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Results for “Ganglionic Eminence”

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PubMed2000

Distribution of SNAP-25 in transient neuronal circuitries of the developing human forebrain.

The distribution of SNAP-25 is demonstrated within prominent transient structures in the developing human forebrain. During early fetal development SNAP-25 is mainly expressed in axons of the intermediate zone and the internal capsule. The fibers appear directed towards the mantle zone of the ganglionic eminence and the perireticular nucleus located within the internal capsule. Cells of these two areas are shown to interact with SNAP-25 immunoreactive structures with the aid of double-labellings. The SNAP-25 immunoreactive fibers may represent corticofugal axons which contact the perireticular nucleus and ganglionic eminence which are regarded as intermediate targets providing a scaffold for growing axons. Anti-SNAP-25, thus, is an appropriate marker of intermediate targets which are involved in brain injuries of preterm infants.

Adult↗

PubMed2006

Developmental appearance of cyclic guanosine monophosphate (cGMP) production and nitric oxide responsiveness in embryonic mouse cortex and striatum.

The second messenger cyclic guanosine monophosphate (cGMP) regulates multiple aspects of both structural development and physiological function in the developing nervous system. Recent in vitro experiments have shown that cGMP also modulates the response of developing vertebrate neurons to guidance molecules. This has led to the proposal that in vivo cGMP plays a critical role in directing the outgrowth of the apical dendrites of developing neurons in the cerebral cortex. Despite this proposed role, the onset, localization, and dynamics of cGMP production in the embryonic cortex are unknown. To investigate the potential contribution of cGMP in the embryo, we have used a pharmacological and immunohistochemical approach to test whether the endogenous production of cGMP, and the capacity to produce cGMP in response to nitric oxide (NO), in the cerebral cortex is compatible with the proposed developmental roles for cGMP. We find that cortical cGMP production and NO sensitivity are regionally and developmentally regulated. Cortical cGMP production begins at E15, later than in the ganglionic eminences, becomes high in the cortical plate but not the ventricular zone, and is dependent on nitric oxide synthase activity. Furthermore, although radially migrating neurons were not NO responsive until they reached the cortical plate, NO exposure revealed an additional population of tangentially migrating presumptive interneurons from the ganglionic eminences with the capacity to produce cGMP. These results provide a new level of understanding of the stage and cell type specific regulation of the NO/cGMP pathway during embryonic development.

Animals↗

PubMed1999

Mash1 regulates neurogenesis in the ventral telencephalon.

Previous studies have shown that mice mutant for the gene Mash1 display severe neuronal losses in the olfactory epithelium and ganglia of the autonomic nervous system, demonstrating a role for Mash1 in development of neuronal lineages in the peripheral nervous system. Here, we have begun to analyse Mash1 function in the central nervous system, focusing our studies on the ventral telencephalon where it is expressed at high levels during neurogenesis. Mash1 mutant mice present a severe loss of progenitors, particularly of neuronal precursors in the subventricular zone of the medial ganglionic eminence. Discrete neuronal populations of the basal ganglia and cerebral cortex are subsequently missing. An analysis of candidate effectors of Mash1 function revealed that the Notch ligands Dll1 and Dll3, and the target of Notch signaling Hes5, fail to be expressed in Mash1 mutant ventral telencephalon. In the lateral ganglionic eminence, loss of Notch signaling activity correlates with premature expression of a number of subventricular zone markers by ventricular zone cells. Therefore, Mash1 is an important regulator of neurogenesis in the ventral telencephalon, where it is required both to specify neuronal precursors and to control the timing of their production.

Animals↗

PubMed2004

Specific beta1 integrins mediate adhesion, migration, and differentiation of neural progenitors derived from the embryonic striatum.

Early inductive signals within the embryonic mammalian forebrain establish two major germinal regions along the dorsal-ventral axis. The dorsal germinal zone eventually forms the cerebral cortex while the ventral ganglionic eminence primarily forms the striatum and globus pallidus. The mechanisms leading to patterning of specific forebrain structures from these distinct germinal regions are not fully understood but may involve the adhesive and migratory properties of regionally specified cells and their interactions with the extracellular environments in which they reside. In the present study, we isolated ganglionic eminence neural progenitor cells (geNPC), precursors of the adult striatum, from the ventral forebrain germinal zone and analyzed adhesion, migration, and differentiation of geNPC on various extracellular matrix (ECM) substrates in vitro. Specifically, we evaluated the role of beta1 integrins, a family of cell surface receptors important in neural development, in mediating geNPC behavior on ECM molecules expressed in embryonic brain tissue. Adhesion and migration of geNPC were significantly enhanced on laminin (LN) and fibronectin (FN) relative to other ECM substrates. Antibody perturbation experiments revealed that although geNPC express several beta1 integrins (alpha1beta1, alpha2beta1, alpha3beta1, alpha5beta1, alpha6beta1, alphavbeta1), adhesion and migration on LN and FN were primarily mediated by alpha6beta1 and alpha5beta1, respectively, and these interactions were confirmed by biochemical cross-link/extraction procedures. Finally, neuronal differentiation of geNPC was enhanced on LN, indicating a role for LN in geNPC differentiation. beta1 integrin-ECM interactions may contribute to basic mechanisms of striatal development and may explain the potent migratory capacity of geNPC transplanted into the adult brain.

Animals↗

PubMed2000

No evidence for infection of human cells with porcine endogenous retrovirus (PERV) after exposure to porcine fetal neuronal cells.

BACKGROUND: Recent demonstration of human cell infection in vitro with porcine endogenous retrovirus (PERV) has raised safety concerns for new therapies that involve transplantation of pig cells or organs to humans. To assess better the specific risk that may be associated with the transplantation of fetal pig neuronal cells to the central nervous system of patients suffering from intractable neurologic disorders (Parkinson's disease, Huntington's disease, and epilepsy), we have performed studies to determine whether there is evidence for in vivo or in vitro transmission of PERV from fetal pig neuronal cells to human cells. METHODS: Ventral mesencephalon (VM) and lateral ganglionic eminence cells were isolated from fetal pigs and transplanted into patients with neurological conditions as part of clinical studies. Blood samples taken from patients at various time points posttransplant were tested for evidence of PERV. In vitro studies to test for PERV infection of human cells after cocultivation with either fetal porcine ventral mesencephalon or porcine fetal lateral ganglionic eminence cells were also performed. RESULTS: We found no evidence of PERV provirus integration in the DNA from PBMC of 24 neuronal transplant recipients. In addition, no PERV was released from cultured fetal porcine neuronal cultures, and there was no transfer of PERV from fetal pig neuronal cells to human cells in vitro. CONCLUSIONS: Our results demonstrate by both examination of transplant patient blood samples and in vitro studies that there is no evidence for transmission of PERV from porcine fetal neural cells to human cells.

Adult↗

PubMed2005

CNTF/LIF/gp130 receptor complex signaling maintains a VZ precursor differentiation gradient in the developing ventral forebrain.

The extrinsic signaling pathways responsible for the formation and maintenance of the unique laminar organization of the forebrain germinal zones are largely unknown. In the present study, we asked whether ciliary neurotrophic factor (CNTF)/leukemia inhibitory factor (LIF)/gp130 signaling plays a role in the development of the germinal layers in the lateral ganglionic eminence. We found that CNTF/LIF/gp130 receptor signaling promotes the self-renewal/expansion of a subpopulation of fibroblast growth factor-responsive ventricular zone (VZ) precursors in the ventral forebrain. Analysis of Lifr-/- mice suggests that CNTF/LIF/gp130 signaling maintains a subpopulation of GSH2+ VZ precursors, which are necessary for normal growth of the early ventral forebrain and for maintaining a gradient of VZ precursor differentiation in the lateral ganglionic eminence, as defined by GSH2, MASH1 and DLX2 expression. Furthermore, addition of exogenous CNTF to embryonic forebrain explant cultures deprived of choroid plexus-derived CNTF, was sufficient to promote a VZ differentiation gradient. In contrast to the forebrain, CNTF/LIF/gp130 signaling reduced, rather than enhanced, precursor self-renewal/expansion in the spinal cord. These results demonstrate a novel region-specific role for CNTF/LIF/gp130 signaling in the development of the germinal layers of the embryonic telencephalon.

Animals↗

PubMed2006

Respiratory inhibition after crying in infants.

BACKGROUND: Among full-term neonates, the authors discovered infants who showed respiratory inhibition after crying which involved a marked decrease in SpO2. The infants were found to present increased echogenicity or a cyst in a cranial region termed the ganglionic eminence, or to have a subependymal cyst. The authors prospectively examined the relationship between respiratory inhibition after crying and these changes to examine the prevention and treatment of the episode. METHODS: The authors conducted cranial ultrasonography to screen 381 full-term neonates who showed no abnormalities at birth and whose parents requested ultrasonographic screening of the head, followed by polygraphy of infants who showed increased echogenicity or a cyst in ganglionic eminence, or had a subependymal cyst. The authors similarly conducted polygraphy for 50 neonates without cranial ultrasound abnormalities; the former constituted the control group. Respiratory inhibition was defined to be central apnea immediately after crying with a decrease in SpO2 to <60%. RESULTS: Among 381 neonates examined, 104 showed cranial ultrasound abnormalities; 60 of the 104 neonates indicated respiratory inhibition after crying. Oxygenation failed to improve the episode in 17 neonates with severe respiratory inhibition. However, theophylline alleviated the episode, and SpO2 no longer decreased to <60%. Theophylline was discontinued successfully by 6 months after birth, while 50 neonates in the control group showed no respiratory inhibition after crying. CONCLUSION: Respiratory inhibition after crying which involved a marked decrease in SpO2 was observed in full-term neonates who showed no abnormalities after birth. These neonates could be screened by cranial ultrasonography.

Apnea↗

PubMed2004

Polarized increase of calcium and nucleokinesis in tangentially migrating neurons.

Cortical interneurons originate from the ganglionic eminences and reach their final position in the cortex via tangential migratory routes. The mechanisms of this migration are poorly understood. Here we have performed confocal time-lapse analysis of cell movement in the intermediate zone of embryonic mouse cortical slices in order to directly visualize their mode of migration. Tangentially migrating neurons moved by nucleokinesis, characterized by active phases of discontinuous advances of the nucleus followed by periods of quiescence. Dissociated cells from the ganglionic eminences also showed nucleokinesis associated with an increase of intracellular calcium, [Ca(2+)](i) Calcium elevation was greatest in the proximal region of the leading process, a zone with a wide distribution of gamma-tubulin. General increases in [Ca(2+)](i) elicited by microperfussion with neurotransmitters did not elicit nucleokinesis. These results show that tangential migration uses nucleokinesis, a cell-intrinsic process in which calcium signalling is local, directional and highly regulated.

Animals↗

PubMed1997

Developmental features of human striatal tissue transplanted in a rat model of Huntington's disease.

Areas of striatal grafts which contain neurons that are characteristic of the striatum are called P-zones. We have investigated whether the paucity of P-zones in human xenografts of lateral ganglionic eminence (LGE) tissue in a rat model of Huntington's disease is due (i) to an absence of the appropriate target cells of LGE neurons or (ii) to the persistence of an immature morphology. Striatal tissue from human embryos of varying sizes (21, 24, and 30 mm in crown-to-rump length) was grafted into the ibotenate-lesioned striatum of immunosuppressed rats, which were killed after 15-17 weeks. In most cases, tissue from the LGE and medial ganglionic eminence (MGE) was transplanted together, whereas some rats received grafts of only LGE tissue. Both types of grafts exhibited positive immunostaining for PCNA (proliferating cells), Vimentin (immature astrocytes), and GAP-43 (outgrowing fibers), which indicates that graft maturation is still ongoing up to 4 months after grafting. Graft survival seemed better when MGE was cografted with LGE, suggesting that the MGE may provide trophic support for LGE neurons and can affect the overall survival of human striatal xenografts. However, the extent of P-zone formation was not increased in MIXED, i.e., LGE plus MGE, grafts.

Acetylcholinesterase↗

PubMed2001

Hepatocyte growth factor/scatter factor is a motogen for interneurons migrating from the ventral to dorsal telencephalon.

Cortical interneurons arise from the proliferative zone of the ventral telencephalon, the ganglionic eminence, and migrate into the developing neocortex. The spatial patterns of migratory interneurons reflect the complementary expression of hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, MET, in the forebrain. Scatter assays on forebrain explants demonstrate regionally specific motogenic activity due to HGF/SF. In addition, exogenous ligand disrupts normal cell migration. Mice lacking the urokinase-type plasminogen activator receptor (u-PAR), a key component of HGF/SF activation, exhibit deficient scatter activity in the forebrain, abnormal interneuron migration from the ganglionic eminence, and reduced interneurons in the frontal and parietal cortex. The data suggest that HGF/SF motogenic activity, which is essential for normal development of other organ systems, is a conserved mechanism that regulates trans-telencephalic migration of interneurons.

Animals↗

PubMed2004

Lhx6 regulates the migration of cortical interneurons from the ventral telencephalon but does not specify their GABA phenotype.

The LIM homeodomain family of transcription factors is involved in many processes in the developing CNS, ranging from cell fate specification to connectivity. A member of this family of transcription factors, lhx6, is expressed in the medial ganglionic eminence (MGE) of the ventral telencephalon, where the vast majority of cortical interneurons are generated. Its expression in the GABA-containing MGE cells that migrate to the cortex suggests that this gene uniquely or in combination with other transcription factors may play a role in the neurochemical identity and migration of these neurons. We performed loss of function studies for lhx6 in mouse embryonic day 13.5 brain slices and dissociated MGE neuronal cultures using Lhx6-targeted small interfering RNA produced by a U6 promoter-driven vector. We found that silencing lhx6 impeded the tangential migration of interneurons into the cortex, although it did not obstruct their dispersion within the ganglionic eminence. Blocking lhx6 expression in dissociated MGE cultured neurons did not interfere with the production of GABA or its synthesizing enzyme. These results indicate that lhx6, unlike the closely related member lhx7, does not regulate neurotransmitter choice in interneurons but plays an important role in their migration from the ventral telencephalon to the neocortex.

Animals↗

PubMed2004

Axon mediated interneuron migration.

Mammalian forebrain development requires extensive cell migration for cells to reach their appropriate location in the adult brain. Defects in this migration result in human malformations and neurologic deficits. Thus, understanding the mechanisms underlying normal cell migration during development is essential to understanding the pathogenesis of human malformations. Radial glia are known to support radial cell migration, while axons have been proposed as substrate for some non-radially migrating cells. Herein we have directly tested the hypothesis that axons can support non-radial cell migration. One population of cells known to migrate non-radially is the inhibitory interneurons that move from the ganglionic eminence to the cerebral cortex. We first show that early born GABAergic cells colocalize with TAG-1-positive (TAG-1+) axons, while later born cells colocalize with intermediate weight neurofilament-positive, TAG-1-negative (TAG-1-) processes, suggesting temporal differences in substrate specificities. We next developed an in vitro assay that allows us to observe cell migration on axons in culture. Using this assay we find that early born medial ganglionic eminence-derived interneurons migrate preferentially on TAG-1+ axons, while later born cells only migrate on neurofilament-positive/TAG-1- processes. These data provide the first direct evidence that ganglionic eminence cells migrate on axons and that there is an age-dependent substrate preference. Furthermore, the assay developed and characterized herein provides a robust method to further study the molecular substrates and guidance cues of axonophilic cell migration in neural development.

Aging↗

PubMed2005

Subpallial origin of part of the calbindin-positive neurons of the claustral complex and piriform cortex.

The aim of the present study was to investigate whether part of the calbindin-positive neurons of the claustral complex and piriform cortex originate in the subpallium. To that end, we prepared organotypic cultures of embryonic telencephalic slices, and applied the cell tracker CMTMR to the ventricular/subventricular zone of the lateral or medial ganglionic eminence. Following 48 h of incubation, we observed a number of CMTMR-labeled cells (showing red fluorescence) of subpallial origin in the claustral complex and piriform cortex. To know whether some of these cells of subpallial origin were calbindin-positive, we performed immunofluorescence for calbindin using an Alexa 488-conjugated secondary antiserum (green fluorescence). Our results showed that some of the CMTMR-labeled cells of subpallial origin in the claustral complex and piriform cortex are calbindin-positive (and possibly GABAergic). The subpallial origin of part of these cells was confirmed by observation of double labeled neurons in the claustral complex that expressed both Lhx6 mRNA (a marker of cells derived from the medial ganglionic eminence) and calbindin. Future studies will be required to analyze the existence of a subpopulation of non-GABAergic calbindin cells in the claustral complex and piriform cortex, and to know their origin.

Animals↗

PubMed2002

Subpallial dlx2-expressing cells give rise to astrocytes and oligodendrocytes in the cerebral cortex and white matter.

The precise origins of postnatal subventricular zone (SVZ) cells are not known. Furthermore, the gliogenic potential of progenitors expressing Dlx genes that migrate ventrodorsally from the ganglionic eminences has not been explored in vivo. Here, we identify the embryonic origins of two distinct populations of postnatal SVZ cells: SVZ border cells, which express Zebrin II, and migratory cells in the central SVZ, which are generally devoid of Zebrin II expression (Staugaitis et al., 2001). Zebrin II is expressed by all cells of the telencephalic primordium, with its expression becoming restricted to astrocytes in the mature telencephalon. As the neuroepithelium folds during corticostriatal sulcus formation (embryonic day 13-15), a wedge of Zebrin II+ cells is created at the presumptive site of the dorsolateral SVZ. At this time, Dlx2-expressing cells and their progeny begin to migrate ventrodorsally along a medial path from the ganglionic eminences. These migratory subpallial cells invade the wedge of Zebrin II+ cells to form the central region of the SVZ. We used a Dlx2/tauLacZ knock-in to perform a short-term lineage analysis of Dlx2-expressing cells throughout SVZ formation and the postnatal peak of gliogenesis. Dlx2/tauLacZ [beta-galactosidase (beta-gal)]-expressing cells populate the central SVZ, whereas Zebrin II-expressing cells form its borders. Furthermore, beta-gal expression demonstrates a lineage relationship between Dlx2-expressing cells and glia residing in the dorsal telencephalon. We propose a model for the formation of the postnatal SVZ and demonstrate that subpallium-derived Dlx2-expressing cells give rise to astrocytes and oligodendrocytes in the white matter and cerebral cortex.

Animals↗

PubMed2003

Dlx2 progenitor migration in wild type and Nkx2.1 mutant telencephalon.

The transcription factor Dlx2 is expressed widely throughout the ventral telencephalon. We have examined the in vitro and in vivo migration of Dlx2 progenitors originating from the different ganglionic eminences of both wild type and Nkx2.1 mutant animals. By examining the expression of tauLacZ targeted into the Dlx2 locus we were able to visualize the distribution of cells expressing this gene at both embryonic and postnatal stages. This analysis suggested that Dlx2-expressing cells traverse a number of characteristic migratory routes to populate both cortical and subcortical regions. We also examined how these patterns of migration were affected in Nkx2.1 mutant animals. In these mutants, the early but not late populations of Dlx2-expressing cells originating in the ventral telencephalon that migrate to the cortex are lost. This recovery may be, at least in part, a result of the late migration of Dlx2 progenitors from the caudal ganglionic eminences (CGE), which, based on our previous work, does not appear to require Nkx2.1 gene function.

Animals↗

PubMedDate not supplied

The age of striatum determines the pattern and extent of dopaminergic innervation: a nigrostriatal double graft study.

In animal models of Parkinson's disease, transplanted fetal mesencephalic dopaminergic neurons can innervate the dopamine-depleted host brain, but it is unclear why large portions of the host striatum are left uninnervated. During normal development, the dopaminergic innervation first occurs in the form of a dense patchy pattern in the striatum, followed by a widespread nerve fiber network. Using intraocular double grafts we have investigated dopaminergic growth patterns initiated when ventral mesencephalic grafts innervate striatal targets. The fetal lateral ganglionic eminence was implanted into the anterior eye chamber. After maturation in oculo, fetal ventral mesencephalon was implanted and placed in contact with the first graft. In other animals the two pieces of tissue were implanted simultaneously. Tyrosine hydroxylase (TH) immunohistochemistry revealed a pattern of dense TH-positive patches throughout the total volume of the striatal grafts in simultaneously transplanted cografts, while a widespread, less dense, pattern was found when mature striatal transplants were innervated by fetal dopaminergic grafts. To investigate which type or types of growth patterns that developed after grafting to striatum in situ of an adult host, fetal ventral mesencephalic tissue was implanted into the lateral ventricle adjacent to the dopamine-lesioned striatum. After maturation of the mesencephalic graft, the fetal lateral ganglionic eminence was implanted into the reinnervated part of the host striatum. TH immunohistochemistry revealed a few nerve fibers within the striatal graft and the growth pattern was of the widespread type. In conclusion, grafted dopaminergic neurons preferably innervate mature striatum with a widespread sparse nerve fiber network, while the innervation of the immature striatum occurs in the form of dense patches. Furthermore, when the patchy pattern is formed, the total volume of the striatal target is innervated while growth of the widespread type terminates prior to reaching distal striatal parts. Thus, the growth pattern seems essential to the final volume that is innervated. Once the widespread growth pattern is initiated, the presence of immature striatum does not change the dopaminergic growth pattern.

Age Factors↗

PubMed2006

In vitro MRI of brain development.

In this review, we demonstrate the developmental appearance, structural features, and reorganization of transient cerebral zones and structures in the human fetal brain using a correlative histological and MRI analysis. The analysis of postmortem aldehyde-fixed specimens (age range: 10 postovulatory weeks to term) revealed that, at 10 postovulatory weeks, the cerebral wall already has a trilaminar appearance and consists of: (1) a ventricular zone of high cell-packing density; (2) an intermediate zone; (3) the cortical plate (in a stage of primary consolidation) with high MRI signal intensity. The anlage of the hippocampus is present as a prominent bulging in the thin limbic telencephalon. The early fetal telencephalon impar also contains the first commissural fibers and fornix bundles in the septal area. The ganglionic eminence is clearly visible as an expanded continuation of the proliferative ventricular zone. The basal ganglia showed an initial aggregation of cells. The most massive fiber system is in the hemispheric stalk, which is in continuity with thalamocortical fibers. During the mid-fetal period (15-22 postovulatory weeks), the typical fetal lamination pattern develops and the cerebral wall consists of the following zones: (a) a marginal zone (visible on MRI exclusively in the hippocampus); (b) the cortical plate with high cell-packing density and high MRI signal intensity; (c) the subplate zone, which is the most prominent zone rich in extracellular matrix and with a very low MRI signal intensity; (d) the intermediate zone (fetal "white matter"); (e) the subventricular zone; (f) the periventricular fiber-rich zone; (g) the ventricular zone. The ganglionic eminence is still a very prominent structure with an intense proliferative activity. During the next period (22-26 postovulatory weeks), there is the developmental peak of transient MRI features, caused by the high content of hydrophyllic extracellular matrix in the subplate zone and the accumulation of waiting afferent axons. The period between 27 and 30 postovulatory weeks is characterized by gradual blurring of the laminar structure in parallel with the formation of cerebral convolutions. In near-term preterm infants, T2-weighted MR images showed better contrast resolution than T1-weighted images. We conclude that transient fetal zones and subcortical structures display characteristic MRI features due to the high content of extracellular matrix in the subplate zone, higher MRI signal intensity of zones with high cell-packing intensity, and the presence of growing fibers.

Brain↗

PubMed1999

Striatal grafts in a rat model of Huntington's disease: time course comparison of MRI and histology.

Survival and integration into the host brain of grafted tissue are crucial factors in neurotransplantation approaches. The present study explored the feasibility of using a clinical MR scanner to study striatal graft development in a rat model of Huntington's disease. Rat fetal lateral ganglionic eminences grown as free-floating roller-tube cultures were grafted into the quinolinic acid-lesioned striatum, and T1- and T2-weighted sequences were acquired at 2, 7, 21, and 99 days posttransplantation. MR images were then compared with images of corresponding histological sections. The lesion-induced striatal degeneration caused a progressive ventricle enlargement, which was significantly different from controls at 21 days posttransplantation. Seven days posttransplantation, T1-weighted images revealed a defined liquid-isointense signal surrounded by a hyperintense rim at the site of graft placement, which was found unaltered for the first 21 days posttransplantation, whereas a hypointense graft signal was detected at 99 days posttransplantation. At 2 days posttransplantation, T2-weighted images showed the graft region as a hyperintense area surrounded by a rim of low signal intensity but at later time-points graft location could not be further verified. Measures for graft size and ventricle size obtained from MR images highly correlated with measures obtained from histologically processed sections (R = 0.8, P < 0.001). In conclusion, the present study shows that fetal rat lateral ganglionic eminences grown as free-floating roller-tube cultures can be successfully grafted in a rat Huntington model and that a clinical MR scanner offers a useful noninvasive tool for studying striatal graft development.

Animals↗