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1.  Faster scaling of visual neurons in cortical areas relative to subcortical structures in non-human primate brains 
Brain structure & function  2012;218(3):805-816.
Cortical expansion, both in absolute terms and in relation to subcortical structures, is considered a major trend in mammalian brain evolution with important functional implications, given that cortical computations should add complexity and flexibility to information processing. Here, we investigate the numbers of neurons that compose 4 structures in the visual pathway across 11 non-human primate species to determine the scaling relationships that apply to these structures and among them. We find that primary visual cortex, area V1, as well as the superior colliculus (SC) and lateral geniculate nucleus scale in mass faster than they gain neurons. Areas V1 and MT gain neurons proportionately to the entire cerebral cortex, and represent fairly constant proportions of all cortical neurons (36 and 3 %, respectively), while V1 gains neurons much faster than both subcortical structures examined. Larger primate brains therefore have increased ratios of cortical to subcortical neurons involved in processing visual information, as observed in the auditory pathway, but have a constant proportion of cortical neurons dedicated to the primary visual representation, and a fairly constant ratio of about 45 times more neurons in primary visual than in primary auditory cortical areas.
PMCID: PMC3727908  PMID: 22684638
Superior colliculus; Visual cortex; Lateral geniculate nucleus; V1; Area MT; Thalamus; Allometry; Brain size; Evolution
2.  How the Cortex Gets Its Folds: An Inside-Out, Connectivity-Driven Model for the Scaling of Mammalian Cortical Folding 
Larger mammalian cerebral cortices tend to have increasingly folded surfaces, often considered to result from the lateral expansion of the gray matter (GM), which, in a volume constrained by the cranium, causes mechanical compression that is relieved by inward folding of the white matter (WM), or to result from differential expansion of cortical layers. Across species, thinner cortices, presumably more pliable, would offer less resistance and hence become more folded than thicker cortices of a same size. However, such models do not acknowledge evidence in favor of a tension-based pull onto the GM from the inside, holding it in place even when the constraint imposed by the cranium is removed. Here we propose a testable, quantitative model of cortical folding driven by tension along the length of axons in the WM that assumes that connections through the WM are formed early in development, at the same time as the GM becomes folded, and considers that axonal connections through the WM generate tension that leads to inward folding of the WM surface, which pulls the GM surface inward. As an important necessary simplifying hypothesis, we assume that axons leaving or entering the WM do so approximately perpendicularly to the WM–GM interface. Cortical folding is thus driven by WM connectivity, and is a function of the fraction of cortical neurons connected through the WM, the average length, and the average cross-sectional area of the axons in the WM. Our model predicts that the different scaling of cortical folding across mammalian orders corresponds to different combinations of scaling of connectivity, axonal cross-sectional area, and tension along WM axons, instead of being a simple function of the number of GM neurons. Our model also explains variations in average cortical thickness as a result of the factors that lead to cortical folding, rather than as a determinant of folding; predicts that for a same tension, folding increases with connectivity through the WM and increased axonal cross-section; and that, for a same number of neurons, higher connectivity through the WM leads to a higher degree of folding as well as an on average thinner GM across species.
PMCID: PMC3270328  PMID: 22347170
allometry; brain size; evolution; white matter; cortical folding; connectivity; axon caliber; cortical thickness
3.  Age-related neuronal loss in the rat brain starts at the end of adolescence 
Aging-related changes in the brain have been mostly studied through the comparison of young adult and very old animals. However, aging must be considered a lifelong process of cumulative changes that ultimately become evident at old age. To determine when this process of decline begins, we studied how the cellular composition of the rat brain changes from infancy to adolescence, early adulthood, and old age. Using the isotropic fractionator to determine total numbers of neuronal and non-neuronal cells in different brain areas, we find that a major increase in number of neurons occurs during adolescence, between 1 and 2–3 months of age, followed by a significant trend of widespread and progressive neuronal loss that begins as early as 3 months of age, when neuronal numbers are maximal in all structures, until decreases in numbers of neurons become evident at 12 or 22 months of age. Our findings indicate that age-related decline in the brain begins as soon as the end of adolescence, a novel finding has important clinical and social implications for public health and welfare.
PMCID: PMC3481355  PMID: 23112765
aging; number of neurons; brain size; atrophy; neuronal loss

Results 1-3 (3)