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SCI論文投稿投稿信模板
Case 1
Dear Editor,
We would like to submit the enclosed manuscript entitled "GDNF Acutely Modulates Neuronal Excitability and A-type Potassium Channels in Midpain 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 midpain dopaminergic neurons, which are degenerated in Parkinson's disease. In this paper, we report an unexpected論文QQ81995535, 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 pain 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 midpain 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 論文QQ81995535
Sincerely yours,
case2
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論文QQ81995535, 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.
Sincerely yours,
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