ROLES OF FIBROBLAST GROWTH FACTOR (B-FGF) AND GAP JUNCTION ON NEOCORTICAL HISTOGENESIS

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We have examined the cell cycle progression in explants cultured with FGF-2 or 1-octanol. FGF-2 is representative of physiologic mitogens respecting the neocortical PVE.1-octanol, on the other hand, has been demonstrated to mediate a countering antimitogenic effect through gap junction blockade.In vivo, there are two options for postmitotic cells, either to exit the cycle and migrate out of the VZ (fate to Q fraction) or to re-enter S phase and continue to cycle (fate to P fraction). In the explants, by contrast, a substantial proportion makes neither of these choices but instead persists in the VZ in an indeterminate state (I fraction). The phenomenon is modulated, in opposing directions and to different degree, by FGF-2 and 1-octanol. Modulation by these mitogenic and antimitogenic agents is observed only in the more advanced region of the neurogenetic gradient. The phenomenon is a relatively selective one in that the majority of other vital properties of the epithelium are little altered : the epithelium maintains its architectonic integrity and there is no interruption of interkinetic nuclear migration, respecting cell cycle phases. Moreover, there is no augmentation in the generally low occurrence rate of pyknosis. That is, these conditions of culture appear to have unmasked relatively selectively mechanisms regulatory to the proliferative fates of cells of the PVE.Importantly, mechanisms by which this effect is modulated by FGF-2 or 1-octanol are evidently developmentally regulated, expressed only in the relatively advanced region of the neurogenetic gradient.