據(jù)12月4日的《科學》雜志報道說,，研究人員已經(jīng)找到了一種存在于神經(jīng)細胞中的特別的離子通道,，當這種離子通道過度活躍的時候會在腦子的海馬回中引起一種“脈沖”活動,，這與在癲癇發(fā)作的時候所經(jīng)歷的情況類似,。這一發(fā)現(xiàn)可能會對癲癇和中風的治療提供一種新型的治療標靶。
Roger Thompson及其同僚培養(yǎng)了海馬回中的神經(jīng)元,，接著用全細胞膜片鉗技術(shù)來激活這些離子通道并記錄它們的活動,。這種方法阻斷了細胞中的依賴于電壓激活的離子通道，使得研究人員可以觀察并記錄通過細胞的繼發(fā)性的電流,。他們發(fā)現(xiàn),，這種繼發(fā)性電流中的一種（由蛋白Pannexin-1所形成的一種半通道）在當某種特別的叫做NMDAR的受體過度激活的時候，容易發(fā)生癲癇樣的活動,。研究人員說,，人們需要對Pannexin-1半通道進行認真的研究以發(fā)現(xiàn)其在癲癇中所起的特別的作用，它可能最終會引領(lǐng)人們找到有效治療某些神經(jīng)系統(tǒng)疾病的途徑,。（生物谷Bioon.com）
生物谷推薦原始出處：
Activation of Pannexin-1 Hemichannels Augments Aberrant Bursting in the Hippocampus
Roger J. Thompson,1* Michael F. Jackson,2 Michelle E. Olah,2 Ravi L. Rungta,1 Dustin J. Hines,1 Michael A. Beazely,2 John F. MacDonald,2 Brian A. MacVicar1
Pannexin-1 (Px1) is expressed at postsynaptic sites in pyramidal neurons, suggesting that these hemichannels contribute to dendritic signals associated with synaptic function. We found that, in pyramidal neurons, N-methyl-D-aspartate receptor (NMDAR) activation induced a secondary prolonged current and dye flux that were blocked with a specific inhibitory peptide against Px1 hemichannels; knockdown of Px1 by RNA interference blocked the current in cultured neurons. Enhancing endogenous NMDAR activation in brain slices by removing external magnesium ions (Mg2+) triggered epileptiform activity, which had decreased spike amplitude and prolonged interburst interval during application of the Px1 hemichannel blocking peptide. We conclude that Px1 hemichannel opening is triggered by NMDAR stimulation and can contribute to epileptiform seizure activity.
1 Department of Psychiatry and Brain Research Centre, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada.
2 Robarts Research Institute, University of Western Ontario, London, ON N6A 5K8, Canada.
