英文論文投稿信coverletter模板-在線瀏覽
2024-09-04 05:11本頁面
【正文】 this paper is our original unpublished work and it has not been submitted to any other journal for reviews. Sincerely,Johnny SmithCase 1Dear Editor,We would like to submit the enclosed manuscript entitled GDNF Acutely Modulates Neuronal Excitability and Atype 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 Atype 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 longterm 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 petition 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,case2Dear Editor,We would like to submit the enclosed manuscript entitled Ca2+binding protein frequenin mediates GDNFinduced 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 longterm 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 longterm, synaptic action of a neurotrophic factor. Our findings may also have general implications in the cell biology of neurotransmitter release.[0630][投稿寫作]某雜志給出的標(biāo)準(zhǔn)Sample Cover Letter[the
公司管理相關(guān)推薦
鄂ICP備17016276號-1