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Choroid Plexus (choroid + plexus)
Terms modified by Choroid Plexus Selected AbstractsGlutamate Export at the Choroid Plexus in Health, Thiamin Deficiency, and Ethanol Intoxication: Review and HypothesisALCOHOLISM, Issue 8 2008Peter F. Nixon Introduction:, The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:, Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin-deficient glucose oxidation. Results:, The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should ,-ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin-deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria-rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke's encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:, Impairment of the CP by ethanol intoxication and by thiamin-deficient carbohydrate metabolism has a common, rational explanation that can guide future research. [source] Multiple sites of L-histidine decarboxylase expression in mouse suggest novel developmental functions for histamineDEVELOPMENTAL DYNAMICS, Issue 1 2001Kaj Karlstedt Abstract Histamine mediates many types of physiologic signals in multicellular organisms. To clarify the developmental role of histamine, we have examined the developmental expression of L-histidine decarboxylase (HDC) mRNA and the production of histamine during mouse development. The predominant expression of HDC in mouse development was seen in mast cells. The HDC expression was evident from embryonal day 13 (Ed13) until birth, and the mast cells were seen in most peripheral tissues. Several novel sites with a prominent HDC mRNA expression were revealed. In the brain, the choroid plexus showed HDC expression at Ed14 and the raphe neurons at Ed15. Close to the parturition, at Ed19, the neurons in the tuberomammillary (TM) area and the ventricular neuroepithelia also displayed a clear HDC mRNA expression and histamine immunoreactivity (HA-ir). From Ed14 until birth, the olfactory and nasopharyngeal epithelia showed an intense HDC mRNA expression and HA-ir. In the olfactory epithelia, the olfactory receptor neurons (ORN) were shown to have very prominent histamine immunoreactivity. The bipolar nerve cells in the epithelium extended both to the epithelial surface and into the subepithelial layers to be collected into thick nerve bundles extending caudally toward the olfactory bulbs. Also, in the nasopharynx, an extensive subepithelial network of histamine-immunoreactive nerve fibers were seen. Furthermore, in the peripheral tissues, the degenerating mesonephros (Ed14) and the convoluted tubules in the developing kidneys (Ed15) showed HDC expression, as did the prostate gland (Ed15). In adult mouse brain, the HDC expression resembled the neuronal pattern observed in rat brain. The expression was restricted to the TM area in the ventral hypothalamus, with the main expression in the five TM subgroups called E1,E5. A distinct mouse HDC mRNA expression was also seen in the ependymal wall of the third ventricle, which has not been reported in the rat. The tissue- and cell-specific expression patterns of HDC and histamine presented in this work indicate that histamine could have cell guidance or regulatory roles in development. © 2001 Wiley-Liss, Inc. [source] Expression and localization of P2 nucleotide receptor subtypes during development of the lateral ventricular choroid plexus of the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2007P. A. Johansson Abstract The choroid plexuses secrete cerebrospinal fluid (CSF) and regulate the brain's internal environment via the blood,CSF barrier. The permeability properties of the blood,CSF interface have been studied previously in adult and immature brains, however, little is known about the development of CSF secretion and its modulation. ATP influences secretion in other epithelia via ionotropic P2X or metabotropic P2Y receptors. P2 receptors have frequently been found to be down-regulated in the postnatal period, suggesting a developmental role for purinergic and pyrimidine signalling. The present study investigated the expression of P2 receptors in lateral ventricular choroid plexus in relation to recent studies of aquaporin-1 expression and rapid expansion of the lateral ventricles in rat embryos. In the present study mRNAs for all known mammalian nucleotide receptor subtypes, except P2X7, were identified from as early as E15. P2X7 mRNA was detected from E18. Indications of differential expression patterns were observed for the different subtypes during development: an apparent increase in expression for P2Y2 and P2X7, a decline in P2X1-2,4, no detectable difference in expression levels for P2X6 and P2Y12-13 and transient expression peaks for P2X3,5 and P2Y1,4,6,14. P2X4,5,7 and P2Y1,4 receptor proteins were detected immunohistochemically in the choroidal epithelium from early in development (E15 or E18). Their differing developmental profiles suggest specific roles in the development of CSF secretion that may have particular relevance for the rapid expansion of the ventricles that occurs in the embryo. P2X5 and P2Y6 were also detected in the developing neuropendyma from P0 and P9, respectively. [source] Aquaporin 4 changes in rat brain with severe hydrocephalusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2006Xiaoyan Mao Abstract Hydrocephalus is characterized by impaired cerebrospinal fluid (CSF) flow with enlargement of the ventricular cavities of the brain and progressive damage to surrounding tissue. Bulk water movement is altered in these brains. We hypothesized that increased expression of aquaporins, which are water-permeable channel proteins, would occur in these brains to facilitate water shifts. We used quantitative (real-time) RT-PCR, Western blotting and immunohistochemistry to evaluate the brain expression of aquaporins (AQP) 1, 4, and 9 mRNA and protein in Sprague,Dawley rats rendered hydrocephalic by injection of kaolin into cistern magna. AQP4 mRNA was significantly up-regulated in parietal cerebrum and hippocampus 4 weeks and 9 months after induction of hydrocephalus (P < 0.05). Although Western blot analysis showed no significant change, there was more intense perivascular AQP4 immunoreactivity in cerebrum of hydrocephalic brains at 3,4 weeks after induction. We did not detect mRNA or protein changes in AQP1 (located in choroid plexus) or AQP9 (located in select neuron populations). Kir4.1, a potassium channel protein linked to water flux, exhibited enhanced immunoreactivity in the cerebral cortex of hydrocephalic rats; the perineuronal distribution was entirely different from that of AQP4. These results suggest that brain AQP4 up-regulation might be a compensatory response to maintain water homeostasis in hydrocephalus. [source] BMP and LIF signaling coordinately regulate lineage restriction of radial glia in the developing forebrainGLIA, Issue 1 2007Hedong Li Abstract The earliest radial glia are neural stem cells that guide neural cell migration away from ventricular zones. Subsequently, radial glia become lineage restricted during development before they differentiate into more mature cell types in the CNS. We have previously shown that subpopulations of radial glial cells express markers for glial and neuronal restricted precursors (GRPs and NRPs) in expression patterns that are temporally and spatially regulated during CNS development. To characterize further the mechanism of this regulation in rat forebrain, we tested whether secreted factors that are present during development effect lineage restriction of radial glia. We show here that in radial glial cultures LIF/CNTF up-regulates, whereas BMP2 down-regulates GRP antigens recognized by monoclonal antibodies A2B5/4D4. These activities combined with secretion of BMPs dorsally and LIF/CNTF from the choroid plexus provide an explanation for the graded distribution pattern of A2B5/4D4 in dorso-lateral ventricular regions in vivo. The regulation by LIF/CNTF of A2B5/4D4 is mediated through the JAK-STAT pathway. BMP2 promotes expression on radial glial cells of the NRP marker polysialic acid most likely by regulating N-CAM expression itself, as well as at least one polysialyl transferase responsible for synthesis of polysialic acid on N-CAM. Taken together, these results suggest that generation of lineage-restricted precursors is coordinately regulated by gradients of the secreted factors BMPs and LIF/CNTF during development of dorsal forebrain. © 2006 Wiley-Liss, Inc. [source] Temporal expression changes during differentiation of neural stem cells derived from mouse embryonic stem cellJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2004Joon-Ik Ahn Abstract Temporal analysis in gene expression during differentiation of neural stem cells (NSCs) was performed by using in-house microarrays composed of 10,368 genes. The changes in mRNA level were measured during differentiation day 1, 2, 3, 6, 12, and 15. Out of 10,368 genes analyzed, 259 genes were up-regulated or down-regulated by 2-fold or more at least at one time-point during differentiation, and were classified into six clusters based on their expression patterns by K-means clustering. Clusters characterized by gradual increase have large numbers of genes involved in transport and cell adhesion; those which showed gradual decrease have much of genes in nucleic acid metabolism, cell cycle, transcription factor, and RNA processing. In situ hybridization (ISH) validated microarray data and it also showed that Fox M1, cyclin D2, and CDK4 were highly expressed in CNS germinal zones and ectonucleotide pyrophosphatase/phosphodiesterase 2 (Enpp2) was highly expressed in choroid plexus where stem/progenitor cells are possibly located. Together, this clustering analysis of expression patterns of functionally classified genes may give insight into understanding of CNS development and mechanisms of NSCs proliferation and differentiation. © 2004 Wiley-Liss, Inc. [source] REVIEW: Vitamin transport and homeostasis in mammalian brain: focus on Vitamins B and EJOURNAL OF NEUROCHEMISTRY, Issue 2 2007Reynold Spector Abstract With the application of genetic and molecular biology techniques, there has been substantial progress in understanding how vitamins are transferred across the mammalian blood,brain barrier and choroid plexus into brain and CSF and how vitamin homeostasis in brain is achieved. In most cases (with the exception of the sodium-dependent multivitamin transporter for biotin, pantothenic acid, and lipoic acid), the vitamins are transported by separate carriers through the blood,brain barrier or choroid plexus. Then the vitamins are accumulated by brain cells by separate, specialized systems. This review focuses on six vitamins (B1, B3, B6, pantothenic acid, biotin, and E) and the newer genetic information including relevant ,knockdown' or ,knockout' models in mice and humans. The overall objective is to integrate this newer information with previous physiological and biochemical observations to achieve a better understanding of vitamin transport and homeostasis in brain. This is especially important in view of the newly described non-cofactor vitamin roles in brain (e.g. of B1, B3, B6, and E) and the potential roles of vitamins in the therapy of brain disorders. [source] Distinct spatio-temporal expression of ABCA and ABCG transporters in the developing and adult mouse brainJOURNAL OF NEUROCHEMISTRY, Issue 1 2005Masanori Tachikawa Abstract Using in situ hybridization for the mouse brain, we analyzed developmental changes in gene expression for the ATP-binding cassette (ABC) transporter subfamilies ABCA1,4 and 7, and ABCG1, 2, 4, 5 and 8. In the embryonic brains, ABCA1 and A7 were highly expressed in the ventricular (or germinal) zone, whereas ABCA2, A3 and G4 were enriched in the mantle (or differentiating) zone. At the postnatal stages, ABCA1 was detected in both the gray and white matter and in the choroid plexus. On the other hand, ABCA2, A3 and A7 were distributed in the gray matter. In addition, marked up-regulation of ABCA2 occurred in the white matter at 14 days-of-age when various myelin protein genes are known to be up-regulated. In marked contrast, ABCA4 was selective to the choroid plexus throughout development. ABCG1 was expressed in both the gray and white matters, whereas ABCG4 was confined to the gray matter. ABCG2 was diffusely and weakly detected throughout the brain at all stages examined. Immunohistochemistry of ABCG2 showed its preferential expression on the luminal membrane of brain capillaries. Expression signals for ABCG5 and G8 were barely detected at any stages. The distinct spatio-temporal expressions of individual ABCA and G transporters may reflect their distinct cellular expressions in the developing and adult brains, presumably, to regulate and maintain lipid homeostasis in the brain. [source] Circulating cell wall components derived from gram-negative, not gram-positive, bacteria cause a profound induction of the gene-encoding Toll-like receptor 2 in the CNSJOURNAL OF NEUROCHEMISTRY, Issue 3 2001Nathalie Laflamme The recent characterization of human homologs of Toll may be the missing link for the transduction events leading to nuclear factor-,B (NF-,B) activity and proinflammatory gene transcription during innate immune response. Mammalian cells may express as many as 10 distinct Toll-like receptors (TLRs), although TLR2 is a key receptor for recognizing cell wall components of Gram-positive bacteria. The present study investigated the effects of circulating bacterial cell wall components on the expression of the gene-encoding TLR2 across the mouse brain. Surprisingly, while Gram-negative components caused a robust increase in TLR2 transcription within the cerebral tissue, peptidoglycan (PGN) and lipoteichoic acid (LTA), either alone or combined, failed to modulate the receptor transcript. Indeed, the mRNA levels for TLR2 in the choroid plexus and few other regions of the brain remained similar between vehicle-, LTA-, PGN-, and LTA/PGN-administered mice at all the times evaluated (i.e. 30 min to 24 h post-intraperitoneal injection). This contrasts with the profound de novo expression of TLR2 following a single systemic injection of the lipopolysaccharide (LPS). The signal was first detected in regions devoid of blood,brain barrier and few blood vessels and microcapillaries. A second wave of TLR2 expression was also detected from these structures to their surrounding parenchymal cells that stained for a microglial marker iba1. The rapid induction of I,B, (index of NF-,B activity) and up-regulation of the adaptor protein MyD88 suggest that LPS-induced TLR2 transcription may be dependent on the NF-,B pathway. These data provide the evidence that TLR2 is not only present in the brain, but its encoding gene is regulated by cell wall components derived from Gram-negative, not Gram-positive, bacteria. The robust wave of TLR2-expressing microglial cells may have a determinant impact on the innate immune response that occurs in the brain during systemic infection by Gram-negative, not Gram-positive, bacteria. [source] Region-Specific Expression and Hormonal Regulation of the First Exon Variants of Rat Prolactin Receptor mRNA in Rat Brain and Anterior Pituitary GlandJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2007H. Nogami Recent studies have revealed the occurrence of five first exon variants of the rat prolactin receptor mRNA, suggesting that multiple promoters direct prolactin receptor transcription in response to different regulatory factors. In the present study, regional expression of these first exon variants, as well as two prolactin receptor subtypes generated by alternative splicing, was examined in the brains and anterior pituitary glands of female rats. Expression of the long-form was detected in the choroid plexus, hypothalamus, hippocampus, cerebral cortex and anterior pituitary gland, whereas the short form was detected only in the choroid plexus. E1-3 mRNA, a first exon variant, was detected in the choroid plexus, hypothalamus, and anterior pituitary gland, whereas E1-4 was detected only in the choroid plexus. Other variants were not detectable by the polymerase chain reaction protocol employed in this study. Ovariectomy increased the short form in the choroid plexus and the E1-3 expression in the choroid plexus and pituitary gland, but changes in the long-form and E1-4 expression were minimal. Replacement of oestrogens and prolactin suggest that oestrogens down-regulate E1-3 expression in the choroid plexus and pituitary gland, and that the negative effect of oestrogen is mediated by prolactin in the pituitary gland. The present results revealed the region-specific promoter usage in prolactin receptor mRNA transcription, as well as the involvement of oestrogens in the regulation of E1-3 mRNA expression in the brain and pituitary gland. [source] Regional and cellular distribution of mitochondrial ferritin in the mouse brainJOURNAL OF NEUROSCIENCE RESEARCH, Issue 14 2010Amanda M. Snyder Abstract Iron and mitochondrial dysfunction are important in many neurodegenerative diseases. Several iron transport proteins have been identified that are associated with mitochondria, most recently mitochondrial ferritin. Here we describe the cellular distribution of mitochondrial ferritin in multiple regions of the brain in C57/BL6 mice. Mitochondrial ferritin was found in all regions of the brain, although staining intensity varied between regions. Mitochondrial ferritin was detected throughout the layers of cerebral cortex and in the cerebellum, hippocampus, striatum, choroid plexus, and ependymal cells. The cell type in the brain that stains most prominently for mitochondrial ferritin is neuronal, but oligodendrocytes also stain strongly in both gray matter and in white matter tracts. Mice deficient in H-ferritin do not differ in the mitochondrial ferritin staining pattern or intensity compared with C57/BL6 mice, suggesting that there is no compensatory expression of these proteins. In addition, by using inbred mouse strains with differing levels of iron content, we have shown that regional brain iron content does not affect expression of mitochondria ferritin. The expression of mitochondria ferritin appears to be more influenced by mitochondrial density. Indeed, at an intracellular level, mitochondrial ferritin immunoreaction product is strongest where mitochondrial density is high, as seen in the ependymal cells. Given the importance and relationship between iron and mitochondrial activity, understanding the role of mitochondrial ferritin can be expected to contribute to our knowledge of mitochondrial dysfunction and neurodegenerative disease. © 2010 Wiley-Liss, Inc. [source] Amphiregulin is a mitogen for adult neural stem cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2002Anna Falk Abstract Neurons are continuously generated from stem cells in the hippocampus and along the lateral ventricles in the adult brain. Neural stem cells can be propagated in vitro in the presence of epidermal growth factor (EGF) or fibroblast growth factor-2. We report here that amphiregulin, a growth factor related to EGF, is a mitogen for adult mouse neural stem cells in vitro and displays potency similar to that of EGF. Neural stem cell cultures can be initiated and the cells propagated as efficiently in the presence of amphiregulin only as with EGF. Furthermore, we show that amphiregulin is expressed in the choroid plexus of the ventricular system and in the hippocampus in the adult brain, suggesting that amphiregulin may participate in the regulation of neural stem cell proliferation and neurogenesis in the adult brain. © 2002 Wiley-Liss, Inc. [source] Glutamate Export at the Choroid Plexus in Health, Thiamin Deficiency, and Ethanol Intoxication: Review and HypothesisALCOHOLISM, Issue 8 2008Peter F. Nixon Introduction:, The earliest observed effect in the pathogenesis of experimental Wernicke's encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF. Methods:, Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin-deficient glucose oxidation. Results:, The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should ,-ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin-deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria-rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke's encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers. Conclusions:, Impairment of the CP by ethanol intoxication and by thiamin-deficient carbohydrate metabolism has a common, rational explanation that can guide future research. [source] Some observations of the structure of the choroid plexus and its cystsPRENATAL DIAGNOSIS, Issue 13 2002Ivan Kraus Abstract The structure of the choroid plexus was studied in five normal human embryos, three normal fetuses and three fetuses with choroid plexus cysts. These were detected by ultrasound and the fetuses were karyotypically normal. The choroid plexus appears in the lateral cerebral ventricles at the seventh developmental week. The early structure is lobulated with vessels running in the mesenchymal stroma and forming capillary nets under the single-layered ependymal epithelium. This embryonal structure is converted into the fetal type during the ninth developmental week as the embryonal capillary net is replaced by elongated loops of wavy capillaries that lie under regular longitudinal epithelial folds. The choroid plexus cysts exhibited accumulation of fluid within distended mesenchymal stroma and did not show the wavy folds on this surface, which was smooth. Within this connective tissue of the cyst wall were distended angiomatous interconnecting thin-walled capillaries. Therefore, filled cavities were not lined by any epithelium. We suggest that fetal choroid plexuses cysts (at least in many cases) are in fact pseudocysts exhibiting angiomatous patterns of capillaries in their walls. Copyright © 2002 John Wiley & Sons, Ltd. [source] Differential expression of p120 catenin in glial cells of the adult rat brainTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2004Norbert Chauvet Abstract p120 catenin (p120ctn) is involved in the regulation of cadherin-mediated adhesion and the dynamic organization of the actin cytoskeleton by modulating RhoGTPase activity. We have previously described the distribution of p120ctn during rat brain development and provided substantial evidence for the potential involvement of p120ctn in morphogenetic events and plasticity in the central nervous system. Here, we analyzed the cellular and ultrastructural distribution of p120ctn in glial cells of the adult rat forebrain. The highest intensity of immunostaining for p120ctn was found in cells of the choroid plexus and ependyma and was mainly restricted to the plasma membrane. However, p120ctn was almost absent from astrocytes. In contrast, in tanycytes, a particular glial cell exhibiting remarkable morphological plasticity, p120ctn, was localized at the plasma membrane and also in the cytoplasm. We show that a large subpopulation of oligodendrocytes expressed multiple isoforms, whereas other neural cells predominantly expressed isoform 1, and that p120ctn immunoreactivity was distributed through the cytoplasm and at certain portions of the plasma membrane. Finally, p120ctn was expressed by a small population of cortical NG2-expressing cells, whereas it was expressed by a large population of these cells in the white matter. However, in both regions, proliferating NG2-positive cells consistently expressed p120ctn. The expression of p120ctn by cells of the oligodendrocyte lineage suggests that p120ctn may participate in oligodendrogenesis and myelination. Moreover, the expression of p120ctn by various cell types and its differential subcellular distribution strongly suggest that p120ctn may serve multiple functions in the central nervous system. J. Comp. Neurol. 479:15,29, 2004. © 2004 Wiley-Liss, Inc. [source] Direct Stimulation of Adult Neural Stem Cells In Vitro and Neurogenesis In Vivo by Vascular Endothelial Growth FactorBRAIN PATHOLOGY, Issue 3 2004Anne Schänzer Hypoxia as well as global and focal ischemia are strong activators of neurogenesis in the adult mammalian central nervous system. Here we show that the hypoxia-inducible vascular endothelial growth factor (VEGF) and its receptor VEGFR-2/Flk-1 are expressed in clonally-derived adult rat neural stem cells in vitro. VEGF stimulated the expansion of neural stem cells whereas blockade of VEGFR-2/Flk-1-kinase activity reduced neural stem cell expansion. VEGF was also infused into the lateral ventricle to study changes in neurogenesis in the ventricle wall, olfactory bulb and hippocampus. Using a low dose (2.4 ng/d) to avoid endothelial proliferation and changes in vascular permeability, VEGF stimulated adult neurogenesis in vivo. After VEGF infusion, we observed reduced apoptosis but unaltered proliferation suggesting a survival promoting effect of VEGF in neural progenitor cells. Strong expression of VEGFR-2/Flk-1 was detected in the ventricle wall adjacent to the choroid plexus, a site of significant VEGF production, which suggests a paracrine function of endogenous VEGF on neural stem cells in vivo. We propose that VEGF acts as a trophic factor for neural stem cells in vitro and for sustained neurogenesis in the adult nervous system. These findings may have implications for the pathogenesis and therapy of neurodegenerative diseases. [source] Sonographic detection of the optic radiationACTA PAEDIATRICA, Issue 10 2005Annemieke Boxma Abstract Objective: To describe a region of hyperechoic white matter adjacent to the atrium of the lateral ventricle of preterms, and to speculate on the relevance of detecting preterm white matter injury. Patients and methods: Cranial ultrasound images of 92 preterms of gestational age (GA) 32 wk or less were reviewed. For each infant, one first week standard coronal image was used for measurement of grey values around the para-atrial region of interest (PAROI) relative to the choroid plexus. For verification of the sonographic anatomy, MR images of an adult brain were used. For reference, neuro-anatomical images were compared in several atlases. In a group of nine preterms of similar GA with cystic periventricular leukomalacia (PVL) or MR-confirmed white matter disease, the disappearance of the PAROI was examined. Results: The hyperechoic para-atrial area, subjectively detected in 84% of the patients, was situated bilaterally between the inner end of the lateral fissure and the upper third of the choroid plexus. In white matter caudal to the atrium, the hyperechoic band could be pursued towards the calcarine area. The average ratio of grey value around the PAROI to the choroid plexus was 0.787 (SD=0.072, median 0.791). There was no correlation between PAROI grey value and gestational age. At 26 wk gestational age, the average ratio was 0.781 (n=14), and 0.789 (n=17) at 31 wk. Location of the PAROI agrees with the angle of the upper loop of the optic radiation. None of the nine infants with white matter damage had PAROIs clearly distinguishable from flaring. Conclusion: The symmetrical and unchanged acoustic character between 26 and 31 wk of gestational age argues in favour of the hypothesis that the PAROI is an anatomical structure. The localization of the hyperechoic band supports the hypothesis that it represents part of the optic radiation. Further study is needed to examine the absence of a hyperechoic para-atrial band as a prognostic marker of the extension and severity of white matter injury. [source] Human brain aminopeptidase A: biochemical properties and distribution in brain nucleiJOURNAL OF NEUROCHEMISTRY, Issue 1 2008Nadia De Mota Abstract Aminopeptidase A (APA) generated brain angiotensin III, one of the main effector peptides of the brain renin angiotensin system, exerting a tonic stimulatory effect on the control of blood pressure in hypertensive rats. The distribution of APA in human brain has not been yet studied. We first biochemically characterized human brain APA (apparent molecular mass of 165 and 130 kDa) and we showed that the human enzyme exhibited similar enzymatic characteristics to recombinant mouse APA. Both enzymes had similar sensitivity to Ca2+. Kinetic studies showed that the Km (190 ,mol/L) of the human enzyme for the synthetic substrate- l -glutamyl-,-naphthylamide was close from that of the mouse enzyme (256 ,mol/L). Moreover, various classes of inhibitors including the specific and selective APA inhibitor, (S)-3-amino-4-mercapto-butyl sulfonic acid, had similar inhibitory potencies toward both enzymes. Using (S)-3-amino-4-mercapto-butyl sulfonic acid, we then specifically measured the activity of APA in 40 microdissected areas of the adult human brain. Significant heterogeneity was found in the activity of APA in the various analyzed regions. The highest activity was measured in the choroids plexus and the pineal gland. High activity was also detected in the dorsomedial medulla oblongata, in the septum, the prefrontal cortex, the olfactory bulb, the nucleus accumbens, and the hypothalamus, especially in the paraventricular and supraoptic nuclei. Immunostaining of human brain sections at the level of the medulla oblongata strengthened these data, showing for the first time a high density of immunoreactive neuronal cell bodies and fibers in the motor hypoglossal nucleus, the dorsal motor nucleus of the vagus, the nucleus of the solitary tract, the Roller nucleus, the ambiguus nucleus, the inferior olivary complex, and in the external cuneate nucleus. APA immunoreactivity was also visualized in vessels and capillaries in the dorsal motor nucleus of the vagus and the inferior olivary complex. The presence of APA in several human brain nuclei sensitive to angiotensins and involved in blood pressure regulation suggests that APA in humans is an integral component of the brain renin angiotensin system and strengthens the idea that APA inhibitors could be clinically tested as an additional therapy for the treatment of certain forms of hypertension. [source] | |||||||||||||