Dear Prof. XXXXX,
Here within enclosed is our paper for consideration to be published on “(Journal name)”. The further information about the paper is in the following:
The Title: XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
The Authors: XXXXXXXXXX XXXXXXXXXXXX and XXXXXXXXXX
The authors claim that none of the material in the paper has been pub
lished or is under consideration for publication elsewhere.
I am the corresponding author and my address and other information is as follows,
Address: Department of XXXXXXXXX,
Thank you very much for consideration!
Dear XX (Editor):
Here is our paper submitted to "(XX Journal)".
The Title: XXXX
The Authors: XXX XXX and XXX
In this paper, we ...
The authors claim that none of the material in the paper has been published or is under consideration for publication elsewhere.
The corresponding author is Dr. XXX and his address and other information is as following:
Address: Department of XXX, XX University, ..., P.R.China
Thank you very much for consideration!
Dear Mr. **
We believe the paper may be of particular interest to the readers of your journal as it ........
1. The work described has not been submitted elsewhere for publication, in whole or in part, and all the authors listed have approved the manuscript that is enclosed.
2. I have read and have abided by the statement of ethical standards for manuscripts submitted to Neuroscience.
Dear Prof. Gil:
This is a manuscript by**and **entitled “.......”. It is submitted to be considered for publication as a “...” in your journal. This paper is new. Neither the entire paper nor any part of its content has been published or has been accepted elsewhere. It is not being submitted to any other journal.
Correspondence should be addressed to **at the following address, phone and fax number, and email address:
Thanks very much for your attention to our paper.
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
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.
Highlights are a short collection of bullet points that convey the core findings and provide readers with a quick textual overview of the article. These three to five bullet points describe the essence of the research (e.g. results or conclusions) and highlight what is distinctive about it. Highlights will be displayed in online search result lists, the contents list and in the online article, but will not (yet) appear in the article PDF file or print. Specifications: Examples
Highlights should be submitted as a separate file in EES by selecting "Highlights" from the drop-down list when uploading files. Please adhere to the specifications below.
Journal of Health Economics, Volume 29, Issue 4, July 2010, 524-535
Highlights are a short collection of bullet points that convey the core findings and provide readers with a quick textual overview of the article. These three to five bullet points describe the essence of the research (e.g. results or conclusions) and highlight what is distinctive about it.
Highlights will be displayed in online search result lists, the contents list and in the online article, but will not (yet) appear in the article PDF file or print.