近日,，日本自然科學(xué)研究機(jī)構(gòu)生理學(xué)研究所的一個(gè)研究小組實(shí)驗(yàn)證實(shí),，精神分裂癥主要癥狀之一的意識(shí)障礙是一種被稱為神經(jīng)膠質(zhì)的細(xì)胞出現(xiàn)構(gòu)造異常所引起的，這種細(xì)胞包圍著神經(jīng)細(xì)胞。
據(jù)介紹，日本研究人員首先培育出一種實(shí)驗(yàn)大鼠，并特意讓這種大鼠神經(jīng)膠質(zhì)細(xì)胞中的一個(gè)基因出現(xiàn)異常,，然后觀察電流信號(hào)在大鼠神經(jīng)細(xì)胞之間傳輸?shù)倪^程中其速度的變化情況。結(jié)果發(fā)現(xiàn),，電流信號(hào)的傳輸速度只有正常大鼠的一半,。
研究人員用電子顯微鏡觀察發(fā)現(xiàn)，出現(xiàn)這種現(xiàn)象的原因就是神經(jīng)膠質(zhì)細(xì)胞的構(gòu)造出現(xiàn)了細(xì)微的異常變化,，即本該完全包住神經(jīng)細(xì)胞突起的神經(jīng)膠質(zhì)細(xì)胞的頂端并沒有完全閉合,，從而使神經(jīng)細(xì)胞突起露出了一部分，這也正是導(dǎo)致患者出現(xiàn)意識(shí)障礙的原因,。
一直以來,，人們都以為是神經(jīng)細(xì)胞本身出了問題才導(dǎo)致意識(shí)障礙，沒想到真正的原因竟是神經(jīng)膠質(zhì)細(xì)胞出現(xiàn)的細(xì)微變化,，這一結(jié)果就連研究人員也連呼意外,。
精神分裂癥是一種具有代表性的精神病，有不少人受這種疾病困擾,。精神分裂癥又分為陽(yáng)性癥狀（妄想和幻覺）,、陰性癥狀（情感障礙，缺乏社交性）和此次研究所涉及的意識(shí)障礙（意志活動(dòng)低下）三大類,。（生物谷Bioon.com）
生物谷推薦原始出處：
The Journal of Neuroscience, July 1, 2009, doi:10.1523/JNEUROSCI.3216-08.2009
Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron–Glia Interactions and Decreased Conduction Velocities
Hisataka Tanaka,1 * Jianmei Ma,1,5 * Kenji F. Tanaka,1 * Keizo Takao,6,7 Munekazu Komada,2,10 Koichi Tanda,6 Ayaka Suzuki,8 Tomoko Ishibashi,8 Hiroko Baba,8 Tadashi Isa,3 Ryuichi Shigemoto,4 Katsuhiko Ono,9 Tsuyoshi Miyakawa,2,6,7,10 and Kazuhiro Ikenaka1,10
1Division of Neurobiology and Bioinformatics, 2Center for Genetic Analysis of Behavior, 3Department of Developmental Physiology, and 4Division of Cerebral Structure, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki, Aichi 444-8787, Japan, 5Department of Anatomy, Dalian Medical University, Dalian, Liaoning 116044, China, 6Genetic Engineering and Functional Genomics Group, Horizontal Medical Research Organization, Kyoto University Faculty of Medicine, Sakyo-ku, Kyoto 606-8501, Japan, 7Division of Systems Medicine, Institute for Comprehensive Medical Science, Fujita Health University, Aichi 470-1192, Japan, 8Department of Molecular Neurobiology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Hachioji 192-0392, Japan, 9Department of Biology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan, and 10Japan Science and Technology Agency, Core Research for Evolutionary Science and Technology, Kawaguchi 332-0012, Japan
Conduction velocity (CV) of myelinated axons has been shown to be regulated by oligodendrocytes even after myelination has been completed. However, how myelinating oligodendrocytes regulate CV, and what the significance of this regulation is for normal brain function remain unknown. To address these questions, we analyzed a transgenic mouse line harboring extra copies of the myelin proteolipid protein 1 (plp1) gene (plp1tg/– mice) at 2 months of age. At this stage, the plp1tg/– mice have an unaffected myelin structure with a normally appearing ion channel distribution, but the CV in all axonal tracts tested in the CNS is greatly reduced. We also found decreased axonal diameters and slightly abnormal paranodal structures, both of which can be a cause for the reduced CV. Interestingly the plp1tg/– mice showed altered anxiety-like behaviors, reduced prepulse inhibitions, spatial learning deficits and working memory deficit, all of which are schizophrenia-related behaviors. Our results implicate that abnormalities in the neuron-glia interactions at the paranodal junctions can result in reduced CV in the CNS, which then induces behavioral abnormalities related to schizophrenia.
