Why is cortex folded

More on the subject: brain research I'm interested in more information … Read all latest stories. Alzheimer's brain neurology research. Neurology The 'thermostat' that prevents our brain from overheating The mechanisms by which the body measures temperature and regulates its own body heat are vital, but still poorly understood. Artificial Intelligence mediaire — mdbrain mediaire GmbH. Subscribe to Newsletter. I am interested in Qualitatively, thinner cerebral cortices are usually found in more convoluted brains, whether across species or in pathological conditions.

In schizophrenia, for example, the cortex may be found to be thinner than usual, with a reduced volume of the superficial layers, and also more folded Sallet et al. These findings are often interpreted as evidence of a thicker cortex resisting buckling.

Our model, however, offers an alternative interpretation: that cortical thickness increases as a consequence of a smaller fraction of neurons connected through the WM, in combination or not to an increased average neuronal size in the WM.

Similarly, the thicker lissencephalic cortex is predicted to be a result of abnormal insufficient cortical connectivity through the WM, possibly due to abnormal neuronal migration Olson and Walsh, , and not simply a cortex that became too thick to be folded. One last and very important aspect of cortical folding is that is has often been considered a means of making more neurons fit into a space-limited brain, as the larger-than-expected cortical surface supposedly allows a larger-than-expected number of neurons for a given cranial volume.

However, this would only be the case if cortical expansion occurred mostly laterally, and with a homogeneous number of neurons per surface area. In contrast, as we have shown previously, cortical expansion can no longer be considered to occur homogeneously across species, nor with a homogeneous number of neurons beneath a unit surface area. This means that it is no longer necessarily true that more convoluted cortices have more neurons than less convoluted cortices. Indeed, the elephant cortex, which has a larger surface area and is more convoluted than the human brain, has been estimated to have fewer neurons than the letter Roth and Dicke, ; Herculano-Houzel, Here we show that cortical folding in mammals can be predicted to happen as a consequence of the folding of the underlying WM under tension of its axons, and not as a simple, linear function of its number of neurons.

Moreover, we show that the scaling of cortical folding with larger numbers of cortical neurons can be predicted, and possibly determined, in different groups of mammals by the scaling of a small number of parameters: 1 the fraction of cortical neurons connected through the WM; 2 the average cross-sectional area of axons in the WM; and 3 the shrinkage, under tension, of average axonal length relative to isometry. Just one further parameter, the scaling of 4 neuronal density, is required next to predict, or determine, both how the thickness of the GM varies, and how the folding of the GM itself scales.

This of course assumes near perpendicular or at least invariant across species incidence of axonal fibers at the WM—GM interface. This is a plausible hypothesis for fibers under longitudinal tension; but the lack of actual systematic measurement of incidence angles that could confirm this hypothesis must be takes as a limitation of the present work.

Such a measurement would be most welcome, allowing us extend our model by introducing another measured coefficient relating the average incidence angle as a power law of N , to recalculate the values of the various coefficients with a source of uncertainty removed, and to independently test our underlying hypothesis since we expect a cortex grown subject to axonal longitudinal tensions to show a marked tendency toward orthogonal incidence. Importantly, while the model is potentially universal, applying across the different orders of mammals, it does not at all imply that there is a single way for the cortex to scale.

Again, our model predicts that cortical thickness is not a determinant of cortical folding, but rather a consequence, depending on the scaling of neuronal density as well as of the connectivity fraction and average cross-sectional area of the axons in the WM. Even in the case that experimental testing eventually shows that causality in cortical folding is not as proposed in our model without the introduction of further variables, the latter has the enormous advantage of allowing one to deduce the scaling of cortical connectivity, axonal length, cross-sectional area, and thus to infer propagation time and computational capability and efficacy, from readily measurable values of A W , V W , N , O W , and D N.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Barres, B. Control of oligodendrocyte number in the developing rat optic nerve.

Neuron 12, — Axonal control of oligodendrocyte development. Cell Biol. Braitenberg, V. Berlin: Springer Verlag.

Caminiti, R. Evolution amplified processing with temporally dispersed slow neuronal connectivity in primates. Chenn, A. Regulation of cerebral cortical size by control of cell cycle exit in neural precursos. Science , — Collins, C. Neuron densities vary across and within cortical areas in primates.

Gabi, M. Cellular scaling rules for the brain of an extended number of primate species. Brain Behav. Goldman-Rakic, P. Morphological consequences of prenatal injury to the primate brain. Brain Res. CrossRef Full Text. Geschwind, and A. Galaburda Cambridge: Harvard University Press , — Gross, C.

Cambridge: MIT Press. Haydar, T. The role of cell death in regulating the size and shape of the mammalian forebrain. Cortex 9, — Herculano-Houzel, S.

The human brain in numbers: a linearly scaled-up primate brain. Not all brains are made the same: new views on brain scaling in evolution.

Cellular scaling rules for primate brains. The basic non-uniformity of the cerebral cortex. Isotropic fractionator: a simple, rapid method for the quantification of total cell and neuron numbers in the brain.

Cellular scaling rules for rodent brains. Connectivity-driven white matter scaling and folding in primate cerebral cortex. Hilgetag, C. Developmental mechanics of the primate cerebral cortex. His, W. Leipzig: FCW Vogel. Hofman, M. Size and shape of the cerebral cortex in mammals. The cortical surface. Kaas, J. Encyclopedia of Neuroscience. Amsterdam: Elsevier, — Kingsbury, M. Non-proliferative effects of lysophosphatidic acid enhance cortical growth and folding. Le Gros Clark, W. Le Gros Clark, and P.

Oxford: Oxford University Press , 1— Mori, S. Imaging cortical association tracts in the human brain using diffusion-tensor-based axonal tracking. Olivares, R. Species differences and similarities in the fine structure of the mammalian corpus callosum. Olson, E.

Smooth, rough and upside-down neocortical development. Pfister, B. Extreme stretch growth of integrated axons. Pillay, P. Order-specific quantitative patterns of cortical gyrification.

For example, thinner regions tend to fold more easily than others, Ronan said. Though the brains' ridges and valleys — called gyri and sulci, respectively — look random, they're actually consistent across individuals, and even some species. Ronan said this consistency is important because it indicates that the folding has meaning. Ultimately, the physical properties and unique folding patterns of each cortex region are linked to its function.

By acquiring the gyrus in the process of evolution, it has become possible to have a large number of neurons, and thus great development of brain functions has been acquired. On the other hand, the mouse, a widely used model animal, has a brain without gyri. This has made it very difficult to do research on the gyrus using the mouse as a model animal; therefore, research on the gyrus has been much retarded. Our group has been developing a research technique for ferrets reported in several articles, which allows analysis of ferrets at the genome level.

Our laboratory is a world leader in research in this field. Furthermore, by using this technique, we have succeeded in developing a ferret disease model that shows impairment in the gyrus, which, we believe, has significantly contributed to genetic approaches to the brain of higher mammals.

This new technique opens a way to a new stage of genetics research of the brain of higher mammals. We have applied the above-mentioned technique to knocking out a gene called Cdk5 in the ferret cerebral cortex and found that gyrus formation was impaired. This result indicates that Cdk5 is an important gene for gyrus formation. We searched for neurons playing important roles in gyrus formation and found that neurons on the upper-layer cerebral cortex were essential.

This finding is the first in the world; it was not known so far which neurons in the brain would play important roles in gyrus formation. These results of the current study indicate that functions of Cdk5 in neurons of the upper-layer cerebral cortex are important for the formation of the gyrus. In this study, our research group has elucidated one of the mechanisms for gyrus formation by developing a research technique for the ferret brain.