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For these goals, we analyzed the cytoarchitectural features, the time of neurogenesis and the cellular phenotype of the heterotopia, by means of Brd U immunocytochemistry and confocal immunofluorescence experiments.Our data demonstrate that the different types of heterotopia in MAM-treated rats are formed through the same altered neurogenetic process, which follows quite organized neurogenetic gradients.We have previously demonstrated that the antiproliferative agent methylazoxymethanol acetate (MAM) is able to induce in rats cerebral heterotopia that share striking similarities with those observed in human periventricular nodular heterotopia (PNH), a cerebral dysgenesis frequently observed in human patients affected by drug-resistant focal epilepsy.In this study, we investigated the time-course of neurogenesis in the cerebral heterotopia of MAM-treated rats, with the idea of understanding why PNH develop in human patients.For these goals, we have employed a combined approach, by analyzing: (i) the cytoarchitectural features of the heterotopia in the early post-natal period; (ii) the birthdating of cells within the heterotopia, by means of the incorporation of the thymidine analog bromodeoxyuridine (Brd U); and (iii) the cellular phenotypes of the heterotopia, by means of confocal immunofluorescence experiments.Our data demonstrate that all heterotopia in MAM-treated rats share a common neurogenesis and suggest that MAM-induced ablation of early generated waves of neurons is sufficient to deeply alter migration and differentiation of the subsequent waves of newly generated neurons, leading to the formation of the different types of heterotopia.The narrow time-window of biological activity of MAM (2–24 h, with maximal activity at 12 h after administration) affects the proliferation of specific neuronal cell populations (Cattaneo , 1999) that share striking similarities with those observed in human peri-ventricular nodular heterotopia (PNH), a cerebral dysgenesis characterized by nodular masses of gray matter located in close apposition to the periventricular germinative neuroepithelium (Battaglia , 1996, 1997).In this study, we investigated neurogenesis in the cerebral heterotopia of MAM-treated rats, with the idea of understanding why periventricular heterotopia develop in human patients.
To assess the contribution of cell death to the observed phenotype, the numbers and radial position of a Casp3-positive cells in the Dicer null cortex were compared with those in wild-type littermates at E17.5 (Figure 5E, F).
Cerebral dysgeneses are developmental malformations of the brain structure determined by impairment of the spatially organized and time-regulated processes of neurogenesis, migration, neuron/glia interaction and cell differentiation, which take place in the developing brain.
In recent years, it has been increasingly recognized that cerebral dysgeneses are a relevant cause of mental and neurological deficits in humans, including epilepsy (Galaburda , 1994).
The MAM-induced ablation of an early wave of cortical neurons is sufficient to alter the migration and differentiation of subsequently generated neurons, which in turn set the base for the formation of the different heterotopic structures.
The neurogenesis of MAM-induced heterotopia may explain the origin and intrinsic epileptogenicity of periventricular nodular heterotopia in human patients.However, in the Dicer null cortex the majority of Brd U neurons were Tbr1 neurons (65%; Figure 5D).