意大利科學(xué)家日前發(fā)現(xiàn),，造成癲癇發(fā)作的不只是神經(jīng)元,，大腦中的一種細(xì)胞也起著重要作用，這種細(xì)胞就是星形膠質(zhì)細(xì)胞,。
意大利帕多瓦神經(jīng)科學(xué)研究所等機構(gòu)的科學(xué)家在新一期美國《科學(xué)公共圖書館·生物學(xué)》雜志上發(fā)表論文說,，癲癇發(fā)作的典型癥狀是抽搐，這是神經(jīng)元活動異常的結(jié)果,。但他們的研究發(fā)現(xiàn),，星形膠質(zhì)細(xì)胞也參與了癲癇的發(fā)作。這種細(xì)胞會與神經(jīng)元持續(xù)交互作用,，這種交互作用使神經(jīng)元活動異常,，從而導(dǎo)致癲癇發(fā)作。
科學(xué)家的研究還證明,，抑制星形膠質(zhì)細(xì)胞的活動可以減輕癲癇發(fā)作時的癥狀,，加強其活動則會使癲癇發(fā)作更為強烈,。
星形膠質(zhì)細(xì)胞普遍存在于哺乳動物大腦中，這種細(xì)胞數(shù)量相當(dāng)多,。過去認(rèn)為這種細(xì)胞在大腦中的作用很小,。(生物谷Bioon.com)
生物谷推薦原文出處：
PLoS Biol. doi:10.1371/journal.pbio.1000352
An Excitatory Loop with Astrocytes Contributes to Drive Neurons to Seizure Threshold
Marta Gómez-Gonzalo1,2#, Gabriele Losi1,2#, Angela Chiavegato1,2, Micaela Zonta1,2, Mario Cammarota1,2, Marco Brondi3,4, Francesco Vetri4, Laura Uva5, Tullio Pozzan1,2,6, Marco de Curtis5, Gian Michele Ratto3,4, Giorgio Carmignoto1,2*
1 Institute of Neuroscience – Consiglio Nazionale delle Ricerche (CNR), University of Padova, Padova, Italy, 2 Department of Experimental Biomedical Sciences, University of Padova, Padova, Italy, 3 National Enterprise for nanoScience and nanoTechnology (NEST), Instituto Nanoscienze CNR, Scuola Normale Superiore, Pisa, Italy, 4 Institute of Neuroscience – CNR, Pisa, Italy, 5 Fondazione Istituto Neurologico Carlo Besta, Milano, Italy, 6 Venetian Institute of Molecular Medicine, Padova, Italy
Seizures in focal epilepsies are sustained by a highly synchronous neuronal discharge that arises at restricted brain sites and subsequently spreads to large portions of the brain. Despite intense experimental research in this field, the earlier cellular events that initiate and sustain a focal seizure are still not well defined. Their identification is central to understand the pathophysiology of focal epilepsies and to develop new pharmacological therapies for drug-resistant forms of epilepsy. The prominent involvement of astrocytes in ictogenesis was recently proposed. We test here whether a cooperation between astrocytes and neurons is a prerequisite to support ictal (seizure-like) and interictal epileptiform events. Simultaneous patch-clamp recording and Ca2+ imaging techniques were performed in a new in vitro model of focal seizures induced by local applications of N-methyl-D-aspartic acid (NMDA) in rat entorhinal cortex slices. We found that a Ca2+ elevation in astrocytes correlates with both the initial development and the maintenance of a focal, seizure-like discharge. A delayed astrocyte activation during ictal discharges was also observed in other models (including the whole in vitro isolated guinea pig brain) in which the site of generation of seizure activity cannot be precisely monitored. In contrast, interictal discharges were not associated with Ca2+ changes in astrocytes. Selective inhibition or stimulation of astrocyte Ca2+ signalling blocked or enhanced, respectively, ictal discharges, but did not affect interictal discharge generation. Our data reveal that neurons engage astrocytes in a recurrent excitatory loop (possibly involving gliotransmission) that promotes seizure ignition and sustains the ictal discharge. This neuron–astrocyte interaction may represent a novel target to develop effective therapeutic strategies to control seizures.
