This study describes the spatio-temporal expression of basic Fibroblast growth factor (FGF-2) during odontogenesis of mouse as revealed by immunohistology. Parasagittal sections of mouse embryo head (13-18 day of gestation) containing various stages of developing tooth were incubated with a polyclonal anti-FGF-2 antibody and positive binding was evidentiated by using Streptavidin-Biotin complex-HRP system and AEC staining. We observed no FGF-2 staining at the dental lamina stage. At the bud stage slight staining is seen, limited to some epithelial cells. The intensity of the staining increases at the cap stage. In the bell stage, the stellate reticulum cells stain intensely. Later, odontoblasts and the dentin matrix stain deeply; but the epithelial cells stain faint. The extra cellular matrix of the dentin and dental papilla stain very intense but the enamel matrix is found negative. These results indicate the participation of FGF-2 in differentiation rather than in proliferation of tooth-forming cells. In particular, it appears that FGF-2 participates in odontoblast differentiation and in dentin matrix deposition. The spatio-temporally specific distribution pattern of FGF-2 in developing mouse tooth reported here emphasizes the importance of FGF-2 in mammalian odontogenesis.

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The influence of chronic maternal morphine on the parvalbumin immunoreactive patterns in developing mouse brain was studied. Female Swiss mice were administered daily saline or morphine (30 or 60 mg/kg) for a period of 7 days before mating, gestation, and 21 days postpartum. Their pups were sacrificed on postnatal day 18 and the brains were examined histologically and immunohistochemically for parvalbumin-positive neurons. Histological observations revealed no significant changes in the cell number of the morphine-exposed neonatal forebrain, whereas the number of parvalbumin-positive neurons increased in layers II-IV of the parietal cortex I. Moreover, the number of parvalbumin-positive dendrites increased remarkably in the cingulate and parietal I cortices of the morphine-exposed neonates, indicating the region-specific increase in the PV immunoreactive profiles. These results are consistent with the key roles played by the above brain regions in the altered behavioral patterns of the maternally addicted neonates, such as impaired somatosensory and cognitive performances. The mechanism of morphine action on parvalbumin expression in neonatal mouse brain is not evident, but alterations in the expression patterns of parvalbumin in specific regions of the developing brain might be one of the cellular mechanisms by which addictive drugs modify the functional aspects of the developing CNS.

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