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Intermittent hypoxia: linkage between OSAS and epilepsy.间歇性缺氧:阻塞性睡眠呼吸暂停低通气综合征与癫痫之间的联系
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本文引用的文献

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Structure and stoichiometry of an accessory subunit TRIP8b interaction with hyperpolarization-activated cyclic nucleotide-gated channels.三聚体 G 蛋白偶联受体相互作用蛋白 8b 亚基与超极化激活环核苷酸门控通道相互作用的结构和化学计量。
Proc Natl Acad Sci U S A. 2012 May 15;109(20):7899-904. doi: 10.1073/pnas.1201997109. Epub 2012 May 1.
2
The GABA excitatory/inhibitory shift in brain maturation and neurological disorders.大脑成熟和神经紊乱中的 GABA 兴奋/抑制转换。
Neuroscientist. 2012 Oct;18(5):467-86. doi: 10.1177/1073858412438697. Epub 2012 Apr 30.
3
Excitatory GABA: How a Correct Observation May Turn Out to be an Experimental Artifact.兴奋性γ-氨基丁酸:正确的观察结果如何可能成为实验假象。
Front Pharmacol. 2012 Apr 19;3:65. doi: 10.3389/fphar.2012.00065. eCollection 2012.
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Distinct regional and subcellular localization of the actin-binding protein filamin A in the mature rat brain.成熟大鼠脑中肌动蛋白结合蛋白细丝蛋白 A 的独特区域性和亚细胞定位。
J Comp Neurol. 2012 Sep 1;520(13):3013-34. doi: 10.1002/cne.23106.
5
Neonatal exposure to phenobarbital potentiates schizophrenia-like behavioral outcomes in the rat.新生期接触苯巴比妥可增强大鼠类似精神分裂症的行为结果。
Neuropharmacology. 2012 Jun;62(7):2337-45. doi: 10.1016/j.neuropharm.2012.02.001. Epub 2012 Feb 15.
6
Regulation of axonal HCN1 trafficking in perforant path involves expression of specific TRIP8b isoforms.调节投射路径轴突 HCN1 的转运涉及特定 TRIP8b 异构体的表达。
PLoS One. 2012;7(2):e32181. doi: 10.1371/journal.pone.0032181. Epub 2012 Feb 21.
7
KCNQ2 encephalopathy: emerging phenotype of a neonatal epileptic encephalopathy.KCNQ2 脑病:一种新生儿癫痫性脑病的新表型。
Ann Neurol. 2012 Jan;71(1):15-25. doi: 10.1002/ana.22644.
8
Neonatal seizures: treatment practices among term and preterm infants.新生儿惊厥:足月和早产儿的治疗实践。
Pediatr Neurol. 2012 Feb;46(2):111-5. doi: 10.1016/j.pediatrneurol.2011.11.006.
9
Concomitant facilitation of GABAA receptors and KV7 channels by the non-opioid analgesic flupirtine.非阿片类镇痛药氟吡汀同时促进 GABAA 受体和 KV7 通道。
Br J Pharmacol. 2012 Jul;166(5):1631-42. doi: 10.1111/j.1476-5381.2011.01821.x.
10
Recessive loss-of-function mutation in the pacemaker HCN2 channel causing increased neuronal excitability in a patient with idiopathic generalized epilepsy.致心律失常性右室发育不良相关心肌病的遗传学研究进展
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寻找治疗小儿癫痫的新靶点。

Searching for new targets for treatment of pediatric epilepsy.

机构信息

Department of Anatomy & Neurobiology, University of California-Irvine, Irvine, CA, USA.

出版信息

Epilepsy Behav. 2013 Mar;26(3):253-60. doi: 10.1016/j.yebeh.2012.09.022. Epub 2012 Dec 6.

DOI:10.1016/j.yebeh.2012.09.022
PMID:23219411
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3595393/
Abstract

The highest incidence of seizures in humans occurs during the first year of life. The high susceptibility to seizures in neonates and infants is paralleled by animal studies showing a high propensity to seizures during early life. The immature brain is highly susceptible to seizures because of an imbalance of excitation and inhibition. While the primary outcome determinant of early-life seizures is etiology, there is evidence that seizures which are frequent or prolonged can result in long-term adverse consequences, and there is a consensus that recurrent early-life seizures should be treated. Unfortunately, seizures in many neonates and children remain refractory to therapy. There is therefore a pressing need for new seizure drugs as well as antiepileptic targets in children. In this review, we focus on mechanisms of early-life seizures, such as hypoxia-ischemia, and novel molecular targets, including the hyperpolarization-activated cyclic nucleotide-gated channels.

摘要

人类癫痫发作的最高发病率发生在生命的第一年。新生儿和婴儿对癫痫发作的高度易感性与动物研究一致,这些研究表明在生命早期癫痫发作的倾向很高。由于兴奋和抑制之间的不平衡,不成熟的大脑极易受到癫痫发作的影响。虽然早期癫痫发作的主要结局决定因素是病因,但有证据表明频繁或长时间的癫痫发作会导致长期的不良后果,并且人们普遍认为反复发生的早期癫痫发作应该得到治疗。不幸的是,许多新生儿和儿童的癫痫发作仍然对治疗有抗药性。因此,迫切需要针对儿童的新型抗癫痫药物和靶点。在这篇综述中,我们专注于生命早期癫痫发作的机制,如缺氧缺血,以及新的分子靶点,包括超极化激活环核苷酸门控通道。