1998 Fiscal Year Final Research Report Summary
Experimental study on pathogenesis of cortical dysplasias
| Project/Area Number |
09670799
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
SHIMADA Morimi Shiga University of Medical Science, School of Medicine, Pediatrics, Professor, 医学部, 教授 (00079873)
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| Co-Investigator(Kenkyū-buntansha) |
TAKANO Tomoyuki Shiga University of Medical Science, School of Medicine, Pediatrics, Assistant P, 医学部, 助手 (80236249)
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| Project Period (FY) |
1997 – 1998
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| Keywords | cortical dysplasia / hydrocephalus / plymicrogyria / mumps virus / hypoxic ischemic encephalopathy / plasticity |
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| Research Abstract |
Pathogenesis of congenital hydrocephalus and polymicrogyria was investigated using model animals which were produced experimentally either by inoculating mumps virus, placing in an hypoxic/ischemic condition or by regional resection of the cortex.
1) Pathogenesis of hydrocephalus : Two groups of Syrian hamsters, either 2- or 30-day-old, were inoculated intracerebrally with 20 ul/g brain of mumps virus. These animals from each group were examined at various days after inoculation. in a group inoculated with mumps virus at 2 days of age, pathologic findings such as periventricular edema, ependymal cell loss, and ventricular dilatation were more prominent than in a group inoculated at 30 days of age. ZO1-immunoreactive tight junctions in hydrocephalic brain of the 2-day group were severely damaged in the choroid plexus and ependyma, and in white matter capillaries as early as 3 days after inoculation. These changes were not apparent in the hydrocephalic brains of the 30-day group. Periventricular edema in the 2-day group was linked to ependymal and blood-brain barrier tight-junction permeability. These results indicate that immaturity and fragility of the tight junction in the developing brain may play a role for cortical dysplasia after the exposure of noxious environmental factors.
2) Pathogenesis of polymicrogyria : Hypoxic/ischemic model was produced by ligating the left common carotid artery of newborn rat and then placed them in hypoxic condition for 2 h. The animals thus treated subsequently developed policystic lesion and/or polymicrogyric changes in the cerebral cortex. In the early stage of treatment, a tentative increase of full-length TrkB receptors and basic fibroblast growth factor (bFGF) in neuron in the former and in astrocyte in the latter around the lesion and related regions. These results indicate that the regional increase in neurotophic factors and neuronal plasticity after damage play an important role for later maldevelopment of the cortex.
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