脳室周囲白質軟化症における脳の可塑性と神経再生に関する免疫組織化学的研究

Abstract

[Purpose] Our previous studies revealed oligodendroglial regeneration around the necrosis of periventricular leukomalacia (PVL). This report describes neuronal compensation and plasticity in the cortex and white matter of PVL brains. [Subjects and Method] An immunohistochemical study was performed on 15 human brains with PVL, using an antibody for PGP9.5, which is expressed predominantly in differentiating neurons. We semiquantitatively evaluated the expression of PGP9.5 in the cerebral cortex and white matter and compared it with that of age-matched controls. [Results] In the white matter, there was an increase of immunoreactivity beside the necrotic lesions of focal type PVL, but there was often a decrease in widespread or diffuse type PVL. In the cortex, close to necrotic lesions, the immunoreactivity was decreased in pyramidal cells of the 3rd and 5th cortical layers, but was increased in granular cells of the 2nd and 4th cortical layers.[Conclusion] The characteristic increase of axons around PVL in the white matter and granular neurons in the cortex close to PVL suggest neuronal compensation for injured axons and plasticity for the transneuronally degenerated pyramidal neurons.

Neuronal Plasticity in the Developing and Aging Cerebral Cortices of Patients with Down Syndrome

“…In current study on the infant group, PGP9.5-positive neurons in the pyramidal cell layers were less prominent in patients with DS than in controls, whereas those in the granule cell layers were not different between patients with DS and controls. Conversely, in the adult groups, patients with DS showed more prominent PGP9.5 expression than controls in both the granule and pyramidal cell layers, consistent with the increased expression of PGP9.5 in the brains of patients with Increased PGP9.5 immunoreactivity has also been observed in the brains with periventricular leukomalacia (PVL) by Nakabayashi et al [10] indeed, marked PGP9.5 expression was observed in white matter and granule cell layers (layers 2 and 4) adjacent to the necrotic lesions of PVL, but not in the pyramidal cell layers [12]. The characteristic increase in the numbers of axons in the white matter and granule neurons closeto PVL lesions most likely reflects compensatory mechanisms in response to axonal damage and transneuronal degeneration of pyramidal neurons.…”

“…After three washes in TBS, the biotinylated second antibodies and peroxidase-conjugated streptoavidin (simplestain MAX-PO (MULTI), Nichirei, Tokyo) were incubated on the sections (for 2 hours at room temperature). After three washes in TBS, the immunoproducts were visualized using diaminobenzidine (Nichirei, Tokyo).The sections were then counterstained with hematoxylin [10].…”