Decision by division: Making cortical maps

Yale University, New Haven, Connecticut, United States
Trends in Neurosciences (Impact Factor: 13.56). 05/2009; 32(5):291-301. DOI: 10.1016/j.tins.2009.01.007
Source: PubMed


In the past three decades, mounting evidence has revealed that specification of the basic cortical neuronal classes starts at the time of their final mitotic divisions in the embryonic proliferative zones. This early cell determination continues during the migration of the newborn neurons across the widening cerebral wall, and it is in the cortical plate that they attain their final positions and establish species-specific cytoarchitectonic areas. Here, the development and evolutionary expansion of the neocortex is viewed in the context of the radial unit and protomap hypotheses. A broad spectrum of findings gave insight into the pathogenesis of cortical malformations and the biological bases for the evolution of the modern human neocortex. We examine the history and evidence behind the concept of early specification of neurons and provide the latest compendium of genes and signaling molecules involved in neuronal fate determination and specification.

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    • "Though some studies have shown similar age effects across different structural methods (Lemaitre et al., 2012), these two measurements are dissociable metrics that are confounded in studies of gray matter volume. Some studies have found either no correlation or a weak correlation between thickness and surface area (Winkler et al., 2010;Hogstrom et al., 2013), consistent with evidence that thickness and area are genetically independent and are affected by distinct neurobiological factors, such as myelin growth, during development (Panizzon et al., 2009;Rakic et al., 2009;Rakic, 2009;White et al., 2010). Additional research is needed to clarify the distinct causes of surface area and cortical thickness changes in late life, and to determine whether or not these two measures are differentially related to clinical and functional outcomes. "
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    ABSTRACT: Age is associated with reductions in surface area and cortical thickness, particularly in prefrontal regions. There is also evidence of greater thickness in some regions at older ages. Non-linear age effects in some studies suggest that age may continue to impact brain structure in later decades of life, but relatively few studies have examined the impact of age on brain structure within middle-aged to older adults. We investigated age differences in prefrontal surface area and cortical thickness in healthy adults between the ages of 51 and 81 years. Participants received a structural 3-Tesla magnetic resonance imaging scan. Based on a priori hypotheses, primary analyses focused on surface area and cortical thickness in the dorsolateral prefrontal cortex, anterior cingulate cortex, and orbitofrontal cortex. We also performed exploratory vertex-wise analyses of surface area and cortical thickness across the entire cortex. We found that older age was associated with smaller surface area in the dorsolateral prefrontal and orbitofrontal cortices but greater cortical thickness in the dorsolateral prefrontal and anterior cingulate cortices. Vertex-wise analyses revealed smaller surface area in primarily frontal regions at older ages, but no age effects were found for cortical thickness. Results suggest age is associated with reduced surface area but greater cortical thickness in prefrontal regions during later decades of life, and highlight the differential effects age has on regional surface area and cortical thickness.
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    • "This lends credence to the idea that the proprioceptive network may be pruned during adolescence through an activity-dependent mechanism where repetitions of evoked activity stabilize functional connections that subserve typical proprioceptive processing and eliminate the others. Besides, such mechanism is also thought to impact upon the structural level, in determining which synaptic connections persist and which are eliminated during development (Changeux and Danchin 1976; Rakic et al. 1994, 2009; Innocenti and Price 2005). Thus, stabilization and regression of functional and structural connections through evoked activation of the proprioceptive network may constitute a unified mechanism by which the network develops during adolescence. "
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    ABSTRACT: Proprioceptive processing is important for appropriate motor control, providing error-feedback and internal representation of movement for adjusting the motor command. Although proprioceptive functioning improves during childhood and adolescence, we still have few clues about how the proprioceptive brain network develops. Here, we investigated developmental changes in the functional organization of this network in early adolescents (n = 18, 12 ± 1 years), late adolescents (n = 18, 15 ± 1), and young adults (n = 18, 32 ± 4), by examining task-evoked univariate activity and patterns of functional connectivity (FC) associated with seeds placed in cortical (supramarginal gyrus) and subcortical (dorsal rostral putamen) regions. We found that although the network is already well established in early adolescence both in terms of topology and functioning principles (e.g., long-distance communication and economy in wiring cost), it is still undergoing refinement during adolescence, including a shift from diffuse to focal FC and a decreased FC strength. This developmental effect was particularly pronounced for fronto-striatal connections. Furthermore, changes in FC features continued beyond adolescence, although to a much lower extent. Altogether, these findings point to a protracted developmental time course for the proprioceptive network, which breaks with the relatively early functional maturation often associated with sensorimotor networks.
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    • "Recently, Chen and colleagues investigated older human adult twins and demonstrated that genetic topography exhibited anterior–posterior and dorsal–ventral organizational gradients on a coarse level (Chen et al. 2011). This level of patterning by opposing gradients is supported by animal studies that used experimental inhibition or overexpression of specific genes (Bishop et al. 2000; O'Leary et al. 2007; Rakic et al. 2009). However, evidence of genetic influences on a finer scale has been sparse. "
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