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【J Neurosci】癫痫发作诱导AMAP受体磷酸化
Sanjay N. Rakhade, Chengwen Zhou, Paven K. Aujla, Rachel Fishman, Nikolaus J. Sucher, and Frances E. Jensen
(see pages 7979–7990)
Seizures in neonates are usually caused by hypoxia and can increase risk of later epilepsy and cognitive impairment. Rakhade et al. induced hypoxic seizures in early postnatal rats to identify molecular changes that increase seizure susceptibility. Seizures increased the amplitude and frequency of miniature and spontaneous EPSCs mediated by AMPA receptors (AMPARs) within 1 h. This increase likely resulted from increased phosphorylation of AMPAR subunits by PKA, PKC, and calcium/calmodulin-dependent kinase II, because the activity of these kinases was elevated. Phosphorylation of GluR1 was increased at sites that increase channel conductance and synaptic insertion, whereas GluR2 was phosphorylated at a site that leads to its internalization. GluR2 internalization can increase the number of calcium-permeant AMPA receptors, which could further increase excitability. In vivo treatment with AMPAR antagonists blocked increases in phosphorylation, EPSC amplitude, and EPSC frequency, and also attenuated susceptibility to later seizures.
http://www.jneurosci.org/cgi/content/full/28/32/i 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Seizure-Induced AMPA Receptor Phosphorylation
癫痫发作-诱发AMPA受体磷酸化
Seizures in neonates are usually caused by hypoxia and can increase risk of later epilepsy and cognitive impairment.
缺氧通常可导致新生儿癫痫发作，而且会增加后天的癫痫与认知功能损伤的风险。
Rakhade et al 编译：
癫痫发作-诱发AMPA受体磷酸化
缺氧通常可导致新生儿癫痫发作，而且会增加后天的癫痫与认知功能损伤的风险。Rakhade et al.可识别分子改变并以此增加发作的敏感性，引发新生大鼠缺血性癫痫发作。癫痫发作在一小时内可增加由AMPARs介导的微小自发兴奋性突触后电流的振幅和频率。这可能是由于PKA,PKC,以及钙/钙依赖性激酶II使AMPAR亚基磷酸化增多，因为此时这些酶的活性也提高了。GluR1的磷酸化增加了通道传导性与突触的嵌入，而GluR2的磷酸化则激活了其内在活性。GluR2的自活化可以增加钙渗透性APMA受体的数量，进而增强其兴奋性。在活体治疗中阻断AMPAR拮抗剂可增加磷酸化，增加EPSC振幅与频率，同时也减轻了后天癫痫发作的损伤 [标签:content1][标签:content2]
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作者:admin@医学,生命科学 2011-04-06 14:07
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