scholarly journals GnRH Receptor Gene Expression in the Developing Rat Hippocampus: Transcriptional Regulation and Potential Roles in Neuronal Plasticity

Endocrinology ◽  
2010 ◽  
Vol 152 (2) ◽  
pp. 568-580 ◽  
Author(s):  
Anne-Laure Schang ◽  
Valérie Ngô-Muller ◽  
Christian Bleux ◽  
Anne Granger ◽  
Marie-Claude Chenut ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Neuronal Plasticity ◽  
Gnrh Receptor ◽  
Lateral Septum ◽  
Rat Hippocampus ◽  
Marker Genes ◽  
Mrna Levels ◽  
Primary Role ◽  
Placental Alkaline Phosphatase ◽  
Human Placental Alkaline Phosphatase

Abstract In the pituitary of mammals, the GnRH receptor (GnRHR) plays a primary role in the control of reproductive function. It is further expressed in the hippocampus, where its function, however, is not well defined. By quantitative RT-PCR analyses, we demonstrate herein that the onset of GnRHR gene (Gnrhr) expression in the rat hippocampus was unexpectedly delayed as compared to the pituitary and only occurred after birth. Using a previously described transgenic mouse model bearing the human placental alkaline phosphatase reporter gene under the control of the rat Gnrhr promoter, we established a positive correlation between the temporal pattern of Gnrhr mRNA levels and promoter activity in the hippocampal formation. The gradual appearance of human placental alkaline phosphatase transgene expression occurred simultaneously in the hippocampus and interconnected structures such as the lateral septum and the amygdala, coinciding with the establishment of hippocampo-septal projections. Analysis of transcription factors together with transient transfection assays in hippocampal neurons indicated that the combinatorial code governing the hippocampus-specific expression of the Gnrhr is distinct from the pituitary, likely involving transactivating factors such as NUR77, cyclic AMP response element binding protein, and Finkel-Biskis-Jinkins murine osteosarcoma virus oncogene homolog. A silencing transcription factor acting via the -3255/-1135 promoter region of the Gnrhr may be responsible for the transcriptional repression observed around birth. Finally, GnRH directly stimulated via activation of its receptor the expression of several marker genes of neuronal plasticity such as Egr1, synaptophysin, and spinophilin in hippocampal primary cultures, suggesting a role for GnRHR in neuronal plasticity. Further characterization of these mechanisms may help unravel important functions of GnRH/GnRHR signaling in the brain.

scholarly journals The Promoter of the Rat Gonadotropin-Releasing Hormone Receptor Gene Directs the Expression of the Human Placental Alkaline Phosphatase Reporter Gene in Gonadotrope Cells in the Anterior Pituitary Gland as well as in Multiple Extrapituitary Tissues

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 983-993 ◽  
Author(s):  
Anne Granger ◽  
Valérie Ngô-Muller ◽  
Christian Bleux ◽  
Céline Guigon ◽  
Hanna Pincas ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Reporter Gene ◽  
Transgene Expression ◽  
Pituitary Cells ◽  
Placental Alkaline Phosphatase ◽  
R Gene ◽  
Glycoprotein Hormone ◽  
Steroidogenic Factor 1 ◽  
Functional Sites ◽  
Human Placental Alkaline Phosphatase

Abstract Previous studies dealing with the mechanisms underlying the tissue-specific and regulated expression of the GnRH receptor (GnRH-R) gene led us to define several cis-acting regulatory sequences in the rat GnRH-R gene promoter. These include functional sites for steroidogenic factor 1, activator protein 1, and motifs related to GATA and LIM homeodomain response elements as demonstrated primarily in transient transfection assays in mouse gonadotrope-derived cell lines. To understand these mechanisms in more depth, we generated transgenic mice bearing the 3.3-kb rat GnRH-R promoter linked to the human placental alkaline phosphatase reporter gene. Here we show that the rat GnRH-R promoter drives the expression of the reporter gene in pituitary cells expressing the LHβ and/or FSHβ subunit but not in TSHβ- or GH-positive cells. Furthermore, the spatial and temporal pattern of the transgene expression during the development of the pituitary was compatible with that characterizing the emergence of the gonadotrope lineage. In particular, transgene expression is colocalized with the expression of the glycoprotein hormone α-subunit at embryonic day 13.5 and with that of steroidogenic factor 1 at later stages of pituitary development. Transgene expression was also found in specific brain areas, such as the lateral septum and the hippocampus. A single promoter is thus capable of directing transcription in highly diverse tissues, raising the question of the different combinations of transcription factors that lead to such a multiple, but nevertheless cell-specific, expressions of the GnRH-R gene.

Use of monoclonal antibodies to detect human placental alkaline phosphatase.

1983 ◽  
Vol 29 (1) ◽  
pp. 115-119 ◽  
Author(s):  
G De Groote ◽  
P De Waele ◽  
A Van de Voorde ◽  
M De Broe ◽  
W Fiers
Keyword(s):  
Monoclonal Antibody ◽  
Alkaline Phosphatase ◽  
Monoclonal Antibodies ◽  
Solid Phase ◽  
Enzymatic Reactions ◽  
Placental Alkaline Phosphatase ◽  
Human Placental Alkaline Phosphatase ◽  
Human Sera ◽  
Starch Gel ◽  
Alkaline Phosphatase Isoenzyme

Abstract Convenient, sensitive, and specific solid-phase immunoassays involving monoclonal antibody are described for the determination of human placental alkaline phosphatase (hPLAP). An endogenous enzyme immunoassay combined the specificity of the immunological and the enzymatic reactions. Alternatively, a solid-phase "sandwich" radioimmunoassay involving immobilized polyclonal rabbit anti-hPLAP in combination with iodinated monoclonal antibody provided some additional advantages. Both tests can be used to detect hPLAP from various sources, e.g., in human sera during pregnancy or as a tumor marker. The radioimmunoassay detected an increase in hPLAP at nine weeks of gestation. We discuss the use of monoclonal antibodies for the differentiation of different alkaline phosphatase isoenzyme types by electrophoresis on starch gel.

scholarly journals Differential fate of multipotent and lineage-restricted neural precursors following transplantation into the adult CNS

2004 ◽  
Vol 1 (2) ◽  
pp. 113-126 ◽  
Author(s):  
ANGELO C. LEPORE ◽  
STEVEN S.W. HAN ◽  
CARLA J. TYLER-POLSZ ◽  
JINGLI CAI ◽  
MAHENDRA S. RAO ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Alkaline Phosphatase ◽  
Placental Alkaline Phosphatase ◽  
Injured Spinal Cord ◽  
Transgenic Rats ◽  
Neuronal Markers ◽  
Multipotent Cells ◽  
Human Placental Alkaline Phosphatase ◽  
Adult Hippocampus ◽  
Developing Spinal Cord

Multiple classes of precursor cells have been isolated and characterized from the developing spinal cord including multipotent neuroepithelial (NEP) stem cells and lineage-restricted precursors for neurons (NRPs) and glia (GRPs). We have compared the survival, differentiation and integration of multipotent NEP cells with lineage-restricted NRPs and GRPs using cells isolated from transgenic rats that express the human placental alkaline phosphatase gene. Our results demonstrate that grafted NEP cells survive poorly, with no cells observed 3 days after transplant in the adult hippocampus, striatum and spinal cord, indicating that most CNS regions are not compatible with transplants of multipotent cells derived from fetal CNS. By contrast, at 3 weeks and 5 weeks post-engraftment, lineage-restricted precursors showed selective migration along white-matter tracts and robust survival in all three CNS regions. The grafted precursors expressed the mature neuronal markers NeuN and MAP2, the astrocytic marker GFAP, the oligodendrocytic markers RIP, NG2 and Sox-10, and the synaptic marker synaptophysin. Similar behavior was observed when these precursors were transplanted into the injured spinal cord. Predifferentiated, multipotent NEP cells also survive and integrate, which indicates that lineage-restricted CNS precursors are well suited for transplantation into the adult CNS and provide a promising cellular replacement candidate.

Sign in / Sign up

Export Citation Format

Share Document