The relationship between corpus callosum size and forebrain volume

Using high-resolution in vivo magnetic resonance morphometry we measured forebrain volume (FBV), midsagittal size of the corpus callosum (CC) and four CC subareas in 120 young and healthy adults (49 women, 71 men). We found moderate linear and quadratic correlations, indicating that the CC and all CC subareas increase with FBV both in men and women (multiple r2 ranging from 0.10 to 0.28). Allometric equations revealed that these increases were less than proportional to FBV (r2 ranging from 0.02 to 0.30). Absolute CC measurements, as well as CC subareas relative to total CC or FBV (the latter measures termed the CC ratios), were further analyzed with regard to possible effects of handedness, gender, or handedness by gender interaction. Contrary to previous reports, left-handers did not show larger CC measurements compared to right-handers. The only apparent influence of gender was on the CC ratios, which were larger in women. However, smaller brains had larger CC ratios which were mainly independent of gender, a result of the less than proportional increase of callosal size with FBV. We suggest that the previously described gender differences in CC anatomy may be better explained by an underlying effect of brain size, with larger brains having relatively smaller callosa. This lends empirical support to the hypothesis that brain size may be an important factor influencing interhemispheric connectivity and lateralizatio

Morphology, electrophysiology and functional input connectivity of pyramidal neurons characterizes a genuine layer va in the primary somatosensory cortex.

Contains fulltext : 49986.pdf (publisher's version ) (Closed access)Cortical layer V classically has been subdivided into sublayers Va and Vb on cytoarchitectonic grounds. In the analysis of cortical microcircuits, however, layer Va has largely been ignored. The purpose of this study was to investigate pyramidal neurons of layer Va in view of their potential role in integrating information from lemniscal and paralemniscal sources. For this we combined detailed electrophysiological and morphological characterization with mapping of intracortical functional connectivity by caged glutamate photolysis in layer Va of rat barrel cortex in vitro. Electrophysiological characterization revealed pyramidal cells of the regular spiking as well as the intrinsically burst firing type. However, all layer Va pyramidal neurons displayed uniform morphological properties and comparable functional input connectivity patterns. They received most of their excitatory and inhibitory inputs from intracolumnar sources, especially from layer Va itself, but also from layer IV. Those two layers were also the main origin for transcolumnar excitatory inputs. Layer Va pyramidal neurons thus may predominantly integrate information intralaminarly as well as from layer IV. The functional connectivity maps clearly distinguish layer Va from layer Vb pyramidal cells, and suggest that layer Va plays a unique role in intracortical processing of sensory information

H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion.

Increase in the size of human neocortex―acquired in evolution―accounts for the unique cognitive capacity of humans. This expansion reflects the evolutionarily enhanced proliferative ability of basal progenitors (BPs), including the basal radial glia and basal intermediate progenitors (bIPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in bIP amplification and cortical expansion. Through epigenetic profiling of sorted bIPs, we show that histone H3 lysine 9 acetylation (H3K9ac) is low in murine bIPs and high in human bIPs. Elevated H3K9ac preferentially increases bIP proliferation, increasing the size and folding of the normally smooth mouse neocortex. H3K9ac drives bIP amplification by increasing expression of the evolutionarily regulated gene, Trnp1, in developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture