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PubMed1993

Volumetric analysis of the telencephalon and tectum during metamorphosis in a flatfish, the turbot Scophthalmus maximus.

The telencephalic hemispheres and the optic tectum of the turbot Scophthalmus maximus were analysed volumetrically during metamorphosis. Both brain regions develop an asymmetry coordinated chronologically with metamorphic events that produce asymmetry in the rest of the animal. Furthermore, the brain asymmetries are correlated with, and may be determined by, the side of origin of their primary afferent inputs, such that the more voluminous side of the brain receives these inputs from the zenithal side. After metamorphosis, the telencephalon remains asymmetric, whereas the optic tectum recovers its bilateral symmetry.

Animals↗
PubMed1993

Auditory projections to the anterior telencephalon in the budgerigar (Melopsittacus undulatus).

The connections of a higher order auditory area in the neostriatum intermedium pars ventrolateralis (NIVL) were mapped with pathway tracing techniques in order to elucidate possible pathways by which auditory feedback may influence vocal learning in the budgerigar (Melopsittacus undulatus). Previous research has shown that NIVL receives projections from Field 'L' as well as adjacent portions of the dorsolateral neostriatum intermedium (NIDL) and hyperstriatum ventrale (HV) and, therefore, may be homologous to previously described auditory centers in the dorsal and lateral portions of the auditory neostriatum of songbirds. The efferent connections of NIVL terminate within a small portion of the rostromedial archistriatum as well as a more rostrally situated area within the medial neostriatum intermedium (NI) and HV. Near by (but not overlapping) fields in NI and HV receive input from the nucleus dorsomedialis posterior thalami (DMP), the archistriatum and ectostriatum. Interestingly, only the DMP projection field overlaps a neural field known to be related to the vocal motor system. The DMP projection field corresponds to that previously described as the magnocellular nucleus of the anterior neostriatum; this nucleus is known to project to the higher vocal center in the budgerigar. In addition to projections from NIVL to medial NI and HIV, auditory information is relayed to the anterolateral telencephalon directly from the brainstem via the ventrolateral nucleus of the lateral lemniscus (VLV). This latter pathway appears comparable to that described in pigeons derived from the intermediate nucleus of the lateral lemniscus. The projection field of VLV overlaps a restricted portion of the caudal and medial aspect of nucleus basalis. These results support the notion that many aspects of telencephalic auditory pathways in birds are primitive characters, although a direct connection between auditory and vocal motor circuits was not found in the present study.

Animals↗
PubMed1976

Telencephalon of the lizard Gekko gecko (Linnaeus): some connections of the cortex and dorsal ventricular ridge.

Interhemispheric connections of the telencephalon in the lizard, Gekko, were studied with anterograde degeneration methods following lesions variously placed in the medial, dorsal, and lateral cortices and/or the dorsal ventricular ridge (D.V.R.). After lesions involving dorsal cortex, the medial wall, and the DVR, the majority of degenerated fibers decussate in the hippocampal commissure and terminate in the septum, medial wall, dorsal cortex, and the lateral edge of the DVR contralaterally. Lesions confined to dorsal cortex result in a similar pattern of degeneration, while lesions confined to the lateral wall result in degeneration in the contralateral lateral cortex, DVR and striatum, mainly via the anterior commissure. Some variation has been reported on the pattern of interhemispheric projections among reptiles studied to date; two possible interpretations of the data are that (1) dorsal cortex may be homologous as a field to parts of both neocortex and the hippocampal formation of mammals or (2) only the lateral part of dorsal cortex may be homologous to neocortex.

Animals↗
PubMed2001

Contribution of reactive oxygen species to 3-hydroxyglutarate neurotoxicity in primary neuronal cultures from chick embryo telencephalons.

Glutaryl-CoA dehydrogenase deficiency is an autosomal recessively inherited neurometabolic disorder with a distinct neuropathology characterized by acute encephalopathic crises during a vulnerable period of brain development. 3-Hydroxyglutarate (3-OH-GA), which accumulates in affected patients, has been identified as an endogenous neurotoxin mediating excitotoxicity via N-methyl-D-aspartate receptors. As increased generation of reactive oxygen species (ROS) and nitric oxide (NO) plays an important role in excitotoxic neuronal damage, we investigated whether ROS and NO contribute to 3-OH-GA neurotoxicity. 3-OH-GA increased mitochondrial ROS generation in primary neuronal cultures from chick embryo telencephalons, which could be prevented by MK-801, confirming the central role of N-methyl-D-aspartate receptor stimulation in 3-OH-GA toxicity. ROS increase was reduced by alpha-tocopherol and--less effectively-by melatonin. alpha-Tocopherol revealed a wider time frame for neuroprotection than melatonin. Creatine also reduced neuronal damage and ROS formation but only if it was administered >or=6 h before 3-OH-GA. NO production revealed only a slight increase after 3-OH-GA incubation. NO synthase inhibitor N(omega)-nitro-L-arginine prevented NO increase but did not protect neurons against 3-OH-GA. The NO donor S-nitroso-N-acetylpenicillamine revealed no effect on 3-OH-GA toxicity at low concentrations (0.5-5 microM), whereas it potentiated neuronal damage at high concentrations (50-500 microM), suggesting that weak endogenous NO production elicited by 3-OH-GA did not affect neuronal viability. We conclude from our results that ROS generation contributes to 3-OH-GA neurotoxicity in vitro and that radical scavenging and stabilization of brain energy metabolism by creatine are hopeful new strategies in glutaryl-CoA dehydrogenase deficiency.

Animals↗
PubMed2004

Retinoic acid signalling specifies intermediate character in the developing telencephalon.

The organisation of the telencephalon into its major structures depends on its early regionalisation along the dorsoventral axis. Previous studies have provided evidence that sonic hedgehog (SHH) is required for the generation of telencephalic cells of ventral character, and that sequential WNT and fibroblast growth factor (FGF) signalling specifies cells of dorsal telencephalic character. However, the signalling mechanisms that specify telencephalic cells of an intermediate character remain to be defined. We provide evidence here that retinoic acid has a crucial role in specifying telencephalic progenitor cells of intermediate character.

Animals↗
PubMed2005

Sonic hedgehog maintains the identity of cortical interneuron progenitors in the ventral telencephalon.

Fate determination in the mammalian forebrain, where mature phenotypes are often not achieved until postnatal stages of development, has been an elusive topic of study despite its relevance to neuropsychiatric disease. In the ventral telencephalon, major subgroups of cerebral cortical interneurons originate in the medial ganglionic eminence (MGE), where the signaling molecule sonic hedgehog (Shh) continues to be expressed during the period of neuronogenesis. To examine whether Shh regulates cortical interneuron specification, we studied mice harboring conditional mutations in Shh within the neural tube. At embryonic day 12.5, NestinCre:Shh(Fl/Fl) mutants have a relatively normal index of S-phase cells in the MGE, but many of these cells do not co-express the interneuron fate-determining gene Nkx2.1. This effect is reproduced by inhibiting Shh signaling in slice cultures, and the effect can be rescued in NestinCre:Shh(Fl/Fl) slices by the addition of exogenous Shh. By culturing MGE progenitors on a cortical feeder layer, cell fate analyses suggest that Shh signaling maintains Nkx2.1 expression and cortical interneuron fate determination by MGE progenitors. These results are corroborated by the examination of NestinCre:Shh(Fl/Fl) cortex at postnatal day 12, in which there is a dramatic reduction in cell profiles that express somatostatin or parvalbumin. By contrast, analyses of Dlx5/6Cre:Smoothened(Fl/Fl) mutant mice suggest that cell-autonomous hedgehog signaling is not crucial to the migration or differentiation of most cortical interneurons. These results combine in vitro and ex vivo analyses to link embryonic abnormalities in Shh signaling to postnatal alterations in cortical interneuron composition.

Animals↗
PubMed1989

Oligodendrocyte progenitors isolated directly from developing telencephalon at a specific phenotypic stage: myelinogenic potential in a defined environment.

Oligodendroglia differentiate asynchronously in the developing central nervous system, passing through a series of stages identified by the sequential expression of specific differentiation antigens, culminating in the formation of the myelin sheath. In the work presented here, oligodendrocyte progenitors at a temporally narrow and well-defined phenotypic stage of development have been isolated in high purity and yield directly from postnatal rat telencephalon. This stage is identified by the expression of the O4 antigen, the earliest recognized surface marker specific for the oligodendroglial lineage, but the absence of the differentiation marker galactosylcerebroside (GalC). These O4+ GalC- progenitors first appear at birth (10(5)/telencephalon), 2-3 days before O4+ GalC+ oligodendrocytes. The work presented here demonstrates that a major subpopulation of O4+ GalC- progenitors (80%), which we have termed 'proligodendrocytes', is fully committed to terminal oligodendrocyte differentiation. A relatively small, maximal set of nutritional supplements are sufficient for proligodendrocytes to carry out the myelinogenic cascade of differentiated gene expression in a temporally normal manner, in quantitatively significant amounts, in normal ratios of myelin protein isoforms, and in a regulated relationship to the inclusion of myelin-specific products into myelin-like membrane sheets. An important corollary is that this step of myelinogenesis does not require contact with other cell types, in particular neurones and astrocytes, nor does it require unknown growth factors unique to these cell types. Additionally under these conditions, there exists a developmentally quiescent subpopulation (20%) of O4+ GalC- cells that may have significance for understanding the progenitors previously described in adult brain and suggested to be instrumental in remyelination under pathological conditions.

Animals↗
PubMed1993

Clonal heterogeneity in the germinal zone of the developing rat telencephalon.

A double-labeling technique, combining retroviral tagging of individual cell lines (one clone per brain hemisphere) with the simultaneous [3H]thymidine-labeling of dividing cells in S phase, was used to study proliferation characteristics of individual precursor cell lines in the germinal zone of the developing rat forebrain. The cortical germinal zone was found to be segregated into three spatially distinct horizontal populations of precursor cell lineages, which differed in cell cycle kinetics, amount of cell death, and synchronous versus asynchronous mode of proliferation. The striatal germinal zone demonstrated a similar heterogeneity in the cell cycle characteristics of proliferating clones, but did not show nearly as distinct a spatial segregation of these different populations. The results demonstrate the clonal heterogeneity among precursor populations in the telencephalon and the differential spatial organization of the cortical and the striatal germinal zones. This germinal zone heterogeneity may predict some of the differences found among cellular phenotypes in the adult forebrain.

Animals↗
PubMed1997

Emx1 and Emx2 functions in development of dorsal telencephalon.

The genes Emx1 and Emx2 are mouse cognates of a Drosophila head gap gene, empty spiracles, and their expression patterns have suggested their involvement in regional patterning of the forebrain. To define their functions we introduced mutations into these loci. The newborn Emx2 mutants displayed defects in archipallium structures that are believed to play essential roles in learning, memory and behavior: the dentate gyrus was missing, and the hippocampus and medial limbic cortex were greatly reduced in size. In contrast, defects were subtle in adult Emx1 mutant brain. In the early developing Emx2 mutant forebrain, the evagination of cerebral hemispheres was reduced and the roof between the hemispheres was expanded, suggesting the lateral shift of its boundary. Defects were not apparent, however, in the region where Emx1 expression overlaps that of Emx2, nor was any defect found in the early embryonic forebrain caused by mutation of the Emx1 gene, of which expression principally occurs within the Emx2-positive region. Emx2 most likely delineates the palliochoroidal boundary in the absence of Emx1 expression during early dorsal forebrain patterning. In the more lateral region of telencephalon, Emx2-deficiency may be compensated for by Emx1 and vice versa. Phenotypes of newborn brains also suggest that these genes function in neurogenesis corresponding to their later expressions.

Animals↗
PubMed2000

Ace/Fgf8 is required for forebrain commissure formation and patterning of the telencephalon.

Fibroblast growth factors (Fgfs) form a large family of secreted signalling proteins that have a wide variety of roles during embryonic development. Within the central nervous system (CNS) Fgf8 is implicated in patterning neural tissue adjacent to the midbrain-hindbrain boundary. However, the roles of Fgfs in CNS tissue rostral to the midbrain are less clear. Here we examine the patterning of the forebrain in zebrafish embryos that lack functional Fgf8/Ace. We find that Ace is required for the development of midline structures in the forebrain. In the absence of Ace activity, midline cells fail to adopt their normal morphology and exhibit altered patterns of gene expression. This disruption to midline tissue leads to severe commissural axon pathway defects, including misprojections from the eye to ectopic ipsilateral and contralateral targets. Ace is also required for the differentiation of the basal telencephalon and several populations of putative telencephalic neurons but not for overall regional patterning of forebrain derivatives. Finally, we show that ace expression co-localises with anterior neural plate cells that have previously been shown to have forebrain patterning activity. Removal of these cells leads to a failure in induction of ace expression indicating that loss of Ace activity may contribute to the phenotypes observed when anterior neural plate cells are ablated. However, as ace mutant neural plate cells still retain at least some inductive activity, then other signals must also be produced by the anterior margin of the neural plate.

Animals↗
PubMed2000

Genetic control of dorsal-ventral identity in the telencephalon: opposing roles for Pax6 and Gsh2.

We have examined the genetic mechanisms that regulate dorsal-ventral identity in the embryonic mouse telencephalon and, in particular, the specification of progenitors in the cerebral cortex and striatum. The respective roles of Pax6 and Gsh2 in cortical and striatal development were studied in single and double loss-of-function mouse mutants. Gsh2 gene function was found to be essential to maintain the molecular identity of early striatal progenitors and in its absence the ventral telencephalic regulatory genes Mash1 and Dlx are lost from most of the striatal germinal zone. In their place, the dorsal regulators, Pax6, neurogenin 1 and neurogenin 2 are found ectopically. Conversely, Pax6 is required to maintain the correct molecular identity of cortical progenitors. In its absence, neurogenins are lost from the cortical germinal zone and Gsh2, Mash1 and Dlx genes are found ectopically. These reciprocal alterations in cortical and striatal progenitor specification lead to the abnormal development of the cortex and striatum observed in Pax6 (small eye) and Gsh2 mutants, respectively. In support of this, double homozygous mutants for Pax6 and Gsh2 exhibit significant improvements in both cortical and striatal development compared with their respective single mutants. Taken together, these results demonstrate that Pax6 and Gsh2 govern cortical and striatal development by regulating genetically opposing programs that control the expression of each other as well as the regionally expressed developmental regulators Mash1, the neurogenins and Dlx genes in telencephalic progenitors.

Animals↗
PubMed2002

MAPK-upstream protein kinase (MUK) regulates the radial migration of immature neurons in telencephalon of mouse embryo.

The radial migration of differentiating neurons provides an essential step in the generation of laminated neocortex, although its molecular mechanism is not fully understood. We show that the protein levels of a JNK activator kinase, MUK/DLK/ZPK, and JNK activity increase potently and temporally in newly generated neurons in developing mouse telencephalon during radial migration. The ectopic expression of MUK/DLK/ZPK in neural precursor cells in utero impairs radial migration, whereas it allows these cells to leave the ventricular zone and differentiate into neural cells. The MUK/DLK/ZPK protein is associated with dotted structures that are frequently located along microtubules and with Golgi apparatus in cultured embryonic cortical cells. In COS-1 cells, MUK/DLK/ZPK overexpression impairs the radial organization of microtubules without massive depolymerization. These results suggest that MUK/DLK/ZPK and JNK regulate radial cell migration via microtubule-based events.

3T3 Cells↗
PubMed2002

Modulation of the notch signaling by Mash1 and Dlx1/2 regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon.

Notch signaling has a central role in cell fate specification and differentiation. We provide evidence that the Mash1 (bHLH) and Dlx1 and Dlx2 (homeobox) transcription factors have complementary roles in regulating Notch signaling, which in turn mediates the temporal control of subcortical telencephalic neurogenesis in mice. We defined progressively more mature subcortical progenitors (P1, P2 and P3) through their combinatorial expression of MASH1 and DLX2, as well as the expression of proliferative and postmitotic cell markers at E10.5-E11.5. In the absence of Mash1, Notch signaling is greatly reduced and 'early' VZ progenitors (P1 and P2) precociously acquire SVZ progenitor (P3) properties. Comparing the molecular phenotypes of the delta-like 1 and Mash1 mutants, suggests that Mash1 regulates early neurogenesis through Notch-and Delta-dependent and -independent mechanisms. While Mash1 is required for early neurogenesis (E10.5), Dlx1 and Dlx2 are required to downregulate Notch signaling during specification and differentiation steps of 'late' progenitors (P3). We suggest that alternate cell fate choices in the developing telencephalon are controlled by coordinated functions of bHLH and homeobox transcription factors through their differential affects on Notch signaling.

Animals↗
PubMed2005

Neuronal migration and ventral subtype identity in the telencephalon depend on SOX1.

Little is known about the molecular mechanisms and intrinsic factors that are responsible for the emergence of neuronal subtype identity. Several transcription factors that are expressed mainly in precursors of the ventral telencephalon have been shown to control neuronal specification, but it has been unclear whether subtype identity is also specified in these precursors, or if this happens in postmitotic neurons, and whether it involves the same or different factors. SOX1, an HMG box transcription factor, is expressed widely in neural precursors along with the two other SOXB1 subfamily members, SOX2 and SOX3, and all three have been implicated in neurogenesis. SOX1 is also uniquely expressed at a high level in the majority of telencephalic neurons that constitute the ventral striatum (VS). These neurons are missing in Sox1-null mutant mice. In the present study, we have addressed the requirement for SOX1 at a cellular level, revealing both the nature and timing of the defect. By generating a novel Sox1-null allele expressing beta-galactosidase, we found that the VS precursors and their early neuronal differentiation are unaffected in the absence of SOX1, but the prospective neurons fail to migrate to their appropriate position. Furthermore, the migration of non-Sox1-expressing VS neurons (such as those expressing Pax6) was also affected in the absence of SOX1, suggesting that Sox1-expressing neurons play a role in structuring the area of the VS. To test whether SOX1 is required in postmitotic cells for the emergence of VS neuronal identity, we generated mice in which Sox1 expression was directed to all ventral telencephalic precursors, but to only a very few VS neurons. These mice again lacked most of the VS, indicating that SOX1 expression in precursors is not sufficient for VS development. Conversely, the few neurons in which Sox1 expression was maintained were able to migrate to the VS. In conclusion, Sox1 expression in precursors is not sufficient for VS neuronal identity and migration, but this is accomplished in postmitotic cells, which require the continued presence of SOX1. Our data also suggest that other SOXB1 members showing expression in specific neuronal populations are likely to play continuous roles from the establishment of precursors to their final differentiation.

Animals↗
PubMed2004

Gene regulation by song in the auditory telencephalon of songbirds.

Inducible gene expression analysis has been successfully used to identify and characterize areas involved in the auditory processing of song in songbirds. When songbirds hear song, zenk, a gene encoding a transcriptional regulator linked to synaptic plasticity, is rapidly and transiently induced in several discrete areas of the telencephalon. This phenomenon is most marked in the caudomedial neostriatum (NCM), a major auditory processing area. zenk induction by song has proven very useful to investigate the functional organization of NCM as well as to characterize song-responding neurons in this brain area. Combined with data from anatomical and electrophysiological studies, the results of gene expression analysis suggest that NCM is involved in the auditory processing of complex sounds such as song and possibly in the formation and/or storage of song auditory memories. Thus, NCM appears to play a prominent role in perceptual aspects of vocal communication, and potentially in the process of vocal learning in songbirds and other vocal learning avian orders, i.e. parrots and hummingbirds.

Acoustic Stimulation↗
PubMed2000

Cell migration and aggregation in the developing telencephalon: pulse-labeling chick embryos with bromodeoxyuridine.

Previous studies had concluded that the avian telencephalon develops according to an outside-in schedule of neurogenesis, with relatively little migration of young neuroblasts past older cells. These previous studies had, however, been based on the "cumulative labeling" method, which is less accurate than the "pulse-labeling" method typically used in mammals. In the present study, we pulse-labeled chick embryos by injecting low doses of the thymidine analog bromodeoxyuridine (BrdU) directly into the circulatory system of chick embryos at 6 d of incubation. The brains of these embryos were then examined for anti-BrdU-labeled cells at postinjection survival times from 30 min to 10 d. Comparisons across different survival times, as well as with cases in which BrdU was injected on day 7, suggested that our effective pulse duration is <24 hr. This was confirmed by injecting tritiated thymidine 24 hr after the BrdU and seeing no double-labeled cells. Several deviations from the previously reported pattern of telencephalic neurogenesis were also noted. Most importantly, the cells born on day 6 in the avian Wulst, the likely homolog of mammalian neocortex, end up homogeneously distributed throughout the Wulst, which suggests that many of them are migrating past older cells. Furthermore, the cells born on day 6 in the ventral hyperstriatum and dorsal neostriatum gradually (over the course of 2-3 d) aggregate into distinct multicellular clusters, which suggests that isochronic cells in these regions adhere preferentially to one another. Finally, the data reveal a proliferative subventricular zone similar to that observed in the ganglionic eminences of mammalian embryos.

Animals↗
PubMed2001

The expression pattern of the cell cycle inhibitor p19(INK4d) by progenitor cells of the rat embryonic telencephalon and neonatal anterior subventricular zone.

In this study we investigated whether the pattern of expression of the cyclin-dependent kinase inhibitor p19(INK4d) by the unique progenitor cells of the neonatal anterior subventricular zone (SVZa) can account for their ability to divide even though they express phenotypic characteristics of differentiated neurons. p19(INK4d) was chosen for analysis because it usually acts to block permanently the cell cycle at the G(1) phase. p19(INK4d) immunoreactivity and the incorporation of bromodeoxyuridine (BrdU) by SVZa cells were compared with that of the more typical progenitor cells of the prenatal telencephalic ventricular zone. In the developing telencephalon, p19(INK4d) is expressed by postmitotic cells and has a characteristic perinuclear distribution depending on the laminar position and state of differentiation of a cell. Moreover, the laminar-specific staining of the developing cerebral cortex revealed that the ventricular zone (VZ) is divided into p19(INK4d)(+) and p19(INK4d)(-) sublaminae, indicating that the VZ has a previously unrecognized level of functional organization. Furthermore, the rostral migratory stream, traversed by the SVZa-derived cells, exhibits an anterior(high)-posterior(low) gradient of p19(INK4d) expression. On the basis of the p19(INK4d) immunoreactivity and BrdU incorporation, SVZa-derived cells appear to exit and reenter the cell cycle successively. Thus, in contrast to telencephalic VZ cells, SVZa cells continue to undergo multiple rounds of division and differentiation before becoming postmitotic.

Animals↗
PubMed2001

[Macrophages in the choroid plexus of the embryonic telencephalon].

Using electron microscopy and immunocytochemistry distribution of macrophages in anlage of telencephalon choroid plexus was studied in 5-9 wks old human embryos. CD68 gene expression by intraepithelial macrophages that appear in anlage of choroid plexus (epithelial plate) was established to begin at 5th week of development. Accumulation of macrophages in embryonic connective tissue of choroid plexus anlage, appearance of intraepithelial macrophages, following appearance of free macrophages and supraependymal cells in brain ventricles (on wk 6-7) indicates that in human embryos choroid plexus anlage is a migration zone for macrophageal serie cells that penetrate into the cavity of the developing brain.

Antibodies, Monoclonal↗