PubMed · 7848192
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J S Robinson, R F Seamark, J A Owens. 1994. Placental function.. https://doi.org/10.1111/j.1479-828x.1994.tb01065.x
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Previous studies reported that telencephalic proliferative zones contribute to the development of the pulvinar thalamic nucleus in the human brain (Rakic and Sidman [1969] Z. Anat. Entwicklungsgesch. 129:53-82). The present study examined their possible contribution to the development of other thalamic nuclei. Postmortem brain tissue from human fetuses ranging between 10.5 and 40 weeks of gestation (wg) was processed by Nissl staining, Golgi impregnation, and MAP2 (microtubule-associated protein 2) immunocytochemistry. The gangliothalamic body, suggested to serve as a conduit for cells migrating from the ganglionic eminence to the thalamus, was found in the period from 15 to 34 wg in all rostrocaudal thalamic regions, particularly at the level of the anterior nuclear complex, mediodorsal and pulvinar nucleus, and in addition, the lateral geniculate nucleus. In Nissl-stained sections, the gangliothalamic body is a thin cellular layer situated beneath the thalamic surface, near the telencephalo-diencephalic junction. In Golgi- and MAP2-stained sections, it is a stream of mostly bipolar cells extending from the ganglionic eminence to the medial thalamus. In addition, MAP2-immunoreactivity confirms the neuronal nature of its cells. The present study further supports the hypothesis that certain neurons migrate from the ganglionic eminence to the thalamus through the transient gangliothalamic body during fetal development. Moreover, our data indicate that both the association (mediodorsal and pulvinar), as well as the anterior (limbic) and specific relay nuclei are potential recipients of the telencephalic neurons.
A prospective observational study of 104 women was performed to study whether the insulin-like growth factor (IGF) system in pregnancy before labour is associated with reduced fetal growth. Fetal blood was obtained by cordocentesis for prenatal diagnosis or at elective caesarean delivery and a maternal sample was also obtained, IGF-1 and IGF-2 and their binding proteins -1 and -3 were measured by RIA. The 35 case were smaller than -2S.D.s by ultrasound abdominal circumference and birthweight and were subdivided into fetal growth retardation (FGR, n = 20) and small for gestational age (SGA, n = 15) by Doppler velocimetry and neonatal outcome. Controls (n = 69) were normally grown. Control maternal IGF-1 (r = 0.65, P < 0.0001) and IGFBP-3 (r = 0.46, P = 0.001) increased with advancing gestational age. In FGR cases, maternal IGF-1 was low (P = 0.0001) and IGFBP-1 was high (P = 0.03) and maternal IGF-2 was low in SGA (P = 0.005). In the SGA fetus, IGF-2 was low (P = 0.0009) and IGFBP-3 (P = 0.02) was high. In FGR, IGFBP-1 (P < 0.0001) and IGFBP-3 (P = 0.002) were both elevated. These data do not support the hypothesis that fetal IGF-1 deficiency is a common cause of FGR. Elevated binding proteins may lead to a relative deficiency of free IGF but changes in binding proteins may be secondary to metabolic changes. In FGR, maternal IGF-1 was low with high binding proteins, so this system may be important in controlling placental transfer.
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