Basic fibroblast growth factor (Fgf2) is necessary for cell proliferation and neurogenesis in the developing cerebral cortex.
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Little is known about regionally specific signals that control the number of neuronal progenitor cells in vivo. We have previously shown that the germline mutation of the basic fibroblast growth factor (Fgf2) gene results in a reduction in the number of cortical neurons in the adult. We show here that Fgf2 is expressed in the pseudostratified ventricular epithelium (PVE) in a dorsoventral gradient and that Fgf2 and its receptor, Fgfr-1, are downregulated by mid to late stages of neurogenesis. In Fgf2 knockout mice, the volume and cell number of the dorsal PVE (the cerebral cortical anlage) are substantially smaller, whereas the volume of the basal PVE is unchanged. The dorsal PVE of Fgf2 knockout mice has a 50% decrease in founder cells and a reduced expansion of the progenitor pool over the first portion of neurogenesis. Despite this reduction, the degree of apoptosis within the PVE is not changed in the Fgf2 knockouts. Cortical neuron number was decreased by 45% in Fgf2 knockout mice by the end of neurogenesis, whereas the number of neurons in the basal ganglia was unaffected. Microscopically, the frontal cerebral cortex of neonatal Fgf2 null mutant mice lacked large neurons in deep cortical layers. We suggest that Fgf2 is required for the generation of a specific class of cortical neurons arising from the dorsal PVE. (+info)
Functional evidence for presence of PEPT2 in rat choroid plexus: studies with glycylsarcosine.
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PEPT2 expression has been established in brain and, in particular, mRNA transcripts and PEPT2 protein have been identified in choroid plexus. However, there is little evidence for the functional presence of this peptide transporter in choroid plexus tissue. In this study, we examined the in vitro uptake of a model dipeptide, glycylsarcosine (GlySar), with whole tissue rat choroid plexus in artificial cerebrospinal fluid. Our findings are consistent with the known transport properties of PEPT2, including its proton dependence, lack of sodium effect, specificity, and high substrate affinity for dipeptides. Kinetic analysis showed saturable transport of GlySar with a Michaelis constant (K(m)) of 129 +/- 32 microM and a maximum velocity (V(max)) of 52.8 +/- 3.6 pmol/mg/min. GlySar uptake (1.88 microM) was not inhibited by 1.0 mM concentrations of amino acids (glycine, sarcosine, L-histidine), organic acids and bases (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid, tetraethylammonium), or non-alpha-amino cephalosporins (cephaloridine, cephalothin). In contrast, di- and tripeptides (GlySar, glycylproline, glycylglycylhistidine), neuropeptides (carnosine), and alpha-amino cephalosporins (cefadroxil, cephalexin) inhibited the uptake of GlySar by 85 to 90% at 1.0 mM. These findings indicate that PEPT2 is functionally active in choroid plexus and that it might play a role in neuropeptide homeostasis of cerebrospinal fluid. The ability of PEPT2 to transport drugs at the choroid plexus also may be important for future drug design, delivery, and tissue-targeting considerations. (+info)
Second trimester ultrasonography may identify 77 to 97% of fetuses with trisomy 18.
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Between 1990 and 1999, 30 second trimester fetuses with trisomy 18 and 2000 control fetuses underwent real-time and color Doppler ultrasonographic examination followed by genetic amniocentesis. Abnormal fetal anatomy was present in 97% of fetuses with trisomy 18, with a false-positive rate of 15.7%. Logistic regression identified six markers (choroid plexus cysts, central nervous system malformations, an abnormal nuchal skin fold, ventricular septal defect, outflow tract abnormalities of the heart, and right-to-left chamber disproportion of the heart) and one interaction between markers (right-to-left chamber disproportion and outflow tract abnormalities) to significantly contribute to the identification of 93% of fetuses with trisomy 18, with a false-positive rate of 8.9%. Noncardiovascular markers (choroid plexus cysts, central nervous system malformations, and abnormal nuchal skin fold) identified 77% of fetuses with trisomy 18, with a false-positive rate of 3.9%. Combining right-to-left chamber disproportion of the heart with choroid plexus cysts, central nervous system malformations, and nuchal skin folds identified 83% of fetuses with trisomy 18, with a false-positive rate of 4.4%. (+info)
Ectopic engrailed 1 expression in the dorsal midline causes cell death, abnormal differentiation of circumventricular organs and errors in axonal pathfinding.
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A series of gain- or loss-of-function experiments performed in different vertebrate species have demonstrated that the Engrailed genes play multiple roles during brain development. In particular, they have been implicated in the determination of the mid/hindbrain domain, in cell proliferation and survival, in neurite formation, tissue polarization and axonal pathfinding. We have analyzed the consequences of a local gain of En function within or adjacent to the endogenous expression domain in mouse and chick embryos. In WEXPZ.En1 transgenic mice (Danielian, P. S. and McMahon, A. P. (1996) Nature 383, 332-334) several genes are induced as a consequence of ectopic expression of En1 in the diencephalic roof (but in a pattern inconsistent with a local di- to mes-encephalon fate change). The development of several structures with secretory function, generated from the dorsal neuroepithelium, is severely compromised. The choroid plexus, subcommissural organ and pineal gland either fail to form or are atrophic. These defects are preceded by an increase in cell death at the dorsal midline. Comparison with the phenotype of Wnt1(sw/sw) (swaying) mutants suggests that subcommissural organ failure is the main cause of prenatal hydrocephalus observed in both strains. The formation of the posterior commissure is also delayed, and errors in axonal pathfinding are frequent. In chick, ectopic expression of En by in ovo electroporation, affects growth and differentiation of the choroid plexus. (+info)
Na/HCO3 cotransporters in rat brain: expression in glia, neurons, and choroid plexus.
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We studied the expression and distribution of Na/HCO(3) cotransporters in rat brain using polynucleotide probes and polyclonal antibodies derived from the electrogenic rat kidney Na/HCO(3) cotransporter (rkNBC). In whole brain, we observed a single mRNA ( approximately 7.5 kb) by Northern hybridization and a major approximately 130 kDa protein by immunoblotting with a polyclonal antiserum directed against the C terminus of rkNBC. NBC mRNA and protein were present in cortex, brainstem-diencephalon, and cerebellum. In situ hybridization revealed NBC mRNA expression throughout the CNS, with particularly high levels in olfactory bulb, hippocampal dentate gyrus, and cerebellum. NBC mRNA was present in glial cells (e.g., Bergmann glia of cerebellum and hippocampal astrocytes) and neurons (e.g., granule cells of dentate gyrus and neurons of cortex or striatum). Double hybridization of mRNA encoding NBC and glutamate transporter 1 (glial marker) confirmed that both glia and neurons express NBC. Indirect immunofluorescence microscopy demonstrated NBC protein throughout the CNS, particularly in hippocampus and cerebellum. Although NBC mRNA was restricted to cell bodies, NBC protein was distributed diffusely, compatible with a localization in cell processes and perhaps cell bodies. Double labeling with glial fibrillary acidic protein (astrocytic marker), microtubule-associated protein 2 (neuronal marker), or 2',3'-cyclic mononucleotide 3'-phosphodiesterase (oligodendrocytic marker) demonstrated expression of NBC protein in specific subpopulations of both glia and neurons. Moreover, NBC protein was present in both cultured hippocampal astrocytes and cortical neurons. NBC mRNA and protein were also present in epithelial cells of choroid plexus, ependyma, and meninges. Our results are thus consistent with multiple novel roles for Na/HCO(3) cotransport in CNS physiology. (+info)
Scanning electron microscopy study of the choroid plexus in the monkey (Cebus apella apella).
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The cells of the choroid plexus of the lateral ventricles of the monkey Cebus apella apella were examined through scanning electron microscopy at contributing to the description of such structures in primates. The animals were anesthetized previously with 3% hypnol intraperitoneally and after perfusion with 2.5% glutaraldehyde, samples of the choroid plexus were collected after exhibition of the central portion and inferior horn of the lateral ventricles. The ventricular surface of those cells presents globose form as well as fine interlaced protrusions named microvilli. Among those, it is observed the presence of some cilia. Resting on the choroid epithelial cells there is a variable number of free cells, with fine prolongations which extend from them. They are probably macrophages and have been compared to Kolmer cells or epiplexus cells, located on choroid epithelium. The choroid plexus of the encephalic lateral ventricles of the monkey Cebus apella apella at scanning electron microscopy is similar to that of other primates, as well as to that of other species of mammals mainly cats and rats, and also humans. (+info)
Choroid plexus changes after temporal lobectomy.
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BACKGROUND AND PURPOSE: Postoperative contrast-enhanced MR imaging of the brain is routinely used when evaluating for residual or recurrent brain tumor. It is imperative to be aware of morphologic changes and imaging features that typically occur in response to surgical manipulation at the postoperative site to avoid misinterpretation of imaging findings. Our purpose was to determine normal postoperative changes and alterations in the choroid plexus among patients who had undergone temporal lobectomy in order to distinguish this appearance from pathologic changes that may be seen in the presence of infection or recurrent tumors. METHODS: We reviewed 159 MR scans from 95 patients with hippocampal sclerosis or gliosis who underwent temporal lobectomy for treatment of intractable epilepsy. Choroid plexus location and size were assessed on contrast-enhanced T1-weighted images. RESULTS: After temporal lobectomy, the choroid plexus enlarged and sagged into the resection site. Increase in the size of the choroid plexus occurred in 58% of cases overall. The degree of enhancement also increased after surgery, sometimes resulting in a nodular pattern of enhancement. The changes were most marked during the 1st week after temporal lobectomy, and showed an enlarged, markedly enhancing choroid plexus on 86% of the scans. CONCLUSION: Postoperative changes of the choroid plexus after temporal lobectomy include sagging into the resection site, an increased size, and an increased degree of enhancement. Normal postoperative morphologic characteristics may mimic neoplastic enhancement pattern. Familiarity with this appearance is important to avoid a pitfall in diagnosis of recurrent postoperative temporal lobe neoplasms. (+info)
Choroid plexus lipocalin 1 (Cpl1) has been isolated from the African clawed toad (Xenopus laevis) and the cane toad (Bufo marinus). Xcpl1 has been used as a marker for studying early neural development. Due to its retinoid binding properties and the fact that it causes dysmorphogenesis when overexpressed in the early embryo, the protein product is considered to be part of the retinoic acid signalling pathway. Later in development and during adulthood, the epithelial cell sheet of the choroid plexus which forms the blood-cerebrospinal fluid barrier expresses cpl1 as the predominant secretory protein. These data, the similarity of Cpl1 to prostaglandin D(2) synthase and its functional homology to transthyretin will be discussed. (+info)