Somato-dendritic morphology and axon origin site specify von Economo neurons as a subclass of modified pyramidal neurons in the human anterior cingulate cortex.

Von Economo neurons (VENs) are modified pyramidal neurons characterized by an extremely elongated rod-shaped soma. They are abundant in layer V of the anterior cingulate cortex (ACC) and fronto-insular cortex (FI) of the human brain, and have long been described as a human-specific neuron type. Recently, VENs have been reported in the ACC of apes and the FI of macaque monkeys.

The Protracted Maturation of Associative Layer IIIC Pyramidal Neurons in the Human Prefrontal Cortex During Childhood: A Major Role in Cognitive Development and Selective Alteration in Autism.

The human specific cognitive shift starts around the age of 2 years with the onset of self-awareness, and continues with extraordinary increase in cognitive capacities during early childhood. Diffuse changes in functional connectivity in children aged 2-6 years indicate an increase in the capacity of cortical network. Interestingly, structural network complexity does not increase during this time and, thus, it is likely to be induced by selective maturation of a specific neuronal subclass.

Extraordinary neoteny of synaptic spines in the human prefrontal cortex.

The major mechanism for generating diversity of neuronal connections beyond their genetic determination is the activity-dependent stabilization and selective elimination of the initially overproduced synapses [Changeux JP, Danchin A (1976) Nature 264:705-712]. The largest number of supranumerary synapses has been recorded in the cerebral cortex of human and nonhuman primates. It is generally accepted that synaptic pruning in the cerebral cortex, including prefrontal areas, occurs at puberty and is completed during early adolescence [Huttenlocher PR, et al.

Effect of environmental enrichment on morphology of deep layer III and layer V pyramidal cells of occipital cortex in oldest-old rat - A quantitative golgi cox study.

Dendrites and dendritic spine density regress extensively during aging in rats housed under standard conditions (SC), which can be ameliorated by housing in the enriched environment (EE). This event is particularly pronounced on neurons where high rates of plasticity are conceivable, such as on projection neurons of archicortical regions of dentate gyrus'. However, effects of EE on neocortical projection neurons are still poorly understood.

Postnatal deletion of Numb/Numblike reveals repair and remodeling capacity in the subventricular neurogenic niche.

Neural stem cells are retained in the postnatal subventricular zone (SVZ), a specialized neurogenic niche with unique cytoarchitecture and cell-cell contacts. Although the SVZ stem cells continuously regenerate, how they and the niche respond to local changes is unclear. Here we generated nestin-creER(tm) transgenic mice with inducible Cre recombinase in the SVZ and removed Numb/Numblike, key regulators of embryonic neurogenesis from postnatal SVZ progenitors and ependymal cells.

Dendritic overgrowth and alterations in laminar phenotypes of neocortical neurons in the newborn with semilobar holoprosencephaly.

We analyzed neuronal phenotypes and dendritic growth in the newborn with semilobar holoprosencephaly and 18p deletion. We found that the holoprosencephalic neocortex retained its basic six-layered lamination but displayed a number of intralaminar and modular architectonic alterations and contained a mixture of normal and aberrant neuronal phenotypes. The most conspicious finding was the presence of the pronounced increase in soma size and total basal dendritic length of holoprosencephalic layer III pyramidal neurons in comparison to age-matched control brains.

Perinatal growth of prefrontal layer III pyramids in Down syndrome.

We analyzed the dendritic differentiation of layer IIIc pyramidal neurons of prefrontal cortex (prospective area 9) in the brains of a premature infant and a 2.5-month-old infant with Down syndrome and two age-matched control subjects during the peak period of dendritic growth and differentiation. Our quantitative analysis supports qualitative observation and revealed no significant differences in the tempo and mode of dendritic differentiation between normal and Down syndrome cases.