survival of midbrain dopaminergic neurons, which are degenerated in Parkinson’s disease. In this paper, we report an unexpected, acute effect of GDNF on A-type potassium channels, leading to a potentiation of neuronal excitability, in the dopaminergic neurons in culture as well as in adult brain slices. Further, we show that GDNF regulates the K+ channels through a mechanism that involves activation of MAP kinase. Thus, this study has revealed, for the first time, an acute modulation of ion channels by GDNF. Our findings challenge the classic view of GDNF as a long-term survival factor for midbrain dopaminergic neurons, and suggest that the normal function of GDNF is to regulate neuronal excitability, and consequently dopamine release. These results may also have implications in the treatment of Parkinson’s disease. Due to a direct competition and conflict of interest, we request that Drs. XXX of Harvard Univ., and YY of Yale Univ. not be considered as reviewers. With thanks for your consideration, I am Sincerely yours, Dear Editor, We would like to submit the enclosed manuscript entitled "Ca2+-binding protein frequenin mediates GDNF-induced potentiation of Ca2+ channels and transmitter release", which we wish to be considered for publication in Neuron. We believe that two aspects of this manuscript will make it interesting to general readers of Neuron. First, we report that GDNF has a long-term regulatory effect on neurotransmitter release at the neuromuscular synapses. This provides the first physiological evidence for a role of this new family of neurotrophic factors in functional synaptic transmission. Second, we show that the GDNF effect is mediated by enhancing the expression of the Ca2+-binding protein frequenin. Further, GDNF and frequenin facilitate synaptic transmission by enhancing Ca2+ channel activity, leading to an enhancement of Ca2+ influx. Thus, this study has identified, for the first time, a molecular target that mediates the long-term, synaptic action of a neurotrophic factor. Our findings may also have general implications in the cell biology of neurotransmitter release. [ Last edited by nxssw on 2008-12-16 at 17:40 ] |
回复此楼» 猜你喜欢
拟解决的关键科学问题还要不要写
已经有11人回复
-
救命帖
已经有5人回复
-
限项规定
已经有5人回复
-
为什么nbs上溴 没有产物点出现呢
已经有9人回复
-
招博士
已经有3人回复
-
存款400万可以在学校里躺平吗
已经有35人回复
-
最失望的一年
已经有18人回复
-
求推荐博导
已经有4人回复
-
求推荐英文EI期刊
已经有5人回复
-
疑惑？
已经有5人回复