The development of the cerebral cortex in the embryonic mouse: An electron microscopic serial section analysis

1978 ◽  
Vol 179 (4) ◽  
pp. 795-830 ◽  
Author(s):  
Gregory M. Shoukimas ◽  
James W. Hinds
Keyword(s):  
Cerebral Cortex ◽  
Serial Section ◽  
Electron Microscopic ◽  
Embryonic Mouse ◽  
Section Analysis

Genetic control of dorsal-ventral identity in the telencephalon: opposing roles for Pax6 and Gsh2

Development ◽  
2000 ◽  
Vol 127 (20) ◽  
pp. 4361-4371 ◽  
Author(s):  
H. Toresson ◽  
S.S. Potter ◽  
K. Campbell
Keyword(s):  
Cerebral Cortex ◽  
Gene Function ◽  
Abnormal Development ◽  
Loss Of Function ◽  
Embryonic Mouse ◽  
Molecular Identity ◽  
Mouse Mutants ◽  
Germinal Zone ◽  
Genetic Mechanisms ◽  
Dlx Genes

We have examined the genetic mechanisms that regulate dorsal-ventral identity in the embryonic mouse telencephalon and, in particular, the specification of progenitors in the cerebral cortex and striatum. The respective roles of Pax6 and Gsh2 in cortical and striatal development were studied in single and double loss-of-function mouse mutants. Gsh2 gene function was found to be essential to maintain the molecular identity of early striatal progenitors and in its absence the ventral telencephalic regulatory genes Mash1 and Dlx are lost from most of the striatal germinal zone. In their place, the dorsal regulators, Pax6, neurogenin 1 and neurogenin 2 are found ectopically. Conversely, Pax6 is required to maintain the correct molecular identity of cortical progenitors. In its absence, neurogenins are lost from the cortical germinal zone and Gsh2, Mash1 and Dlx genes are found ectopically. These reciprocal alterations in cortical and striatal progenitor specification lead to the abnormal development of the cortex and striatum observed in Pax6 (small eye) and Gsh2 mutants, respectively. In support of this, double homozygous mutants for Pax6 and Gsh2 exhibit significant improvements in both cortical and striatal development compared with their respective single mutants. Taken together, these results demonstrate that Pax6 and Gsh2 govern cortical and striatal development by regulating genetically opposing programs that control the expression of each other as well as the regionally expressed developmental regulators Mash1, the neurogenins and Dlx genes in telencephalic progenitors.

scholarly journals The Expression and Distributions of ANP32A in the Developing Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Shanshan Wang ◽  
Yunliang Wang ◽  
Qingshan Lu ◽  
Xinshan Liu ◽  
Fuyu Wang ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Fetal Brain ◽  
Tissue Expression ◽  
Developing Brain ◽  
Adult Brain ◽  
Mammalian Brain ◽  
Dependent Manner ◽  
Growing Up ◽  
Embryonic Mouse ◽  
And Function

Acidic (leucine-rich) nuclear phosphoprotein 32 family, member A (ANP32A), has multiple functions involved in neuritogenesis, transcriptional regulation, and apoptosis. However, whether ANP32A has an effect on the mammalian developing brain is still in question. In this study, it was shown that brain was the organ that expressed the most abundant ANP32A by human multiple tissue expression (MTE) array. The distribution of ANP32A in the different adult brain areas was diverse dramatically, with high expression in cerebellum, temporal lobe, and cerebral cortex and with low expression in pons, medulla oblongata, and spinal cord. The expression of ANP32A was higher in the adult brain than in the fetal brain of not only humans but also mice in a time-dependent manner. ANP32A signals were dispersed accordantly in embryonic mouse brain. However, ANP32A was abundant in the granular layer of the cerebellum and the cerebral cortex when the mice were growing up, as well as in the Purkinje cells of the cerebellum. The variation of expression levels and distribution of ANP32A in the developing brain would imply that ANP32A may play an important role in mammalian brain development, especially in the differentiation and function of neurons in the cerebellum and the cerebral cortex.

scholarly journals In vitro formation of osteoclasts from long-term cultures of bone marrow mononuclear phagocytes.

1982 ◽  
Vol 156 (6) ◽  
pp. 1604-1614 ◽  
Author(s):  
E H Burger ◽  
J W Van der Meer ◽  
J S van de Gevel ◽  
J C Gribnau ◽  
G W Thesingh ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Electron Microscopic Examination ◽  
Osteoclast Formation ◽  
Mononuclear Phagocytes ◽  
Long Bone ◽  
Embryonic Liver ◽  
Blood Monocytes ◽  
Electron Microscopic ◽  
Embryonic Mouse

The origin of osteoclasts was studied in an in vitro model using organ cultures of periosteum-free embryonic mouse long-bone primordia, which were co-cultured with various cell populations. The bone rudiments were freed of their periosteum-perichondrium by collagenase treatment in a stage before cartilage erosion and osteoclast formation, and co-cultured for 7 d with either embryonic liver or mononuclear phagocytes from various sources. Light and electron microscopic examination of the cultures showed that mineralized matrix-resorbing osteoclasts developed only in bones co-cultured with embryonic liver or with cultured bone marrow mononuclear phagocytes but not when co-cultured with blood monocytes or resident or exudate peritoneal macrophages. Osteoclasts developed from the weakly adherent, but not from the strongly adherent cells of bone marrow cultures, whereas 1,000 rad irradiation destroyed the capacity of such cultures to form osteoclasts. In bone cultures to which no other cells were added, osteoclasts were virtually absent. Bone-resorbing activity of in vitro formed osteoclasts was demonstrated by 45Ca release studies. These studies demonstrate that osteoclasts develop from cells present in cultures of proliferating mononuclear phagocytes and that, at least in our system, monocytes and macrophages are unable to form osteoclasts. The most likely candidates for osteoclast precursor cells seem to be monoblasts and promonocytes.

Effect of maternal protein malnutrition on the developing cerebral cortex of mouse embryo: An electron microscopic study

1980 ◽  
Vol 68 (2) ◽  
pp. 228-239 ◽  
Author(s):  
Tsunekazu Yamano ◽  
Morimi Shimada ◽  
Syosaku Yamazaki ◽  
Masakatsu Goto ◽  
Noriaki Ohoya
Keyword(s):  
Cerebral Cortex ◽  
Microscopic Study ◽  
Electron Microscopic Study ◽  
Mouse Embryo ◽  
Protein Malnutrition ◽  
Electron Microscopic
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