近日，日本自然科学研究机构生理学研究所的一个研究小组实验证实，精神分裂症主要症状之一的意识障碍是一种被称为神经胶质的细胞出现构造异常所引起的，这种细胞包围着神经细胞。

据介绍，日本研究人员首先培育出一种实验大鼠，并特意让这种大鼠神经胶质细胞中的一个基因出现异常，然后观察电流信号在大鼠神经细胞之间传输的过程中其速度的变化情况。结果发现，电流信号的传输速度只有正常大鼠的一半。

研究人员用电子显微镜观察发现，出现这种现象的原因就是神经胶质细胞的构造出现了细微的异常变化，即本该完全包住神经细胞突起的神经胶质细胞的顶端并没有完全闭合，从而使神经细胞突起露出了一部分，这也正是导致患者出现意识障碍的原因。

一直以来，人们都以为是神经细胞本身出了问题才导致意识障碍，没想到真正的原因竟是神经胶质细胞出现的细微变化，这一结果就连研究人员也连呼意外。

精神分裂症是一种具有代表性的精神病，有不少人受这种疾病困扰。精神分裂症又分为阳性症状（妄想和幻觉）、阴性症状（情感障碍，缺乏社交性）和此次研究所涉及的意识障碍（意志活动低下）三大类。（ 生物谷 Bioon.com）

生物谷推荐原始出处：

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 (plp1^tg/–   mice)   at 2 months of age. At this stage, the   plp1^tg/–   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   plp1^tg/–   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.