Renewed focus on the developing human neocortex

Clowry, Gavin J.; Molnár, Zoltán; Rakić, Paško

doi:10.1111/j.1469-7580.2010.01281.x

Cited by 128 publications

(102 citation statements)

References 114 publications

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“…However, based on its connection to the visual cortex, it is also reasonable to hypothesize that it shares some origins with the dLGN. Therefore, it may be premature to conclude that there is no pulvinar in rodents, as suggested in the literature (Fosse and Fonnum, 1987;Jones, 2007;Bystron et al, 2008;Clowry et al, 2010). This controversy highlights the point that direct anatomical comparisons or gene expression comparison between rodent pulvinar/LP and primate pulvinar is not an easy task.…”

Section: Evolution Of the Cortical Area Mapmentioning

confidence: 89%

Comparative Anatomy of Marmoset and Mouse Cortex from Genomic Expression

et al. 2012

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Advances in mouse neural circuit genetics, brain atlases, and behavioral assays provide a powerful system for modeling the genetic basis of cognition and psychiatric disease. However, a critical limitation of this approach is how to achieve concordance of mouse neurobiology with the ultimate goal of understanding the human brain. Previously, the common marmoset has shown promise as a genetic model system toward the linking of mouse and human studies. However, the advent of marmoset transgenic approaches will require an understanding of developmental principles in marmoset compared to mouse. In this study, we used gene expression analysis in marmoset brain to pose a series of fundamental questions on cortical development and evolution for direct comparison to existing mouse brain atlas expression data. Most genes showed reliable conservation of expression between marmoset and mouse. However, certain markers had strikingly divergent expression patterns. The lateral geniculate nucleus and pulvinar in the thalamus showed diversification of genetic organization between marmoset and mouse, suggesting they share some similarity. In contrast, gene expression patterns in early visual cortical areas showed marmoset-specific expression. In prefrontal cortex, some markers labeled architectonic areas and layers distinct between mouse and marmoset. Core hippocampus was conserved, while afferent areas showed divergence. Together, these results indicate that existing cortical areas are genetically conserved between marmoset and mouse, while differences in areal parcellation, afferent diversification, and layer complexity are associated with specific genes. Collectively, we propose that gene expression patterns in marmoset brain reveal important clues to the principles underlying the molecular evolution of cortical and cognitive expansion.

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Section: Evolution Of the Cortical Area Mapmentioning

confidence: 89%

Comparative Anatomy of Marmoset and Mouse Cortex from Genomic Expression

et al. 2012

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“…The formation of the six-layered cerebral cortex requires a complex spatiotemporal coordination of different cellular and intracellular processes, such as neuronal proliferation, migration, differentiation, and circuitry formation (25,26). Newborn neurons must reach their final laminar positions at the established time to undergo morphofunctional changes enabling them to integrate intracortical inputs (27).…”

Section: Discussionmentioning

confidence: 99%

TBC1D24 regulates neuronal migration and maturation through modulation of the ARF6-dependent pathway

Falace

Buhler

Fadda

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Alterations in the formation of brain networks are associated with several neurodevelopmental disorders. Mutations in TBC1 domain family member 24 (TBC1D24) are responsible for syndromes that combine cortical malformations, intellectual disability, and epilepsy, but the function of TBC1D24 in the brain remains unknown. We report here that in utero TBC1D24 knockdown in the rat developing neocortex affects the multipolar-bipolar transition of neurons leading to delayed radial migration. Furthermore, we find that TBC1D24-knockdown neurons display an abnormal maturation and retain immature morphofunctional properties. TBC1D24 interacts with ADP ribosylation factor (ARF)6, a small GTPase crucial for membrane trafficking. We show that in vivo, overexpression of the dominant-negative form of ARF6 rescues the neuronal migration and dendritic outgrowth defects induced by TBC1D24 knockdown, suggesting that TBC1D24 prevents ARF6 activation. Overall, our findings demonstrate an essential role of TBC1D24 in neuronal migration and maturation and highlight the physiological relevance of the ARF6-dependent membrane-trafficking pathway in brain development.dendritogenesis | synaptogenesis | epileptic encephalopathies | gene | RNA interferenceT he mammalian cerebral cortex is a multilayered structure derived from cells of the neural tube (1). Cortical projection neurons are generated from proliferating progenitor cells located in the ventricular zone (VZ) adjacent to the lateral ventricle (2). After their final mitotic division, the majority of neurons migrate radially, along radial glia fibers, from the VZ toward the pial surface, where each successive generation passes one another and settles in an inside-out pattern within the cortical plate (CP) (3, 4). When neurons reach their final destination, they stop migrating and order themselves into specific "architectonic" patterns, according to a complex signaling pathway, guiding cells to the correct location in the brain (5). Overall, these steps lead to the formation of a six-layered cortex that plays a key role in cognitive processes. It is therefore not surprising that disruption of early cortical development causes severe neurological conditions usually featuring intellectual disabilities (IDs) and epilepsy, which may be associated with brain malformations (6).Over the past decades, advances in our understanding of the genetics of ID and epilepsy have revolutionized the diagnostic and the clinical approach to these disorders, and an increasing number of pathogenic gene mutations have been identified. TBC1D24 is a novel epilepsy-related gene mutated in different autosomal recessive forms of early-onset epilepsy, which can be accompanied by variable degrees of ID (7-11). The TBC1D24 gene encodes a protein of 553 aa that contains a Tre2/Bub2/Cdc16 (TBC) domain, shared by Rab GTPase-activating proteins (Rab-GAPs) and a TLDc domain of unknown function (8). The TBC1D24 protein is expressed in the brain and interacts with the ADP ribosylation factor (ARF) 6, a small GTP-binding prot...

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“…It is appealing to speculate that this projection might be unique to humans because specifically involved in language. Differences between the human and nonhuman primates can be expected considering that there are additional human-specific traits (Clowry et al 2010) and many molecular and cellular differences even between close relatives such as chimpanzees and humans (Geschwind and Rakic 2013). In particular, other connectional differences between the human and the monkey brains are beginning to emerge.…”

Section: Dt Topographymentioning

confidence: 99%

The Crossed Projection to the Striatum in Two Species of Monkey and in Humans: Behavioral and Evolutionary Significance

et al. 2016

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The corpus callosum establishes the anatomical continuity between the 2 hemispheres and coordinates their activity. Using histological tracing, single axon reconstructions, and diffusion tractography, we describe a callosal projection to n caudatus and putamen in monkeys and humans. In both species, the origin of this projection is more restricted than that of the ipsilateral projection. In monkeys, it consists of thin axons (0.4-0.6 μm), appropriate for spatial and temporal dispersion of subliminal inputs. For prefrontal cortex, contralateral minus ipsilateral delays to striatum calculated from axon diameters and conduction distance are <2 ms in the monkey and, by extrapolation, <4 ms in humans. This delay corresponds to the performance in Poffenberger's paradigm, a classical attempt to estimate central conduction delays, with a neuropsychological task. In both species, callosal cortico-striatal projections originate from prefrontal, premotor, and motor areas. In humans, we discovered a new projection originating from superior parietal lobule, supramarginal, and superior temporal gyrus, regions engaged in language processing. This projection crosses in the isthmus the lesion of which was reported to dissociate syntax and prosody. The projection might originate from an overproduction of callosal projections in development, differentially pruned depending on species.

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Renewed focus on the developing human neocortex

Cited by 128 publications

References 114 publications

Comparative Anatomy of Marmoset and Mouse Cortex from Genomic Expression

Comparative Anatomy of Marmoset and Mouse Cortex from Genomic Expression

TBC1D24 regulates neuronal migration and maturation through modulation of the ARF6-dependent pathway

The Crossed Projection to the Striatum in Two Species of Monkey and in Humans: Behavioral and Evolutionary Significance

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