英文論文投稿信coverletter模板(編輯修改稿)
2024-08-21 05:11 本頁面
【文章內(nèi)容簡介】 p: I met Dr. Gate only once at a conference in 1999. I didn39。t know him personally.Assoc Prof. Dr. John Adams Director of Network Research Center College of Business Australian University 123, Harbor Drive Sydney, Australia 56789 phone: +61888888888 fax: +61888888886 jadams@ Expertise: published a related paper (Creating Mobile Agents) in IEEE TOSE, 18(8), pp. 8898. Relationship: None. I have never met Dr. Adams.Assoc Prof. Dr. ChiaHo Chen Chair of MIS Department College of Management Open University 888, Putong Road Keelung, Taiwan 100 phone: +886288888888 fax: +886288888886 chchen@ Expertise: published a related paper (Network Management for ECommerce) in IJ Electronic Business, 1(4), pp. 1828. Relationship: Former professor, dissertation chairman.Mr. Frank Young Partner, ABC Consulting 888, Seashore Highway Won Kok, Kowloon Hong Kong phone: +85288888888 fax: +85288888886 fyoung@ Expertise: Mr. Young provides consulting services extensively to his clients regarding network management practices. Relationship: I have worked with Mr. Young in several consulting projects in the past three years. Finally, this paper is our original unpublished work and it has not been submitted to any other journal for reviews.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
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