Intraventricular administration of neurotrophic factor midkine ameriolates hippocampal delayed neuronal death following transient global ischemia in gerbils.

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  • 神経栄養因子ミドカイン（ＭＫ）のスナネズミ遅発性神経細胞死に対する抑制作用

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Abstract

Upon experimental cerebral infarction of rats midkine (MK) is expressed 1 to 4 days after the onset of infarction at the surrounding zone of the infarct. We examined the effect of intraventricular administration of MK to mongolian gerbils on the hippocumpal delayed neuronal death of CA-1. The yeast producing MK was injected into the ventricle. Thereafter, the bilateral common arteries were occluded for 5 min. The animals were sacrificed 7 days after th ischemic insult. The coronal 5 μm-thick sections for hematoxylin-eosin staining included the hippocampal area at 1.4-1.8 mm posterior to bregma. Hippocampal nuclear number was 272 ± 44/mm in sham operated group (n= 13, mean ± S.D.), 10 ± 10/ mm in vehicle administration group (n=11), 236 ± 40/mm in 2, ug administration group (n=4), 222 ± 11/ mm in 1 μg group (n=5), 232 ± 18/mm in 0.5 beg group (n=4), and 50 ± 91/mm in 0.25 pg group (n=6). A significant F ratio was found in one-way analysis of varience, then post-hoc Fisher's protected least significant differences test was performed, which showed the significances in the administration groups of 2, 1, and 0.5 ug (p<0.0001), and 0.25 ug (p<0.5). This results indicated small amount of MK protein had neurotrophic activity in the inhibition of hippocampal delayed neuronal death.

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