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Quick Scroll Q 15 brain lipid binding protein 10.01.03 (5 years ago) #1

Brain lipid binding protein is expressed by which of the following
Mature astrocytes
Oligodendrcytes
Purkinje cells
pyramidal neurons




oligodendrocytes are definitely out.......mature astrocytes sounds like a trap but seems the best choice..


heres what i found on the net
Gomori-positive (GP) astrocytes are a subset of brain astrocytes with highly stained cytoplasmic granules that arise from the degradation of mitochondria. The GP granules of these astrocytes are most prominent in the arcuate nucleus of the hypothalamus, but can also be detected in the olfactory bulbs, hippocampus, habenula, and other selected brain regions. The cause and functional effects of this mitochondrial Pathology in these glia are not yet known with certainty. In other tissues, mitochondrial dysfunction is associated with elevations in cytoplasmic lipids and lipid-binding proteins, due to impaired mitochondrial oxidation of lipids. To see if GP astrocytic mitochondrial Pathology is also associated with an elevation in lipid binding proteins, rat brain sections were stained for brain fatty acid binding protein (B-FABP), using immunocytochemistry. Astrocytes immunoreactive for B-FABP were much more abundant in brain regions enriched in GP astrocytes than in other brain regions. Semi-thin sections revealed that astrocytic B-FABP immunoreactivity was often, but not always, associated with GP cytoplasmic granules. These data suggest that GP astrocytes have an unusual lipid metabolism, which may relate to degenerative processes occurring in the selected brain regions that contain GP astrocytes.


Fatty acid binding proteins (FABPs) are a multigene family of small intracellular proteins that bind hydrophobic ligands. In this report we describe the cloning and expression pattern of a novel member of this gene family that is specifically expressed in the developing and adult nervous system and thus was designated brain (B)-FABP. B-FABP is closely related to heart (H)-FABP with 67% amino acid identity. B-FABP expression was first detected at mouse embryonic day 10 in neuroepithelial cells and its pattern correlates with early neuronal differentiation. Upon further development, B-FABP was confined to radial glial cells and immature astrocytes. B-FABP mRNA and protein were found in glial cells of the peripheral nervous system such as satellite cells of spinal and cranial ganglia and ensheathing cells of the olfactory nerve layer from as early as embryonic day 11 until adulthood. In the adult mouse brain, B-FABP was found in the glia limitans, in radial glial cells of the hippocampal dentate gyrus and Bergman glial cells. These findings suggest a function of B-FABP during neurogenesis or neuronal migration in the developing nervous system. The partially overlapping expression pattern with that of cellular retinoid binding proteins suggests that B-FABP is involved in the metabolism of a so far unknown hydrophobic ligand with potential morphogenic activity during CNS development

cell-specific regulation of the brain lipid-binding protein (BLBP) gene in Bergmann glia, astrocytes, and migrating granule cells is conferred by 1.7 kb of 5' flanking sequences and that Purkinje cell-specific expression of the calbindin D28k gene in cerebellar cortex can be achieved with 1.1 kb of flanking DNA

Blbp, 10-Fdh
Brain lipid-binding protein (Blbp, GC9) and 10-formyltetrahydrofolate dehydrogenase (10-Fdh, GC44) were first identified in our lab in the context of a large screen for dynamically regulated genes that mark specific cerebellar cell types. Subsequent studies confirmed that these genes are coexpressed in developing Bergmann glia, and in radial glial cells at many sites in the developing CNS. Our lab also showed that Blbp is a carrier for a docosahexanoic acid, an essential fatty acid that is enriched in the CNS and critical for its development. Studies in other laboratories have demonstrated that Blbp is also expressed in neural stem cells. In the context of studies of the transcriptional regulation of Blbp in vivo, we have recently discovered that the Blbp gene is transcribed in a specific subset of neural stem cells and that the regulatory elements controlling its transcription in these cells are distinct from those important for Blbp regulation in Bergmann glia. We believe that further lineage-tracing studies with Blbp will provide access to a previously unidentified subpopulation of neural stem cells.


Neural Differentiation in the Developing Cerebellum. The differentiation of specific cell types in the cerebellum requires complex molecular subprograms that provide distinct functions for differentiating cells. Many of these functions are generally important for neuronal differentiation, being shared by different cell types to accomplish a given task. One example of such a subroutine is glial guided neuronal migration, which is necessary for the translocation of many different neurons from their place of birth in the neural tube to the eventual sites of their maturation in the developing brain. During the past year, studies in our laboratory and in collaboration with Dr. Mary E. Hatten of The Rockefeller University, have yielded important insights into this problem. Previous studies in our laboratories have established that the brain lipid binding protein (BLBP) is critical for the differentiation of primary glial cells in vitro, and that this protein is produced in radial glial cells only during the period of neuronal migration. During the past year, we have identified a transcriptional regulatory element that is critical for the regulation of BLBP transcription in radial cells in vivo, and have shown that this same element can program expression of the BLBP gene in glial cells in primary culture only if differentiating neurons are present. These results suggest that the dynamic regulation of BLBP expression in vivo, and hence radial glial function, is a consequence of neuron:glial interactions that maintain glial differentiation. Additional studies have led to the cloning of the mouse astrotactin gene, to its identification as a novel neuron specific signaling molecule, and to the demonstration that it is involved in migration and assembly of differentiating neurons into cortical structures of the mammalian brain. This work, and additional studies of other molecules important for cellular differentiation in the developing cerebellum, remain an important priority in the laboratory. (These studies are partially supported by the National Institutes of Health
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