@article{oai:niigata-u.repo.nii.ac.jp:00021735,
 author = {阿部, 博史},
 issue = {12},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Dec},
 note = {Using the model of middle cerebral artery (MCA) occlusion in gerbils, in which infarction was produced in the ipsilateral cortex and striatum, the author investigated neuronal damage and sequential changes of local cerebral glucose utilization ipsilaterally in the hippocampus, thalamus, lateral geniculate body (LGB), medial geniculate body (MGB), globus pallidus (GP), and substantia nigra pars reticulata (SNR), all of which are outside the ischemic area, and protein synthesis in the hippocampus. Neuronal damage was determined by histopathological change and the regional distribution of ^<45>Ca on ^<45>Ca autoradiograms. Local cerebral glucose utilization (LCGU) was evaluated by ^<14>C-deoxyglucose autoradiography, and protein synthesis by ^<14>C-valine autoradiography. In the ipsilateral hippocampus, a marked increase in LCGU was present and ^<45>Ca accumulation was observed in the dendritic region of the pyramidal cells during the 2 hours after MCA occlusion. Reduced protein synthesis in the CA1 neurons was evident 2 to 12 hours after MCA occlusion and reversible dendritic damage of the CA1 neurons was demonstrated using the antibody against microtubule-associated protein 2. However, in the ipsilateral thalamus, LGB, MGB, GP and SNR, degenerated neurons were found 1 week after MCA occlusion, and a marked atrophy was observed during and after the second week following MCA occlusion. The ventral posterior nucleus of the ipsilateral thalamus suffered the greatest neuronal loss. In the thalamus, LGB and MGB, which all send efferent fibers to the cortex in the territory of the MCA, a decrease in LCGU was observed during the first week after the occlusion, and ^<45>Ca accumulation occured during and after the second day following MCA occlusion. In contrast, in the GP and SNR, which receive striatal input, LCGU increased during the first 12 hours, and ^<45>Ca started to accumulate from the 4 th day after the onset of ischemia. These results demonstrate there are two types of neuronal damage in areas remote to the infarction following focal cerebral ischemia. One is a reversible change in the acute stage of ischemia and the other is a progressive degeneration in the areas having direct connections with the ischemic focus. The latter could be caused by some different mechanisms such as retrograde degeneration, antegrade transsynaptic degeneration, and neuronal disinhibition conseqent to loss of inhibitory inputs, in which the type of neurotransmitter and the direction of transmission are important factors.},
 pages = {1013--1025},
 title = {砂ネズミ中大脳動脈閉塞モデルにおける遠隔病変},
 volume = {104},
 year = {1990}
}