Prenatal cannabinoid exposure and gene expression for neural adhesion molecule L1 in the fetal rat brain

2003 ◽  
Vol 147 (1-2) ◽  
pp. 201-207 ◽  
Author(s):  
Marı́a Gómez ◽  
Mariluz Hernández ◽  
Björn Johansson ◽  
Rosario de Miguel ◽  
José Antonio Ramos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Brain ◽  
Adhesion Molecule ◽  
Fetal Rat ◽  
Neural Adhesion Molecule ◽  
Fetal Rat Brain

Prenatal Δ9-tetrahydrocannabinol exposure modifies proenkephalin gene expression in the fetal rat brain: sex-dependent differences

2000 ◽  
Vol 120 (1) ◽  
pp. 77-81 ◽  
Author(s):  
Alberto Pérez-Rosado ◽  
Jorge Manzanares ◽  
Javier Fernández-Ruiz ◽  
José A Ramos
Keyword(s):  
Gene Expression ◽  
Rat Brain ◽  
Fetal Rat ◽  
Fetal Rat Brain

scholarly journals Lack of Action of Exogenously Administered T3 on the Fetal Rat Brain Despite Expression of the Monocarboxylate Transporter 8

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1713-1721 ◽  
Author(s):  
Carmen Grijota-Martínez ◽  
Diego Díez ◽  
Gabriella Morreale de Escobar ◽  
Juan Bernal ◽  
Beatriz Morte
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Rat Brain ◽  
Organic Anion ◽  
Fetal Brain ◽  
Monocarboxylate Transporter ◽  
Anion Transporter ◽  
Fetal Rat ◽  
Fetal Rat Brain

Abstract Mutations of the monocarboxylate transporter 8 gene (MCT8, SLC16A2) cause the Allan-Herndon-Dudley syndrome, an X-linked syndrome of severe intellectual deficit and neurological impairment. Mct8 transports thyroid hormones (T4 and T3), and the Allan-Herndon-Dudley syndrome is likely caused by lack of T3 transport to neurons during critical periods of fetal brain development. To evaluate the role of Mct8 in thyroid hormone action in the fetal brain we administered T4 or T3 to thyroidectomized pregnant dams treated with methyl-mercapto-imidazol to produce maternal and fetal hypothyroidism. Gene expression was then measured in the fetal cerebral cortex. T4 increased Camk4, Sema3c, and Slc7a3 expression, but T3 was without effect. To investigate the cause for the lack of T3 action we analyzed the expression of organic anion transport polypeptide (Oatp14, Slco1c1), a T4 transporter, and Mct8 (Slc16a2), a T4 and T3 transporter, by confocal microscopy. Both proteins were present in the brain capillaries forming the blood-brain barrier and in the epithelial cells of the choroid plexus forming the blood-cerebrospinal fluid barrier. It is concluded that T4 from the maternal compartment influences gene expression in the fetal cerebral cortex, possibly after transport via organic anion transporter polypeptide and/or Mct8, and conversion to T3 in the astrocytes. On the other hand, T3 does not reach the target neurons despite the presence of Mct8. The data indicate that T4, through local deiodination, provides most T3 in the fetal rat brain. The role of Mct8 as a T3 transporter in the fetal rat brain is therefore uncertain.

scholarly journals Acute Changes in Maternal Thyroid Hormone Induce Rapid and Transient Changes in Gene Expression in Fetal Rat Brain

2000 ◽  
Vol 20 (6) ◽  
pp. 2255-2265 ◽  
Author(s):  
Amy L. S. Dowling ◽  
Gabriel U. Martz ◽  
Jack L. Leonard ◽  
R. Thomas Zoeller
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Rat Brain ◽  
Fetal Rat ◽  
Maternal Thyroid ◽  
Acute Changes ◽  
Fetal Rat Brain

Development of Monoamine Oxidase and Aldehyde Dehydrogenase in Reaggregating Cultures of Fetal Rat Brain Cells

1989 ◽  
Vol 16 (3) ◽  
pp. 281-286
Author(s):  
Olof Tottmar ◽  
Maria Söderbäck ◽  
Anders Aspberg
Keyword(s):  
Monoamine Oxidase ◽  
Rat Brain ◽  
Aldehyde Dehydrogenase ◽  
Brain Cells ◽  
Mao B ◽  
Adult Rat ◽  
Fetal Rat ◽  
Adult Rat Brain ◽  
Mao A ◽  
Fetal Rat Brain

The development of monoamine oxidase (MAO) and aldehyde dehydrogenase (ALDH) in reaggregation cultures of fetal rat brain cells was compared with that of enzymatic markers for glial and neuronal cells. Only MAO-A was detected in the cultures during the first week, but, during the following three weeks, the activity of MAO-B increased more rapidly than that of MAO-A. The ratio MAO-A/MAO-B in four-week aggregates was close to that found in the adult rat brain. The activity of ALDH started to increase rapidly after 15 days, and the developmental pattern was intermediate to those of the glial and neuronal markers. The activity after four weeks was close to that found in the adult rat brain. Epidermal growth factor (EGF) caused a slight decrease in the activities of the low-Km ALDH (after four weeks) and the neuronal marker, choline acetyltransferase (after two weeks), whereas the other markers were not affected. By contrast, the activities of MAO-A and MAO-B were greatly increased during almost the entire culture period. It is suggested that this effect of EGF was the result of increased mitotic activity and/or biochemical differentiation of other cell types present in the cell aggregates, e.g. capillary endothelial cells.

scholarly journals Polychlorinated biphenyls (PCBs) exert thyroid hormone-like effects in the fetal rat brain but do not bind to thyroid hormone receptors.

2004 ◽  
Vol 112 (5) ◽  
pp. 516-523 ◽  
Author(s):  
Kelly J Gauger ◽  
Yoshihisa Kato ◽  
Koichi Haraguchi ◽  
Hans-Joachim Lehmler ◽  
Larry W Robertson ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Polychlorinated Biphenyls ◽  
Rat Brain ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors ◽  
Fetal Rat ◽  
Fetal Rat Brain
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