منابع مشابه
Excitotoxic damage to white matter.
Glutamate kills neurons by excitotoxicity, which is caused by sustained activation of glutamate receptors. In recent years, it has been shown that glutamate can also be toxic to white matter oligodendrocytes and to myelin by this mechanism. In particular, glutamate receptor-mediated injury to these cells can be triggered by activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid,...
متن کاملNBQX attenuates excitotoxic injury in developing white matter.
The excitatory neurotransmitter glutamate is released from axons and glia under hypoxic/ischemic conditions. In vitro, oligodendrocytes (OLs) express non-NMDA glutamate receptors (GluRs) and are susceptible to GluR-mediated excitotoxicity. We evaluated the role of GluR-mediated OL excitotoxicity in hypoxic/ischemic white matter injury in the developing brain. Hypoxic/ischemic white matter injur...
متن کاملDamage to white matter fiber tracts in acute spatial neglect.
Previous statistical voxelwise lesion-behavior mapping (VLBM) studies have demonstrated that spatial neglect is associated with cortical and subcortical gray matter damage. However, it has also been suggested that the disorder may result from white matter injury. Our aim was to investigate the white matter connectivity in a large sample of 140 stroke patients. We combined a VLBM approach with t...
متن کاملWhite matter damage impairs access to consciousness in multiple sclerosis
Global neuronal workspace theory predicts that damage to long-distance white matter (WM) tracts should impair access to consciousness during the perception of brief stimuli. To address this issue, we studied visual backward masking in 18 patients at the very first clinical stage of multiple sclerosis (MS), a neurological disease characterized by extensive WM damage, and in 18 matched healthy su...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Anatomy
سال: 2007
ISSN: 0021-8782,1469-7580
DOI: 10.1111/j.1469-7580.2007.00733.x