Effect of Intrauterine Growth Restriction on Cell Proliferation in the Fetal Cerebellum of the Guinea Pig / 체질인류학회지

Intrauterine growth restriction (IUGR) is a risk factor for neurological and behavioral deficits in children although the precise underlying biological mechanisms are unclear. It is also unclear whether IUGR affects cell proliferation in the cerebellum, which is vulnerable to prenatal insults during brain development. The aim of this study is to determine whether IUGR affects the alteration of cell proliferation in the fetal cerebellum and whether this change correlate with reduction in the growth of cerebellum. IUGR was induced via unilateral ligation of the uterine artery in pregnant guinea pigs at 30 days of gestation (dg; term ~67 dg) to produce growth restricted (GR) fetuses. Fetal (control, n=7 and GR, n=7) body and organ weights at 60 dg were measured and Ki67 immunohistochemistry was performed to detect cell proliferation. The width of the external granular layer (EGL) was also measured at 60 dg. The mean body and organ weights of GR fetuses at 60 dg were significantly reduced. The proportion of proliferating cells to the total cell number in the EGL was not different in GR compared with control animals but the width of the EGL was significantly increased in GR animals. These results demonstrate that significant reductions in the growth of the cerebellum do not have a well-defined relationship to cell proliferation in IUGR guinea pig fetuses. In addition, despite there was no difference in the proportion of proliferating to post-mitotic cells between control and GR fetuses in the EGL at 60 dg, the width of the EGL was increased in GR fetuses compared to controls. This could be interpreted as a delay in the process of cell production or migration.

Effect of Maternal Thyroxine Treatment on the Postnatal Development of Brain-derived Neurotrophic Factor-containing Neuron in the Brain of Pups of Alcohol Abused Mother / 대한해부학회지

Maternal alcohol abuse is thought to be the common cause of mental retardation. Especially, continuous alcohol consumption during critical period of brain development induce fetal alcohol effects. In this study, the authors investigated the effects of maternal alcohol drinking on the postnatal changes of BDNF contents and patterns of BDNF-containing neuron in neonatal rat brain, and, the influence of maternal thyroxine treatment on the brain of pups of alcohol abused mother. Pregnant rats were divided into three groups. Alcohol-fed group (n=4) received 35 calories of liquid alcohol diet daily from gestation day 6; control pair-fed group (n=4) was fed a liquid diet in dextrin replaced alcohol isocalorically; alcohol+T4 group (n=4) received 35 calories liquid alcohol diet and exogenous thyroxine (5 microgram/kg/day) subcutaneously. The amount of BDNF was significantly higher in the alcohol+T4 group as compared to the alcohol group at P7, P14 and P21, especially, alcohol+T4-exposed pups showed a significant increase of BDNF at P7. The decrease in BDNF was found in alcohol group compared to control pair-fed group at all ages. In alcohol+T4 group, BDNF-containing Purkinje cells exhibited mature pattern and monolayer arrangement at P14. Alcohol+T4 group showed mature pattern and numerical increase of BDNF-containing cells in cerebral cortex, hypothalamus and hippocampus at P7. The BDNF immunoreactivity of hippocampus continued to show prominent configuration in alcohol+T4 group at P28. These results indicate that the increase of the BDNF-containing neurons and BDNF amount in pups of thyroxinesupplemented alcohol-exposed dams as compared to control pair-fed and alcohol-exposed pups at P7, presumably suggest the early postnatal growth stimulatory effect of the exogenously supplemented thyroxine. Therefore, the increase of BDNF synthesis caused by maternal administration of exogenous thyroxine may ameliorate fetal alcohol effects, one of the ill effects as a result of the dysthyroid state following maternal alcohol abuse.

Morphological Studies on the Calbindin D-28K and Parvalbumin Immunoreactive Neurons in the Medulla Oblongata and Ventral Horn of the Spinal Cord Gray Matter after Spinal Cord Injury in Rats / 체질인류학회지

This study was examined and compared the immunocytochemical distribution of the two calcium-binding proteins calbindin D-28K and parvalbumin immunreactive neurons in the medulla oblongata and spinal cord after transection of spinal cord in rats. In this experiment, calbindin D-28K immnunoreactive neurons were mainly found in many pyramidal cells distributed medulla oblongata and spina1 cord of rats. Parvalbumin immunoreactive cells were demonstrated in all lamina of the gray matter of the spinal cord. These immunoreactive cells had the most high density in the severa1 nuclei of the ventra1 horn of the all segments of the spina1 cord. Calbindin D-28K neuropil labeling was strongly noted in spina1 all segments of the spinal cord. In contrast parva1bumin immunoreactive, little differences were found in distribution, size and morphology of calbindin D-28K cell body or neuropil staining in the spinal cord. The number of parvalbumin immunoreactive cells were more than twice in the medulla oblongata and spinal cord compared to the calbindin D-28K immunoreactive cells. Calbindin D-28K and parvalbumin-immmoreactive somata were round, ova1, spind1e and polygona1 in shape, and the immunoreactive neurons were unipolar, bipolar, multipolar and horizontal in shape. The diameters of the somata of the two immunoreactive neurons were 40 ~50 micrometer, respectively. Also dendrites of two immunoreactive neurons were densely arrayed in network. These results suggest that CB-IR and PV-IR most high density in the of the VII~X layers in the ventra1 horn of the all segments of the spina1 cord.