Hypobaric-ischemic conditions produce glutamate-like cytopathology in infant rat brain.

作者: C Ikonomidou , MT Price , JL Mosinger , G Frierdich , J Labruyere

DOI: 10.1523/JNEUROSCI.09-05-01693.1989

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摘要: We present a new animal model of perinatal hypoxic/ischemic brain damage and compare this type with the excitotoxic previously described in brains infant rats monkeys treated systemically glutamate (Glu). Ten-d-old unilateral occlusion common carotid artery were subjected to hypobaric conditions for 75 min sacrificed 0–4 hr later light electron microscopic examination. The mortality rate was relatively low (12%), evident ipsilateral ligated 94% surviving animals 4 after termination event. Regions most frequently affected medial habenulum, dentate gyrus, caudate nucleus, frontoparietal neocortices, olfactory tubercle, several thalamic nuclei. acute cytopathological changes, primarily edematous degeneration neuronal dendrites cell bodies, evolved very rapidly, some neurons manifesting end-stage necrosis at 0 (immediately exposure) others developing such changes over 1–4-hr period. conclude that neurodegenerative reaction induced rat by hypoxia/ischemia is indistinguishable from exogenous Glu known cause. Moreover, companion study (Olney et al., 1989) we show MK-801, powerful antagonist N-methyl-D-aspartate receptor complex (subtype receptor), protects against hypobaric/ischemic model. Our results reinforce other recent evidence suggesting mediated endogenous or related excitotoxins.

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