Unequal gains of function are a headache for migraine mechanisms.
作者信息
Uchitel Osvaldo D
机构信息
Institute of Physiology, Molecular Biology and Neuroscience, CONICET, Departamento de Fisiología, Biología Molecular y Celular, Universidad de Buenos Aires, Argentina.
出版信息
J Physiol. 2012 Jan 1;590(1):1-2. doi: 10.1113/jphysiol.2011.223545.
Abstract
摘要
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1
Unequal gains of function are a headache for migraine mechanisms.功能获得不均衡是偏头痛发病机制中的一个棘手问题。
J Physiol. 2012 Jan 1;590(1):1-2. doi: 10.1113/jphysiol.2011.223545.
2
Trigeminal ganglion neuron subtype-specific alterations of Ca(V)2.1 calcium current and excitability in a Cacna1a mouse model of migraine.偏头痛 Cacna1a 小鼠模型中海马神经节神经元亚型特异性钙通道电流和兴奋性改变。
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Immunohistochemical characterization of calcitonin gene-related peptide in the trigeminal system of the familial hemiplegic migraine 1 knock-in mouse.家族性偏瘫性偏头痛 1 型嵌合小鼠三叉神经系统中降钙素基因相关肽的免疫组织化学特征。
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本文引用的文献
1
Trigeminal ganglion neuron subtype-specific alterations of Ca(V)2.1 calcium current and excitability in a Cacna1a mouse model of migraine.偏头痛 Cacna1a 小鼠模型中海马神经节神经元亚型特异性钙通道电流和兴奋性改变。
J Physiol. 2011 Dec 1;589(Pt 23):5879-95. doi: 10.1113/jphysiol.2011.220533. Epub 2011 Oct 17.
2
Calcitonin gene-related peptide does not cause migraine attacks in patients with familial hemiplegic migraine.降钙素基因相关肽不会引起家族性偏瘫性偏头痛患者的偏头痛发作。
Headache. 2011 Apr;51(4):544-53. doi: 10.1111/j.1526-4610.2011.01861.x.
3
Gain of function in FHM-1 Cav2.1 knock-in mice is related to the shape of the action potential.FHM-1 Cav2.1 敲入小鼠中的功能获得与动作电位的形态有关。
J Neurophysiol. 2010 Jul;104(1):291-9. doi: 10.1152/jn.00034.2010. Epub 2010 May 19.
4
Insights into migraine mechanisms and CaV2.1 calcium channel function from mouse models of familial hemiplegic migraine.家族性偏瘫性偏头痛小鼠模型对偏头痛发病机制和 Cav2.1 钙通道功能的深入了解。
J Physiol. 2010 Jun 1;588(Pt 11):1871-8. doi: 10.1113/jphysiol.2010.188003. Epub 2010 Mar 1.
5
Spreading depression: from serendipity to targeted therapy in migraine prophylaxis.扩散性抑制：从偶然发现到偏头痛预防的靶向治疗
Cephalalgia. 2009 Oct;29(10):1095-114. doi: 10.1111/j.1468-2982.2009.01982.x.
6
Origin of pain in migraine: evidence for peripheral sensitisation.偏头痛疼痛的起源：外周敏化的证据。
Lancet Neurol. 2009 Jul;8(7):679-90. doi: 10.1016/S1474-4422(09)70090-0.
7
Enhanced excitatory transmission at cortical synapses as the basis for facilitated spreading depression in Ca(v)2.1 knockin migraine mice.皮质突触处兴奋性传递增强作为Ca(v)2.1基因敲入偏头痛小鼠中扩散性抑制易化的基础。
Neuron. 2009 Mar 12;61(5):762-73. doi: 10.1016/j.neuron.2009.01.027.
8
A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression.一种对皮层扩散性抑制敏感性增加的Cacna1a基因敲入偏头痛小鼠模型。
Neuron. 2004 Mar 4;41(5):701-10. doi: 10.1016/s0896-6273(04)00085-6.
9
Familial hemiplegic migraine mutations increase Ca(2+) influx through single human CaV2.1 channels and decrease maximal CaV2.1 current density in neurons.家族性偏瘫性偏头痛突变可增加通过单个人类CaV2.1通道的Ca(2+)内流，并降低神经元中CaV2.1电流的最大密度。
Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13284-9. doi: 10.1073/pnas.192242399. Epub 2002 Sep 16.
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