英文论文投稿信Cover-letter-模板
英文论文投稿信Cover letter模板
qiusuo BY - 2006-1-17 8:59:00 Dear Editor,
We would like to submit the enclosed manuscript entitled \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, case2 Dear Editor,
We would like to submit the enclosed manuscript entitled \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.
[0630][投稿写作]某杂志给出的标准Sample Cover Letter[the example used is the IJEB] Case 3
Sample Cover Letter[the example used is the IJEB]
Dear Editor of the [please type in journal title or acronym]:
Enclosed is a paper, entitled \Network Management.\Please accept it as a candidate for publication in the [journal title]. Below are our responses to your submission requirements.