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Journal articles on the topic 'Developing telencephalon'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Grove, E. A., S. Tole, J. Limon, L. Yip, and C. W. Ragsdale. "The hem of the embryonic cerebral cortex is defined by the expression of multiple Wnt genes and is compromised in Gli3-deficient mice." Development 125, no. 12 (June 15, 1998): 2315–25. http://dx.doi.org/10.1242/dev.125.12.2315.

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In the developing vertebrate CNS, members of the Wnt gene family are characteristically expressed at signaling centers that pattern adjacent parts of the neural tube. To identify candidate signaling centers in the telencephalon, we isolated Wnt gene fragments from cDNA derived from embryonic mouse telencephalon. In situ hybridization experiments demonstrate that one of the isolated Wnt genes, Wnt7a, is broadly expressed in the embryonic telencephalon. By contrast, three others, Wnt3a, 5a and a novel mouse Wnt gene, Wnt2b, are expressed only at the medial edge of the telencephalon, defining the hem of the cerebral cortex. The Wnt-rich cortical hem is a transient, neuron-containing, neuroepithelial structure that forms a boundary between the hippocampus and the telencephalic choroid plexus epithelium (CPe) throughout their embryonic development. Indicating a close developmental relationship between the cortical hem and the CPe, Wnt gene expression is upregulated in the cortical hem both before and just as the CPe begins to form, and persists until birth. In addition, although the cortical hem does not show features of differentiated CPe, such as expression of transthyretin mRNA, the CPe and cortical hem are linked by shared expression of members of the Bmp and Msx gene families. In the extra-toesJ (XtJ) mouse mutant, telencephalic CPe fails to develop. We show that Wnt gene expression is deficient at the cortical hem in XtJ/XtJ mice, but that the expression of other telencephalic developmental control genes, including Wnt7a, is maintained. The XtJ mutant carries a deletion in Gli3, a vertebrate homolog of the Drosophila gene cubitus interruptus (ci), which encodes a transcriptional regulator of the Drosophila Wnt gene, wingless. Our observations indicate that Gli3 participates in Wnt gene regulation in the vertebrate telencephalon, and suggest that the loss of telencephalic choroid plexus in XtJ mice is due to defects in the cortical hem that include Wnt gene misregulation.

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2

Striedter, Georg F., and Christine J. Charvet. "Telencephalon enlargement by the convergent evolution of expanded subventricular zones." Biology Letters 5, no. 1 (October 7, 2008): 134–37. http://dx.doi.org/10.1098/rsbl.2008.0439.

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Some mammals and birds independently evolved an enlarged telencephalon. They appear to have done so, at least in part, by developing a thick telencephalic subventricular zone (SVZ). We suggest that this correlation between telencephalic enlargement and SVZ expansion is due to a mechanical constraint acting on the proliferative ventricular zone (VZ). Essentially, we argue that rapid proliferation in the VZ after post-mitotic cells in the overlying mantle zone have begun to form limits the VZ's tangential expandability and forces some proliferating cells to emigrate from the VZ and expand the pool of proliferating cells that comprise the SVZ.

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3

Shinya, Minori, Sumito Koshida, Atsushi Sawada, Atsushi Kuroiwa, and Hiroyuki Takeda. "Fgf signalling through MAPK cascade is required for development of the subpallial telencephalon in zebrafish embryos." Development 128, no. 21 (November 1, 2001): 4153–64. http://dx.doi.org/10.1242/dev.128.21.4153.

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The telencephalon is formed in the most anterior part of the central nervous system (CNS) and is organised into ventral subpallial and dorsal pallial domains. In mice, it has been demonstrated that Fgf signalling has an important role in induction and patterning of the telencephalon. However, the precise role of Fgf signalling is still unclear, owing to overlapping functions of Fgf family genes. To address this, we have examined, in zebrafish embryos, the activation of Ras/mitogen-activated protein kinase (MAPK), one of the major downstream targets of Fgf signalling. Immunohistochemical analysis reveals that an extracellular signal-regulated kinase (ERK), a vertebrate MAPK is activated in the anterior neural boundary (ANB) of the developing CNS at early segmentation stages. Experiments with Fgf inhibitors reveal that ERK activation at this stage is totally dependent on Fgf signalling. Interestingly, a substantial amount of ERK activation is observed in ace mutants in which fgf8 gene is mutated. We then examine the function of Fgf signalling in telencephalic development by use of several inhibitors to Fgf signalling cascade, including dominant-negative forms of Ras (RasN17) and the Fgf receptor (Fgfr), and a chemical inhibitor of Fgfr, SU5402. In treated embryos, the induction of telencephalic territory normally proceeded but the development of the subpallial telencephalon was suppressed, indicating that Fgf signalling is required for the regionalisation within the telencephalon. Finally, antisense experiments with morpholino-modified oligonucleotides suggest that zebrafish fgf3, which is also expressed in the ANB, co-operates with fgf8 in subpallial development.

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4

Chapouton, P., A. Gartner, and M. Gotz. "The role of Pax6 in restricting cell migration between developing cortex and basal ganglia." Development 126, no. 24 (December 15, 1999): 5569–79. http://dx.doi.org/10.1242/dev.126.24.5569.

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It is not clear to what extent restricted cell migration contributes to patterning of the developing telencephalon, since both restricted and widespread cell migration have been observed. Here, we have analysed dorso-ventral cell migration in the telencephalon of Pax6 mutant mice (Small Eye). The transcription factor Pax6 is expressed in the dorsal telencephalon, the cerebral cortex. Focal injections of adenoviral vectors containing the green fluorescent protein were used to follow and quantify cell movements between two adjacent regions in the developing telencephalon, the cerebral cortex and the ganglionic eminence (the prospective basal ganglia). The analysis in wild-type mice confirmed that the cortico-striatal boundary acts as a semipermeable filter and allows a proportion of cells from the ganglionic eminence to invade the cortex, but not vice versa. Ventro-dorsal cell migration was strongly enhanced in the Pax6 mutant. An essential function of Pax6 in the regionalisation of the telencephalon is then to limit the invasion of the cortex by cells originating in the ganglionic eminence. Cortical cells, however, remain confined to the cortex in the Pax6 mutant. Thus, dorsal and ventral cells are restricted to their respective territories by distinct mechanisms.

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5

Smith, D. "Retinoic Acid Synthesis for the Developing Telencephalon." Cerebral Cortex 11, no. 10 (October 1, 2001): 894–905. http://dx.doi.org/10.1093/cercor/11.10.894.

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6

Girós, Amparo, Javier Morante, Cristina Gil-Sanz, Alfonso Fairén, and Mercedes Costell. "Perlecan controls neurogenesis in the developing telencephalon." BMC Developmental Biology 7, no. 1 (2007): 29. http://dx.doi.org/10.1186/1471-213x-7-29.

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7

Pineda, Daniel, Beatriz García, José Luis Olmos, José Carlos Dávila, María Ángeles Real, and Salvador Guirado. "Semaphorin5A expression in the developing chick telencephalon." Brain Research Bulletin 66, no. 4-6 (September 2005): 436–40. http://dx.doi.org/10.1016/j.brainresbull.2005.02.011.

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8

Tichy, Julia, Jenny Zinke, Benedikt Bunz, Richard Meyermann, Patrick N. Harter, and Michel Mittelbronn. "Expression Profile of Sonic Hedgehog Pathway Members in the Developing Human Fetal Brain." BioMed Research International 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/494269.

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The Sonic Hedgehog (SHH) pathway plays a central role in the developing mammalian CNS. In our study, we aimed to investigate the spatiotemporalSHHpathway expression pattern in human fetal brains. We analyzed 22 normal fetal brains for Shh, Patched, Smoothened, and Gli1-3 expression by immunohistochemistry. In the telencephalon, strongest expression of Shh, Smoothened, and Gli2 was found in the cortical plate (CP) and ventricular zone. Patched was strongly upregulated in the ventricular zone and Gli1 in the CP. In the cerebellum,SHHpathway members were strongly expressed in the external granular layer (EGL).SHHpathway members significantly decreased over time in the ventricular and subventricular zone and in the cerebellar EGL, while increasing levels were found in more superficial telencephalic layers. Our findings show thatSHHpathway members are strongly expressed in areas important for proliferation and differentiation and indicate a temporal expression gradient in telencephalic and cerebellar layers probably due to decreased proliferation of progenitor cells and increased differentiation. Our data about the spatiotemporal expression ofSHHpathway members in the developing human brain serves as a base for the understanding of both normal and pathological CNS development.

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9

Zappone, M. V., R. Galli, R. Catena, N. Meani, S. De Biasi, E. Mattei, C. Tiveron, et al. "Sox2 regulatory sequences direct expression of a (beta)-geo transgene to telencephalic neural stem cells and precursors of the mouse embryo, revealing regionalization of gene expression in CNS stem cells." Development 127, no. 11 (June 1, 2000): 2367–82. http://dx.doi.org/10.1242/dev.127.11.2367.

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Sox2 is one of the earliest known transcription factors expressed in the developing neural tube. Although it is expressed throughout the early neuroepithelium, we show that its later expression must depend on the activity of more than one regionally restricted enhancer element. Thus, by using transgenic assays and by homologous recombination-mediated deletion, we identify a region upstream of Sox2 (−5.7 to −3.3 kb) which can not only drive expression of a (beta)-geo transgene to the developing dorsal telencephalon, but which is required to do so in the context of the endogenous gene. The critical enhancer can be further delimited to an 800 bp fragment of DNA surrounding a nuclease hypersensitive site within this region, as this is sufficient to confer telencephalic expression to a 3.3 kb fragment including the Sox2 promoter, which is otherwise inactive in the CNS. Expression of the 5.7 kb Sox2(beta)-geo transgene localizes to the neural plate and later to the telencephalic ventricular zone. We show, by in vitro clonogenic assays, that transgene-expressing (and thus G418-resistant) ventricular zone cells include cells displaying functional properties of stem cells, i.e. self-renewal and multipotentiality. We further show that the majority of telencephalic stem cells express the transgene, and this expression is largely maintained over two months in culture (more than 40 cell divisions) in the absence of G418 selective pressure. In contrast, stem cells grown in parallel from the spinal cord never express the transgene, and die in G418. Expression of endogenous telencephalic genes was similarly observed in long-term cultures derived from the dorsal telencephalon, but not in spinal cord-derived cultures. Thus, neural stem cells of the midgestation embryo are endowed with region-specific gene expression (at least with respect to some networks of transcription factors, such as that driving telencephalic expression of the Sox2 transgene), which can be inherited through multiple divisions outside the embryonic environment.

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10

Rakic, Sonja, and Nada Zecevic. "Programmed cell death in the developing human telencephalon." European Journal of Neuroscience 12, no. 8 (August 2000): 2721–34. http://dx.doi.org/10.1046/j.1460-9568.2000.00153.x.

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11

Howard, Brian, Yanhui Chen, and Nada Zecevic. "Cortical progenitor cells in the developing human telencephalon." Glia 53, no. 1 (2005): 57–66. http://dx.doi.org/10.1002/glia.20259.

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12

Cheng, Lin, Zhiliang Tian, Ruizhen Sun, Zhendong Wang, Jingling Shen, Zhiyan Shan, Lianhong Jin, and Lei Lei. "ApoER2 and VLDLR in the developing human telencephalon." European Journal of Paediatric Neurology 15, no. 4 (July 2011): 361–67. http://dx.doi.org/10.1016/j.ejpn.2011.03.011.

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13

Caric, Damira, Heather Raphael, Jane Viti, Angela Feathers, Debbie Wancio, and Laura Lillien. "EGFRs mediate chemotactic migration in the developing telencephalon." Development 128, no. 21 (November 1, 2001): 4203–16. http://dx.doi.org/10.1242/dev.128.21.4203.

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Epidermal growth factor receptors (EGFRs) have been implicated in the control of migration in the telencephalon, but the mechanism underlying their contribution is unclear. We show that expression of a threshold level of EGFRs confers chemotactic competence in stem cells, neurons and astrocytes in cortical explants. This level of receptor expression is normally achieved by a subpopulation of cells during mid-embryonic development. Cells that express high levels of EGFR are located in migration pathways, including the tangential pathway to the olfactory bulb via the rostral migratory stream (RMS), the lateral cortical stream (LCS) leading to ventrolateral cortex and the radial pathway from proliferative zones to cortical plate. The targets of these pathways express the ligands HB-EGF and/or TGFα. To test the idea that EGFRs mediate chemotactic migration these pathways, we increased the size of the population of cells expressing threshold levels of EGFRs in vivo by viral transduction. Our results suggest that EGFRs mediate migration radially to the cortical plate and ventrolaterally in the LCS, but not tangentially in the RMS. Within the bulb, however, EGFRs also mediate radial migration. Our findings suggest that developmental changes in EGFR expression, together with changes in ligand expression regulate the migration of specific populations of cells in the telencephalon by a chemoattractive mechanism.

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14

Anderson, S. A., O. Marin, C. Horn, K. Jennings, and J. L. Rubenstein. "Distinct cortical migrations from the medial and lateral ganglionic eminences." Development 128, no. 3 (February 1, 2001): 353–63. http://dx.doi.org/10.1242/dev.128.3.353.

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Recent evidence suggests that projection neurons and interneurons of the cerebral cortex are generally derived from distinct proliferative zones. Cortical projection neurons originate from the cortical ventricular zone (VZ), and then migrate radially into the cortical mantle, whereas most cortical interneurons originate from the basal telencephalon and migrate tangentially into the developing cortex. Previous studies using methods that label both proliferative and postmitotic cells have found that cortical interneurons migrate from two major subdivisions of the developing basal telencephalon: the medial and lateral ganglionic eminences (MGE and LGE). Since these studies labeled cells by methods that do not distinguish between the proliferating cells and those that may have originated elsewhere, we have studied the contribution of the MGE and LGE to cortical interneurons using fate mapping and genetic methods. Transplantation of BrdU-labeled MGE or LGE neuroepithelium into the basal telencephalon of unlabeled telencephalic slices enabled us to follow the fate of neurons derived from each of these primordia. We have determined that early in neurogenesis GABA-expressing cells from the MGE tangentially migrate into the cerebral cortex, primarily via the intermediate zone, whereas cells from the LGE do not. Later in neurogenesis, LGE-derived cells also migrate into the cortex, although this migration occurs primarily through the subventricular zone. Some of these LGE-derived cells invade the cortical plate and express GABA, while others remain within the cortical proliferative zone and appear to become mitotically active late in gestation. In addition, by comparing the phenotypes of mouse mutants with differential effects on MGE and LGE migration, we provide evidence that the MGE and LGE may give rise to different subtypes of cortical interneurons.

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15

Marteau, Léna, Emilie Pacary, Samuel Valable, Myriam Bernaudin, François Guillemot, and Edwige Petit. "Angiopoietin-2 Regulates Cortical Neurogenesis in the Developing Telencephalon." Cerebral Cortex 21, no. 7 (December 2, 2010): 1695–702. http://dx.doi.org/10.1093/cercor/bhq243.

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16

Gohlke, Julia M., Pat S. Stockton, Stella Sieber, Julie Foley, and Christopher J. Portier. "AhR-mediated gene expression in the developing mouse telencephalon." Reproductive Toxicology 28, no. 3 (November 2009): 321–28. http://dx.doi.org/10.1016/j.reprotox.2009.05.067.

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17

Gohlke, J. M., P. Stockton, S. Sieber, J. Foley, and C. J. Portier. "AhR-mediated gene expression in the developing mouse telencephalon." Neurotoxicology and Teratology 31, no. 4 (July 2009): 241. http://dx.doi.org/10.1016/j.ntt.2009.04.021.

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18

Markenscoff-Papadimitriou, Eirene, Sean Whalen, Pawel Przytycki, Reuben Thomas, Fadya Binyameen, Tomasz J. Nowakowski, Arnold R. Kriegstein, et al. "A Chromatin Accessibility Atlas of the Developing Human Telencephalon." Cell 182, no. 3 (August 2020): 754–69. http://dx.doi.org/10.1016/j.cell.2020.06.002.

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19

Visel, Axel, Leila Taher, Hani Girgis, Dalit May, Olga Golonzhka, Renee V. Hoch, Gabriel L. McKinsey, et al. "A High-Resolution Enhancer Atlas of the Developing Telencephalon." Cell 152, no. 4 (February 2013): 895–908. http://dx.doi.org/10.1016/j.cell.2012.12.041.

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20

Schuurmans, Carol, and François Guillemot. "Molecular mechanisms underlying cell fate specification in the developing telencephalon." Current Opinion in Neurobiology 12, no. 1 (February 2002): 26–34. http://dx.doi.org/10.1016/s0959-4388(02)00286-6.

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21

Marklund, M. "Retinoic acid signalling specifies intermediate character in the developing telencephalon." Development 131, no. 17 (September 1, 2004): 4323–32. http://dx.doi.org/10.1242/dev.01308.

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22

Striedter, Georg F., and Sarah Beydler. "Distribution of radial glia in the developing telencephalon of chicks." Journal of Comparative Neurology 387, no. 3 (October 27, 1997): 399–420. http://dx.doi.org/10.1002/(sici)1096-9861(19971027)387:3<399::aid-cne6>3.0.co;2-w.

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23

Qin, Shenyue, Mayur Madhavan, Ronald R. Waclaw, Masato Nakafuku, and Kenneth Campbell. "Characterization of a newGsx2-creline in the developing mouse telencephalon." genesis 54, no. 10 (September 29, 2016): 542–49. http://dx.doi.org/10.1002/dvg.22980.

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24

Veney, Sean L., Camilla Peabody, George W. Smith, and Juli Wade. "Sexually dimorphic neurocalcin expression in the developing zebra finch telencephalon." Journal of Neurobiology 56, no. 4 (August 8, 2003): 372–86. http://dx.doi.org/10.1002/neu.10246.

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25

Luk, Kelvin C., and Abbas F. Sadikot. "Glutamate and Regulation of Proliferation in the Developing Mammalian Telencephalon." Developmental Neuroscience 26, no. 2-4 (2004): 218–28. http://dx.doi.org/10.1159/000082139.

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26

Hamasaki, T. "Early-generated Preplate Neurons in the Developing Telencephalon: Inward Migration into the Developing Striatum." Cerebral Cortex 11, no. 5 (May 1, 2001): 474–84. http://dx.doi.org/10.1093/cercor/11.5.474.

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27

Chun, J. J. M., M. J. Nakamura, and C. J. Shatz. "Transient cells of the developing mammalian telencephalon are peptide-immunoreactive neurons." Nature 325, no. 6105 (February 1987): 617–20. http://dx.doi.org/10.1038/325617a0.

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28

Szele, Francis G., Helen K. Chin, Marisa A. Rowlson, and Constance L. Cepko. "Sox-9 and cDachsund-2 expression in the developing chick telencephalon." Mechanisms of Development 112, no. 1-2 (March 2002): 179–82. http://dx.doi.org/10.1016/s0925-4773(01)00641-4.

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29

Szele, Francis G., and Constance L. Cepko. "The Dispersion of Clonally Related Cells in the Developing Chick Telencephalon." Developmental Biology 195, no. 2 (March 1998): 100–113. http://dx.doi.org/10.1006/dbio.1997.8725.

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30

Acklin, S. E., and D. van der Kooy. "Clonal heterogeneity in the germinal zone of the developing rat telencephalon." Development 118, no. 1 (May 1, 1993): 175–92. http://dx.doi.org/10.1242/dev.118.1.175.

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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.

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31

Radhakrishnan, Balachandar, and A. Alwin Prem Anand. "Role of miRNA-9 in Brain Development." Journal of Experimental Neuroscience 10 (January 2016): JEN.S32843. http://dx.doi.org/10.4137/jen.s32843.

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MicroRNAs (miRNAs) are a class of small regulatory RNAs involved in gene regulation. The regulation is effected by either translational inhibition or transcriptional silencing. In vertebrates, the importance of miRNA in development was discovered from mice and zebrafish dicer knockouts. The miRNA-9 (miR-9) is one of the most highly expressed miRNAs in the early and adult vertebrate brain. It has diverse functions within the developing vertebrate brain. In this article, the role of miR-9 in the developing forebrain (telencephalon and diencephalon), midbrain, hindbrain, and spinal cord of vertebrate species is highlighted. In the forebrain, miR-9 is necessary for the proper development of dorsoventral telencephalon by targeting marker genes expressed in the telencephalon. It regulates proliferation in telencephalon by regulating Foxg1, Pax6, Gsh2, and Meis2 genes. The feedback loop regulation between miR-9 and Nr2e1/Tlx helps in neuronal migration and differentiation. Targeting Foxp1 and Foxp2, and Map1b by miR-9 regulates the radial migration of neurons and axonal development. In the organizers, miR-9 is inversely regulated by hairy1 and Fgf8 to maintain zona limitans interthalamica and midbrain-hindbrain boundary (MHB). It maintains the MHB by inhibiting Fgf signaling genes and is involved in the neurogenesis of the midbrain-hindbrain by regulating Her genes. In the hindbrain, miR-9 modulates progenitor proliferation and differentiation by regulating Her genes and Elav3. In the spinal cord, miR-9 modulates the regulation of Foxp1 and Onecut1 for motor neuron development. In the forebrain, midbrain, and hindbrain, miR-9 is necessary for proper neuronal progenitor maintenance, neurogenesis, and differentiation. In vertebrate brain development, miR-9 is involved in regulating several region-specific genes in a spatiotemporal pattern.

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32

Moore, Nicholas S., Robert A. Mans, Mackenzee K. McCauley, Colton S. Allgood, and Keri A. Barksdale. "Critical Effects on Akt Signaling in Adult Zebrafish Brain Following Alterations in Light Exposure." Cells 10, no. 3 (March 12, 2021): 637. http://dx.doi.org/10.3390/cells10030637.

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Evidence from human and animal studies indicate that disrupted light cycles leads to alterations of the sleep state, poor cognition, and the risk of developing neuroinflammatory and generalized health disorders. Zebrafish exhibit a diurnal circadian rhythm and are an increasingly popular model in studies of neurophysiology and neuropathophysiology. Here, we investigate the effect of alterations in light cycle on the adult zebrafish brain: we measured the effect of altered, unpredictable light exposure in adult zebrafish telencephalon, homologous to mammalian hippocampus, and the optic tectum, a significant visual processing center with extensive telencephalon connections. The expression of heat shock protein-70 (HSP70), an important cell stress mediator, was significantly decreased in optic tectum of adult zebrafish brain following four days of altered light exposure. Further, pSer473-Akt (protein kinase B) was significantly reduced in telencephalon following light cycle alteration, and pSer9-GSK3β (glycogen synthase kinase-3β) was significantly reduced in both the telencephalon and optic tectum of light-altered fish. Animals exposed to five minutes of environmental enrichment showed significant increase in pSer473Akt, which was significantly attenuated by four days of altered light exposure. These data show for the first time that unpredictable light exposure alters HSP70 expression and dysregulates Akt-GSK3β signaling in the adult zebrafish brain.

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33

Pratt, T., T. Vitalis, N. Warren, J. M. Edgar, J. O. Mason, and D. J. Price. "A role for Pax6 in the normal development of dorsal thalamus and its cortical connections." Development 127, no. 23 (December 1, 2000): 5167–78. http://dx.doi.org/10.1242/dev.127.23.5167.

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The transcription factor Pax6 is widely expressed throughout the developing nervous system, including most alar regions of the newly formed murine diencephalon. Later in embryogenesis its diencephalic expression becomes more restricted. It persists in the developing anterior thalamus (conventionally termed “ventral” thalamus) and pretectum but is downregulated in the body of the posterior (dorsal) thalamus. At the time of this downregulation, the dorsal thalamus forms its major axonal efferent pathway via the ventral telencephalon to the cerebral cortex. This pathway is absent in mice lacking functional Pax6 (small eye homozygotes: Sey/Sey). We tested whether the mechanism underlying this defect includes abnormalities of the dorsal thalamus itself. We exploited a new transgenic mouse ubiquitously expressing green fluorescent protein tagged with tau, in which axonal tracts are clearly visible, and co-cultured dorsal thalamic explants from Pax6(+/+)or Pax6(Sey/Sey)embryos carrying the transgene with wild-type tissues from other regions of the forebrain. Whereas Pax6(+/+)thalamic explants produced strong innervation of wild-type ventral telencephalic explants in a pattern that mimicked the thalamocortical tract in vivo, Pax6(Sey)(/Sey) explants did not, indicating a defect in the ability of mutant dorsal thalamic cells to respond to signals normally present in ventral telencephalon. Pax6(Sey)(/Sey) embryos also showed early alterations in the expression of regulatory genes in the region destined to become dorsal thalamus. Whereas in normal mice Nkx2.2 and Lim1/Lhx1 are expressed ventral to this region, in the mutants their expression domains are throughout it, suggesting that a primary action of Pax6 is to generate correct dorsoventral patterning in the diencephalon. Our results suggest that normal thalamocortical development requires the actions of Pax6 within the dorsal thalamus itself.

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34

Hamasaki, T. "Inward migration of the early-generated preplate neurons in the developing telencephalon." Neuroscience Research 38 (2000): S128. http://dx.doi.org/10.1016/s0168-0102(00)81614-4.

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35

Haydar, T. F., E. Ang, and P. Rakic. "Mitotic spindle rotation and mode of cell division in the developing telencephalon." Proceedings of the National Academy of Sciences 100, no. 5 (February 14, 2003): 2890–95. http://dx.doi.org/10.1073/pnas.0437969100.

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36

Corbin, J. G., N. Gaiano, R. P. Machold, A. Langston, and G. Fishell. "The Gsh2 homeodomain gene controls multiple aspects of telencephalic development." Development 127, no. 23 (December 1, 2000): 5007–20. http://dx.doi.org/10.1242/dev.127.23.5007.

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Homeobox genes have recently been demonstrated to be important for the proper patterning of the mammalian telencephalon. One of these genes is Gsh2, whose expression in the forebrain is restricted to the ventral domain. In this study, we demonstrate that Gsh2 is a downstream target of sonic hedgehog and that lack of Gsh2 results in profound defects in telencephalic development. Gsh2 mutants have a significant decrease in the expression of numerous genes that mark early development of the lateral ganglionic eminence, the striatal anlage. Accompanying this early loss of patterning genes is an initial expansion of dorsal telencephalic markers across the cortical-striatal boundary into the lateral ganglionic eminence. Interestingly, as development proceeds, there is compensation for this early loss of markers that is coincident with a molecular re-establishment of the cortical-striatal boundary. Despite this compensation, there is a defect in the development of distinct subpopulations of striatal neurons. Moreover, while our analysis suggests that the migration of the ventrally derived interneurons to the developing cerebral cortex is not significantly affected in Gsh2 mutants, there is a distinct delay in the appearance of GABAergic interneurons in the olfactory bulb. Taken together, our data support a model in which Gsh2, in response to sonic hedgehog signaling, plays a crucial role in multiple aspects of telencephalic development.

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Denaxa, Myrto, Chun-Hung Chan, Melitta Schachner, John G. Parnavelas, and Domna Karagogeos. "The adhesion molecule TAG-1 mediates the migration of cortical interneurons from the ganglionic eminence along the corticofugal fiber system." Development 128, no. 22 (November 15, 2001): 4635–44. http://dx.doi.org/10.1242/dev.128.22.4635.

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Cortical nonpyramidal cells, the GABA-containing interneurons, originate mostly in the medial ganglionic eminence of the ventral telencephalon and follow tangential migratory routes to reach the dorsal telencephalon. Although several genes that play a role in this migration have been identified, the underlying cellular and molecular cues are not fully understood. We provide evidence that the neural cell adhesion molecule TAG-1 mediates the migration of cortical interneurons. We show that the migration of these neurons occurs along the TAG-1-expressing axons of the developing corticofugal system. The spatial and temporal pattern of expression of TAG-1 on corticofugal fibers coincides with the order of appearance of GABAergic cells in the developing cortex. Blocking the function of TAG-1, but not of L1, another adhesion molecule and binding partner of TAG-1, results in a marked reduction of GABAergic neurons in the cortex. These observations reveal a mechanism by which the adhesion molecule TAG-1, known to be involved in axonal pathfinding, also takes part in neuronal migration.

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Kim, Anthony S., Daniel H. Lowenstein, and Samuel J. Pleasure. "Wnt receptors and Wnt inhibitors are expressed in gradients in the developing telencephalon." Mechanisms of Development 103, no. 1-2 (May 2001): 167–72. http://dx.doi.org/10.1016/s0925-4773(01)00342-2.

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39

v. Frowein, Julia, Kenneth Campbell, and Magdalena Götz. "Expression of Ngn1, Ngn2, Cash1, Gsh2 and Sfrp1 in the developing chick telencephalon." Mechanisms of Development 110, no. 1-2 (January 2002): 249–52. http://dx.doi.org/10.1016/s0925-4773(01)00590-1.

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Hutton, Scott R., and Larysa H. Pevny. "SOX2 expression levels distinguish between neural progenitor populations of the developing dorsal telencephalon." Developmental Biology 352, no. 1 (April 2011): 40–47. http://dx.doi.org/10.1016/j.ydbio.2011.01.015.

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Liao, Wen-Lin, Hsiao-Fang Wang, Hsiu-Chao Tsai, Pierre Chambon, Michael Wagner, Akira Kakizuka, and Fu-Chin Liu. "Retinoid signaling competence and RAR?-mediated gene regulation in the developing mammalian telencephalon." Developmental Dynamics 232, no. 4 (2005): 887–900. http://dx.doi.org/10.1002/dvdy.20281.

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Chen, Chun-Chun, Candace M. Winkler, Andreas R. Pfenning, and Erich D. Jarvis. "Molecular profiling of the developing avian telencephalon: Regional timing and brain subdivision continuities." Journal of Comparative Neurology 521, no. 16 (September 25, 2013): 3666–701. http://dx.doi.org/10.1002/cne.23406.

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43

Schlinger, BA, S. Amur-Umarjee, P. Shen, AT Campagnoni, and AP Arnold. "Neuronal and non-neuronal aromatase in primary cultures of developing zebra finch telencephalon." Journal of Neuroscience 14, no. 12 (December 1, 1994): 7541–52. http://dx.doi.org/10.1523/jneurosci.14-12-07541.1994.

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Hellbach, Nicole, Stefan Weise, and Tanja Vogel. "ISDN2014_0056: Tgfbr2 conditional knock‐out in the developing telencephalon results in neurovascular defects." International Journal of Developmental Neuroscience 47, Part_A (December 2015): 12. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.043.

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45

Yun, Kyuson, Seth Fischman, Jane Johnson, Martin Hrabe de Angelis, Gerry Weinmaster, and John L. R. Rubenstein. "Modulation of the notch signaling by Mash1 and Dlx1/2regulates sequential specification and differentiation of progenitor cell types in the subcortical telencephalon." Development 129, no. 21 (November 1, 2002): 5029–40. http://dx.doi.org/10.1242/dev.129.21.5029.

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Notch signaling has a central role in cell fate specification and differentiation. We provide evidence that the Mash1 (bHLH) andDlx1 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 ofMash1, 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.

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Eze, Ugomma C., Aparna Bhaduri, Maximilian Haeussler, Tomasz J. Nowakowski, and Arnold R. Kriegstein. "Single-cell atlas of early human brain development highlights heterogeneity of human neuroepithelial cells and early radial glia." Nature Neuroscience 24, no. 4 (March 15, 2021): 584–94. http://dx.doi.org/10.1038/s41593-020-00794-1.

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AbstractThe human cortex comprises diverse cell types that emerge from an initially uniform neuroepithelium that gives rise to radial glia, the neural stem cells of the cortex. To characterize the earliest stages of human brain development, we performed single-cell RNA-sequencing across regions of the developing human brain, including the telencephalon, diencephalon, midbrain, hindbrain and cerebellum. We identify nine progenitor populations physically proximal to the telencephalon, suggesting more heterogeneity than previously described, including a highly prevalent mesenchymal-like population that disappears once neurogenesis begins. Comparison of human and mouse progenitor populations at corresponding stages identifies two progenitor clusters that are enriched in the early stages of human cortical development. We also find that organoid systems display low fidelity to neuroepithelial and early radial glia cell types, but improve as neurogenesis progresses. Overall, we provide a comprehensive molecular and spatial atlas of early stages of human brain and cortical development.

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Cheng, Y., S. Leung, and D. Mangoura. "Transient suppression of cortactin ectopically induces large telencephalic neurons towards a GABAergic phenotype." Journal of Cell Science 113, no. 18 (September 15, 2000): 3161–72. http://dx.doi.org/10.1242/jcs.113.18.3161.

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Excitatory and inhibitory neuronal cell fates require specific expression of both neurotransmitter and morphological phenotypes. The role of the F-actin cytoskeleton in morphological phenotypes has been well documented, but its role in neurotransmitter phenotype expression remains unknown. Here we present evidence that the F-actin binding protein cortactin participates in determining both aspects of cell fate in large telencephalic neurons. We show that the expression of cortactin was upregulated early in development just prior to appearance of GABAergic neurons in the chick telencephalon at embryonic day 6. This program was faithfully maintained in primary neuronal cultures derived from E6 telencephalon, where immature neurons differentiate either to large pyramidal and large stellate excitatory neurons or to small inhibitory GABAergic neurons. Immunostaining revealed that cortactin was enriched in areas of membrane budding, growth cones, and in the cell cortex of immature neurons. With differentiation, intense punctate staining was also observed in an extraction-resistant cytosolic compartment of the soma and processes. More importantly, suppression of cortactin by inhibition of cortactin mRNA translation with antisense oligonucleotides caused permanent phenotypic changes. Specifically, a transient suppression of cortactin was achieved in immature neurons with a single exposure to antisense oligonucleotides. This inhibition first induced both the expression of mRNA and the enzymatic activity of GAD significantly earlier than in control neurons. Second, cortactin-suppressed large projectional neurons exhibited significantly shorter processes and growth cones with protrusive filopodia and an enlarged lamellipodia veil. Most importantly, this remodeling of neuritic outgrowth in projectional somata was accompanied by the ectopic induction of GABA (*-aminobutyric acid) expression. Considering this data altogether, it appears that cortactin may function to suppress concurrently several parameters of the GABAergic program in large developing neurons.

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Hsing, Hsiang-Wei, Zi-Hui Zhuang, Zhen-Xian Niou, and Shen-Ju Chou. "Temporal Differences in Interneuron Invasion of Neocortex and Piriform Cortex during Mouse Cortical Development." Cerebral Cortex 30, no. 5 (December 14, 2019): 3015–29. http://dx.doi.org/10.1093/cercor/bhz291.

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Abstract Establishing a balance between excitation and inhibition is critical for brain functions. However, how inhibitory interneurons (INs) generated in the ventral telencephalon integrate with the excitatory neurons generated in the dorsal telencephalon remains elusive. Previous studies showed that INs migrating tangentially to enter the neocortex (NCx), remain in the migratory stream for days before invading the cortical plate during late corticogenesis. Here we show that in developing mouse cortices, INs in the piriform cortex (PCx; the major olfactory cortex) distribute differently from those in the NCx. We provide evidence that during development INs invade and mature earlier in PCx than in NCx, likely owing to the lack of CXCR4 expression in INs from PCx compared to those in NCx. We analyzed IN distribution patterns in Lhx2 cKO mice, where projection neurons in the lateral NCx are re-fated to generate an ectopic PCx (ePCx). The PCx-specific IN distribution patterns found in ePCx suggest that properties of PCx projection neurons regulate IN distribution. Collectively, our results show that the timing of IN invasion in the developing PCx fundamentally differs from what is known in the NCx. Further, our results suggest that projection neurons instruct the PCx-specific pattern of IN distribution.

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Poitras, Luc, Noël Ghanem, Gary Hatch, and Marc Ekker. "Molecular analysis of the genetic cascade controlling Dlx1/2 expression in the developing telencephalon." Developmental Biology 306, no. 1 (June 2007): 351. http://dx.doi.org/10.1016/j.ydbio.2007.03.218.

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UCHIDA, Shinsuke, Tomohiro IMAGAWA, Aya SHINOZAKI, Masato FURUE, Safwat ALI, Yoshinao HOSAKA, and Masato UEHARA. "Distribution of Astroglial Lineage Cells in Developing Chicken Telencephalon from Embryo to Young Chick." Journal of Veterinary Medical Science 72, no. 12 (2010): 1597–602. http://dx.doi.org/10.1292/jvms.10-0209.

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