scholarly journals Inhibited maturation of astrocytes caused by maternal n-3 polyunsaturated fatty acid intake deficiency hinders the development of brain glial cells in neonatal rats

2021 ◽  
pp. 1-26
Author(s):  
Tatsuro Yamamoto ◽  
Ayako Yamamoto ◽  
Hiroki Tanabe ◽  
Naomichi Nishimura
Keyword(s):  
Glial Cells ◽  
Lipid Binding ◽  
Brain Cell ◽  
Neonatal Rats ◽  
Pufa Intake ◽  
Radial Glial Cells ◽  
Somatosensory Cortices ◽  
Radial Glial ◽  
The Impact ◽  
The Brain

Abstract The brain is rich in long chain polyunsaturated fatty acids (PUFAs), which play an essential role in its development and functions. Here we examined the impact of maternal n-3 PUFA intake deficiency during gestation and lactation on the development of glial cells in the pup’s developing cerebral cortex. In addition, using myelination as indicator and the anti-myelin basic protein (MBP) as measurement to establish the relationship between the number of glial fibrillary acidic protein (GFAP)-positive cells and the development of oligodendrocytes, we determined the myelination state of the somatosensory cortex at day 14 postnatal. Rat dams were fed either a control (Cont) or an n-3 PUFA-deficient (Def) diet for 60 days (acclimatisation :14 days; gestation: 21 days; lactation:21 days). Pups lactated from dams throughout the experiment. The distribution pattern of astrocytes in pups on day 7 postnatal was immunohistochemically analysed using GFAP and brain lipid binding protein (BLBP) as markers for mature astrocytes and astrocyte-specific radial glial cells, respectively. It was observed that, when compared with Cont pups, GFAP-positive cells decreased, BLBP-positive cells increased and myelinated structures were sparser in the somatosensory cortices of Def pups. In the open field test on day 21 postnatal, behavioural parameters did not differ between groups. Our results indicated that inhibited maturation of astrocytes caused by maternal n-3 PUFA deficiency hindered the development of brain glial cells of neonatal rats and hence, maternal n-3 PUFA intake during the gestation and lactation periods may have been crucial for the brain cell composition of pups.

scholarly journals ANO1/TMEM16A regulates process maturation in radial glial cells in the developing brain

2019 ◽  
Vol 116 (25) ◽  
pp. 12494-12499 ◽  
Author(s):  
Gyu-Sang Hong ◽  
Sung Hoon Lee ◽  
Byeongjun Lee ◽  
Jae Hyouk Choi ◽  
Soo-Jin Oh ◽  
...  
Keyword(s):  
Glial Cells ◽  
Ventricular Zone ◽  
Trophic Factors ◽  
Early Developmental Stage ◽  
Anoctamin 1 ◽  
Radial Glial Cells ◽  
Radial Glial ◽  
Early Developmental ◽  
The Brain ◽  
Deficient Mice

Neural stem cells (NSCs) are primary progenitor cells in the early developmental stage in the brain that initiate a diverse lineage of differentiated neurons and glia. Radial glial cells (RGCs), a type of neural stem cell in the ventricular zone, are essential for nurturing and delivering new immature neurons to the appropriate cortical target layers. Here we report that Anoctamin 1 (ANO1)/TMEM16A, a Ca2+-activated chloride channel, mediates the Ca2+-dependent process extension of RGCs. ANO1 is highly expressed and functionally active in RGCs of the mouse embryonic ventricular zone. Knockdown of ANO1 suppresses RGC process extension and protrusions, whereas ANO1 overexpression stimulates process extension. Among various trophic factors, brain-derived neurotrophic factor (BDNF) activates ANO1, which is required for BDNF-induced process extension in RGCs. More importantly, Ano1-deficient mice exhibited disrupted cortical layers and reduced cortical thickness. We thus conclude that the regulation of RGC process extension by ANO1 contributes to the normal formation of mouse embryonic brain.

scholarly journals Expression of Aromatase in Radial Glial Cells in the Brain of the Japanese Eel Provides Insight into the Evolution of the cyp191a Gene in Actinopterygians

PLoS ONE ◽  
2012 ◽  
Vol 7 (9) ◽  
pp. e44750 ◽  
Author(s):  
Shan-Ru Jeng ◽  
Wen-Shiun Yueh ◽  
Yi-Ting Pen ◽  
Marie-Madeleine Gueguen ◽  
Jérémy Pasquier ◽  
...  
Keyword(s):  
Glial Cells ◽  
Japanese Eel ◽  
Radial Glial Cells ◽  
Radial Glial ◽  
The Brain ◽  
Insight Into

Cxcr4 and Cxcl12 expression in radial glial cells of the brain of adult zebrafish

2010 ◽  
Vol 518 (24) ◽  
pp. 4855-4876 ◽  
Author(s):  
Nicolas Diotel ◽  
Colette Vaillant ◽  
Marie-Madeleine Gueguen ◽  
Svetlana Mironov ◽  
Isabelle Anglade ◽  
...  
Keyword(s):  
Glial Cells ◽  
Adult Zebrafish ◽  
Cxcl12 Expression ◽  
Radial Glial Cells ◽  
Radial Glial ◽  
The Brain

Role of GGF/neuregulin signaling in interactions between migrating neurons and radial glia in the developing cerebral cortex

Development ◽  
1997 ◽  
Vol 124 (18) ◽  
pp. 3501-3510 ◽  
Author(s):  
E.S. Anton ◽  
M.A. Marchionni ◽  
K.F. Lee ◽  
P. Rakic
Keyword(s):  
Cerebral Cortex ◽  
Glial Cells ◽  
Neuronal Migration ◽  
Lipid Binding ◽  
Soluble Form ◽  
Dependent Manner ◽  
Radial Glial Cells ◽  
Glial Development ◽  
Radial Glial

During neuronal migration to the developing cerebral cortex, neurons regulate radial glial cell function and radial glial cells, in turn, support neuronal cell migration and differentiation. To study how migrating neurons and radial glial cells influence each others' function in the developing cerebral cortex, we examined the role of glial growth factor (a soluble form of neuregulin), in neuron-radial glial interactions. Here, we show that GGF is expressed by migrating cortical neurons and promotes their migration along radial glial fibers. Concurrently, GGF also promotes the maintenance and elongation of radial glial cells, which are essential for guiding neuronal migration to the cortex. In the absence of GGF signaling via erbB2 receptors, radial glial development is abnormal. Furthermore, GGF's regulation of radial glial development is mediated in part by brain lipid-binding protein (BLBP), a neuronally induced, radial glial molecule, previously shown to be essential for the establishment and maintenance of radial glial fiber system. The ability of GGF to influence both neuronal migration and radial glial development in a mutually dependent manner suggests that it functions as a mediator of interactions between migrating neurons and radial glial cells in the developing cerebral cortex.

Differentiating neurons activate transcription of the brain lipid-binding protein gene in radial glia through a novel regulatory element

Development ◽  
1995 ◽  
Vol 121 (6) ◽  
pp. 1719-1730 ◽  
Author(s):  
L. Feng ◽  
N. Heintz
Keyword(s):  
Glial Cells ◽  
Radial Glia ◽  
Lipid Binding ◽  
Radial Glial Cell ◽  
Specific Element ◽  
Radial Glial ◽  
And Migration ◽  
The Brain

Formation and maintenance of a radial glial scaffold is fundamental for development of the vertebrate central nervous system. In mammals, radial glia arise in the neuroepithelium immediately prior to differentiation and migration of neurons away from the ventricular zones, and they are maintained until neuronal migration subsides. We have previously shown that expression of the brain lipid-binding protein (BLBP) in radial glia throughout the developing CNS is strictly correlated with the differentiation and migration of neurons upon these cells, and that BLBP function is required to maintain differentiation of primary cerebellar glial cells in vitro (Feng, L., Hatten, M. E. and Heintz, N. (1994). Neuron 12, 895–908). In this study, we demonstrate that BLBP transcription in vivo involves multiple regulatory elements, and that the dynamic temporal and spatial pattern of BLBP expression in radial and Bergmann glial cells throughout the developing CNS is programmed by a single radial glial cell-specific element (RGE). Furthermore, we demonstrate that BLBP expression in primary cerebellar glial cells requires coculture with differentiating neurons, and that this induction is regulated by the radial glia-specific element. The fact that transcription of BLBP in response to neurons in vitro and its dynamic regulation in radial glia throughout the CNS in vivo are both controlled by the RGE provides the first direct evidence supporting a role for differentiating neurons in the epigenetic regulation of radial glial cell function in vivo.

Mutations affecting neurogenesis and brain morphology in the zebrafish, Danio rerio

Development ◽  
1996 ◽  
Vol 123 (1) ◽  
pp. 205-216 ◽  
Author(s):  
Y.J. Jiang ◽  
M. Brand ◽  
C.P. Heisenberg ◽  
D. Beuchle ◽  
M. Furutani-Seiki ◽  
...  
Keyword(s):  
Cell Types ◽  
Brain Morphology ◽  
Abnormal Development ◽  
Radial Glial Cells ◽  
Complementation Groups ◽  
Early Neurogenesis ◽  
Radial Glial ◽  
General Organization ◽  
Neurogenic Mutants ◽  
The Brain

In a screen for embryonic mutants in the zebrafish a large number of mutants were isolated with abnormal brain morphology. We describe here 26 mutants in 13 complementation groups that show abnormal development of large regions of the brain. Early neurogenesis is affected in white tail (wit). During segmentation stages, homozygous wit embryos display an irregularly formed neural keel, particularly in the hindbrain. Using a variety of molecular markers, a severe increase in the number of various early differentiating neurons can be demonstrated. In contrast, late differentiating neurons, radial glial cells and some nonneural cell types, such as the neural crest-derived melanoblasts, are much reduced. Somitogenesis appears delayed. In addition, very reduced numbers of melanophores are present posterior to the mid-trunk. The wit phenotype is reminiscent of neurogenic mutants in Drosophila, such as Notch or Delta. In mutant parachute (pac) embryos the general organization of the hindbrain is disturbed and many rounded cells accumulate loosely in the hindbrain and midbrain ventricles. Mutants in a group of 6 genes, snakehead(snk), natter (nat), otter (ott), fullbrain (ful), viper (vip) and white snake (wis) develop collapsed brain ventricles, before showing signs of general degeneration. atlantis (atl), big head (bid), wicked brain (win), scabland (sbd) and eisspalte (ele) mutants have different malformation of the brain folds. Some of them have transient phenotypes, and mutant individuals may grow up to adults.

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