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PubMed1999

Formation of cortical fields on a reduced cortical sheet.

Theories of both cortical field development and cortical evolution propose that thalamocortical projections play a critical role in the differentiation of cortical fields (; ). In the present study, we examined how changing the size of the immature neocortex before the establishment of thalamocortical connections affects the subsequent development and organization of the adult neocortex. This alteration in cortex is consistent with one of the most profound changes made to the mammalian neocortex throughout evolution: cortical size. Removing the caudal one-third to three-fourths of the cortical neuroepithelial sheet unilaterally at an early stage of development in marsupials resulted in normal spatial relationships between visual, somatosensory, and auditory cortical fields on the remaining cortical sheet. Injections of neuroanatomical tracers into the reduced cortex revealed in an altered distribution of thalamocortical axons; this alteration allowed the maintenance of their original anteroposterior distribution. These results demonstrate the capacity of the cortical neuroepithelium to accommodate different cortical fields at early stages of development, although the anteroposterior and mediolateral relationships between cortical fields appear to be invariant. The shifting of afferents and efferents with cortical reduction or expansion at very early stages of development may have occurred naturally in different lineages over time and may be sufficient to explain much of the phenotypic variation in cortical field number and organization in different mammals.

Aging↗
PubMed2000

Specificity and efficiency of Cre-mediated recombination in Emx1-Cre knock-in mice.

Emx1 is a mouse homologue of the Drosophila homeobox gene empty spiracles and its expression is restricted to the neurons in the developing and adult cerebral cortex and hippocampus. We reported previously the creation of a line of transgenic mice in which the cre gene was placed directly downstream of the putative Emx1 promoter using ES cell technology. We showed that Cre protein was present in the cerebral cortex of the transgenic mice and was able to mediate loxP-specific recombination in vitro. In the present study, the specificity and efficiency of the cre-mediated recombination were determined using three independent lines of reporter mice and a combination of histochemical staining, neuronal culture, and Southern detection of the genomic DNA. Our results showed that the recombination was highly efficient in all three lines of reporter mice tested and confirmed that the deletion was restricted to the neurons in the cerebral cortex and hippocampus. Furthermore, we have determined that the recombination efficiency in the cerebral cortex was 91%. Our results suggest that Emx1 is not expressed in every neuron in the developing and adult cerebral cortex. This line of cre mice should contribute to the studies of cortical development and plasticity.

Animals↗
PubMed2000

Visual behaviour mediated by retinal projections directed to the auditory pathway.

An unresolved issue in cortical development concerns the relative contributions of intrinsic and extrinsic factors to the functional specification of different cortical areas. Ferrets in which retinal projections are redirected neonatally to the auditory thalamus have visually responsive cells in auditory thalamus and cortex, form a retinotopic map in auditory cortex and have visual receptive field properties in auditory cortex that are typical of cells in visual cortex. Here we report that this cross-modal projection and its representation in auditory cortex can mediate visual behaviour. When light stimuli are presented in the portion of the visual field that is 'seen' only by this projection, 'rewired' ferrets respond as though they perceive the stimuli to be visual rather than auditory. Thus the perceptual modality of a neocortical region is instructed to a significant extent by its extrinsic inputs. In addition, gratings of different spatial frequencies can be discriminated by the rewired pathway, although the grating acuity is lower than that of the normal visual pathway.

Animals↗
PubMed2002

Differential modulation of BMP signaling promotes the elaboration of cerebral cortical GABAergic neurons or oligodendrocytes from a common sonic hedgehog-responsive ventral forebrain progenitor species.

During cerebral cortical development, excitatory glutamatergic projection neurons are generated from neural stem cells intrinsic to the early embryonic cortical ventricular zone by a process of radial migration, whereas most inhibitory gamma-aminobutyric acid (GABA)ergic interneurons and oligodendrocytes (OLs) appear to be elaborated from ventral forebrain stem cells that initially undergo tangential cortical migration before terminal lineage maturation. In contrast to the more compartmentalized developmental organization of the spinal cord, the generation of neurons and OLs from a common ventral forebrain stem cell would expose these cells to the sequential actions of ventral and dorsal gradient morphogens [sonic hedgehog (Shh) and bone morphogenetic proteins (BMPs)] that normally mediate opposing developmental programs. Here we report that Shh promotes GABAergic neuronalOL lineage restriction of forebrain stem cells, in part, by activation of the basic helix-loop-helix transcription factors, Olig2 and Mash1. In mutant mice with a generalized defect in tangential cortical migration (Dlx12--), there is a profound and selective reduction in the elaboration of both cortical GABAergic neurons and OLs. Our studies further demonstrate that the sequential elaboration of cortical GABAergic neurons and OLs from common Shh-responsive ventral forebrain progenitors requires the spatial and temporal modulation of cortical BMP signaling by BMP ligands and the BMP antagonist, noggin, respectively. These findings suggest an integrative model for cerebral cortical GABAergic neuronal and OL lineage maturation that would incorporate the sequential contributions of the ventral and dorsal forebrain, and the potential role of regional developmental cues in modulating transcriptional codes within evolving neural lineage species.

Animals↗
PubMed1992

Late appearance of parvalbumin-immunoreactive neurons in the rodent cerebral cortex does not follow an 'inside-out' sequence.

Parvalbumin (PARV), a Ca(2+)-binding protein believed to play a role in neuronal excitability, is contained in certain GABAergic inhibitory neurons of the cerebral cortex. Here we report that expression of PARV in the developing neocortex of rats and mice occurs with a sequence which does not follow the usual 'inside-out' gradient of cortical development. Thus, PARV-immunoreactive neurons appear first in layer V and only thereafter in the remaining cortical layers. An adult-like pattern of immunoreactivity is reached simultaneously in layers II-III and VIb. These observations indicate that the mechanisms regulating the functional maturation of PARV-containing inhibitory neurons are different from those that generally govern developmental processes in the cortex.

Animals↗
PubMed2005

Analysis of shape and positioning of the hippocampal formation: an MRI study in patients with partial epilepsy and healthy controls.

The purpose of this study was to evaluate systematically shape and positioning of the hippocampal formation (HF) in patients with partial epilepsy related to malformations of cortical development (MCD) and those with temporal lobe epilepsy (TLE). We studied 76 patients with MCD, including focal cortical dysplasia (n = 29; lesions located outside the temporal lobe in all), heterotopia (lesions outside of the temporal lobe, n = 14; lesions extending into the temporal lobe, n = 16), polymicrogyria (bilateral perisylvian, n = 14; unilateral perisylvian, n = 3) and 30 patients with TLE (hippocampal atrophy, n = 15; normal hippocampal volumes, n = 15). Shape and positioning of the HF were evaluated using a set of eight predefined morphological characteristics. In addition, the degree of hippocampal vertical orientation and medial positioning were assessed quantitatively. Patients were compared with 50 healthy controls. At least three criteria describing abnormal HF shape and positioning were found in 5/50 (10%) healthy controls, 37/76 (49%) MCD and 13/30 (43%) TLE patients. An association with all criteria was found in MCD and TLE, but not in healthy controls. In MCD there was no association between the side of HF shape abnormalities and the side of the cortical malformation or the EEG focus. Likewise, in TLE, HF abnormalities were not related to the side of the EEG focus. In both MCD and TLE patients who had hippocampal atrophy, no association was found between the side of HF shape abnormalities and the side of atrophy. Abnormal HF shape and positioning are found in a similar proportion in MCD and TLE. In TLE, they may be a marker of a more extensive disorder of brain development and may participate in the development of this condition.

Adolescent↗
PubMedDate not supplied

Cerebral cortical progenitors are fated to produce region-specific neuronal populations.

The mammalian cerebral cortex is characterized by its organization into anatomically and functionally discrete regions. During cortical development, a homogeneous-appearing population of cells along the ventricular surface generates the neurons and glia that ultimately form these cytoarchitectonic areas. The limbic system-associated membrane protein (LAMP) is a neuronal, cell surface glycoprotein that identifies neurons restricted to limbic cerebral cortical areas (Levitt, 1984). LAMP is expressed early in development (Horton and Levitt, 1988), and transplantation studies in the rat suggest that cells in the cerebral wall are committed to a limbic or nonlimbic molecular phenotype by embryonic day 14 (E14) (Barbe and Levitt, 1991). However, at E12, cells destined for the cerebral cortex are still multipotential and presumably depend on local, extrinsic signals to adopt a limbic phenotype. We have developed an in vitro assay system for examining the fate of these multipotential progenitors and identifying potential environmental regulators of neuronal differentiation. Regions of the lateral (limbic) and dorsal (nonlimbic) cerebral wall at E12 are dissected, dissociated, and grown in low-density cultures in defined medium. The cells are examined by immunocytochemistry for expression of MAP2, a neuronal cytoskeletal protein, and LAMP to define neuronal differentiation and the expression of a limbic molecular phenotype, respectively. We find that after 4 d in culture, up to 75% of the progenitor cells from presumptive limbic cortex express LAMP upon differentiation. In contrast, only 20-30% of the differentiated cells from presumptive sensorimotor cortex express LAMP. Thus, most cortical progenitors are fated to a limbic or nonlimbic phenotype early in development, and the decision by neuronal stem cells to differentiate into neurons exhibiting this molecular phenotype occurs prior to the completion of neurogenesis, in the absence of subcortical environmental cues.

Animals↗
PubMed1991

A target-derived chemoattractant controls the development of the corticopontine projection by a novel mechanism of axon targeting.

Here, we review our studies in rats of target recognition by developing cortical axons focusing on their innervation of the basilar pons, a major hindbrain target. The corticopontine projection develops by a 'delayed interstitial budding' of collaterals from layer 5 corticospinal axons, rather than by a direct ingrowth of primary axons or by bifurcation of the growth cone. Branches form de novo from the axon cylinder in the pathway overlying the basilar pons and extend directly into it. Co-cultures of cortex and basilar pons in 3-dimensional collagen matrices show that a diffusible chemotropic signal released by the basilar pons directs the growth of collateral branches from layer 5 axons in a target and neuron specific manner. 'Delayed' co-cultures suggest that a diffusible, pontine-derived signal also initiates the selective branching of layer 5 axons. In vivo experiments support this chemotropic mechanism. First, corticospinal axons form collateral branches at novel locations directly over ectopic aggregations of basilar pontine neurons induced by X-irradiation; no branches form at positions that would normally overlie the appropriate region of basilar pons which is absent because of the X-irradiation. Thus, the basilar pons, rather than local cues in the axon pathway, appears to control the location of corticospinal axon branching. Second, in a series of experiments in which different subsets of corticospinal axons are prevented from innervating the basilar pons, remaining corticospinal axons extend collaterals in a directed manner to regions of the basilar pons deprived of cortical input, a behavior consistent with a response to a diffusible chemoattractant emanating from these regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Brain development: integrins and the Reelin pathway.

Integrins link the extracellular matrix to the intracellular environment. They have been implicated in the Reelin pathway in cortical development. But new genetic studies have revealed that, while beta(1) integrin plays a role in formation of the basement membrane, it is not essential for neuronal migration.

Animals↗
PubMedDate not supplied

Homotopic, but not heterotopic, fetal cortical transplants can result in functional sparing following neonatal damage to the frontal cortex in rats.

Experiments involving the heterotopic transplantation of neocortex during development have indicated that the efferent connections maintained by the transplant as well as other organizational features are appropriate to the transplant's regional locale within the host cortex, rather than to its site of origin within the donor cortex. These findings would seem to be consistent with the idea that developing cortical neurons lack any rigid regional specification. To examine this further, we made lesions in the rostral cortex of newborn rats and placed pieces of either rostral or occipital fetal cortex into the lesion site. Additional cases with similar lesions, but with no transplants, were also prepared. When the animals matured, behavioral testing was done to identify any residual deficits. Compared with lesioned animals that had received no transplants, animals with homotopic transplants show a substantial sparing in certain forelimb placing and somatosensory tasks. In marked contrast, animals with heterotopic transplants did not show any sparing. Indeed, when placing reactions were elicited by vibrissal stimulation (vibrissae-->forelimb placing; extinction-placing) the animals with heterotopic transplants showed a greater impairment than the lesioned animals that received no transplants. These results indicate that while homotopic fetal cortical transplants may help ameliorate behavioral deficits that normally follow neonatal lesions of the rostral cortex, heterotopic transplants do not, and may in fact exacerbate the deficits, despite the fact that such heterotopic transplants have been shown to maintain projections that seemingly are appropriate to their locale.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Automated detection of focal cortical dysplasia lesions using computational models of their MRI characteristics and texture analysis.

Focal cortical dysplasia (FCD), a malformation of cortical development, is a frequent cause of pharmacologically intractable epilepsy. FCD is characterized on Tl-weighted MRI by cortical thickening, blurring of the gray-matter/white-matter interface, and gray-level hyperintensity. We have previously used computational models of these characteristics to enhance visual lesion detection. In the present study we seek to improve our methods by combining these models with features derived from texture analysis of MRI, which allows measurement of image properties not readily accessible by visual analysis. These computational models and texture features were used to develop a two-stage Bayesian classifier to perform automated FCD lesion detection. Eighteen patients with histologically confirmed FCD and 14 normal controls were studied. On the MRI volumes of the 18 patients, 20 FCD lesions were manually labeled by an expert observer. Three-dimensional maps of the computational models and texture features were constructed for all subjects. A Bayesian classifier was trained on the computational models to classify voxels as cerebrospinal fluid, gray-matter, white-matter, transitional, or lesional. Voxels classified as lesional were subsequently reclassified based on the texture features. This process produced a 3D lesion map, which was compared to the manual lesion labels. The automated classifier identified 17/20 manually labeled lesions. No lesions were identified in controls. Thus, combining models of the T1-weighted MRI characteristics of FCD with texture analysis enabled successful construction of a classifier. This computer-based, automated method may be useful in the presurgical evaluation of patients with severe epilepsy related to FCD.

Adult↗
PubMed2006

Towards the classification of subpopulations of layer V pyramidal projection neurons.

The nature of cerebral cortical circuitry has been increasingly clarified by markers for the identification of precise cell types with specific morphology, connectivity and distinct physiological properties. Molecular markers are not only helpful in dissecting cortical circuitry, but also give insight into the mechanisms of cortical neuronal specification and differentiation. The two principal neuronal types of the cerebral cortex are the pyramidal and GABAergic cells. Pyramidal cells are excitatory and project to distant targets, while GABAergic neurons are mostly inhibitory non-pyramidal interneurons. Reliable markers for specific subtypes of interneurons are available and have been employed in the classification and functional analysis of cortical circuitry. Until recently, cortical pyramidal neurons have been considered a homogeneous class of cells. This concept is now changing as the powerful tools of molecular biology and genetics identify molecular tags for subtypes of pyramidal cells such as: Otx-1 [Frantz, G.D., Bohner, A.P., Akers, R.M., McConnell, S.K., 1994. Regulation of the POU domain gene SCIP during cerebral cortical development. J. Neurosci. 14, 472-485; Weimann, J.M., Zhang, Y.A., Levin, M.E., Devine, W.P., Brulet, P., McConnell, S.K., 1999. Cortical neurons require Otx1 for the refinement of exuberant axonal projections to subcortical targets. Neuron 24, 819-831]; SMI-32, N200 and FNP-7 [Voelker, C.C., Garin, N., Taylor, J.S., Gahwiler, B.H., Hornung, J.P., Molnár, Z., 2004. Selective neurofilament (SMI-32, FNP-7 and N200) expression in subpopulations of layer V pyramidal neurons in vivo and in vitro. Cereb. Cortex 14, 1276-1286]; ER81 [Hevner, R.F., Daza, R.A., Rubenstein, J.L., Stunnenberg, H., Olavarria, J.F., Englund, C., 2003. Beyond laminar fate: toward a molecular classification of cortical projection/pyramidal neurons. Dev. Neurosci. 25 (2-4), 139-151; Yoneshima, H., Yamasaki, S., Voelker, C., Molnár, Z., Christophe, E., Audinat, E., Takemoto, M., Tsuji, S., Fujita, I., Yamamoto, N., 2006. ER81 is expressed in a subpopulation of layer 5 projection neurons in rodent cerebral cortices. Neuroscience, 137, 401-412]; Lmo4 [Bulchand, S., Subramanian, L., Tole, S., 2003. Dynamic spatiotemporal expression of LIM genes and cofactors in the embryonic and postnatal cerebral cortex. Dev. Dyn. 226, 460-469; Arlotta, P., Molyneaux, B.J., Chen, J., Inoue, J., Kominami, R., Macklis, J.D., 2005. Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo. Neuron 45 (2), 207-221]; CTIP2 [Arlotta, P., Molyneaux, B.J., Chen, J., Inoue, J., Kominami, R., Macklis, J.D., 2005. Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo. Neuron 45 (2), 207-221]; Fez1 [Molyneaux, B.J., Arlotta, P., Hirata, T., Hibi, M., Macklis, J.D., 2005. Fez1 is required for the birth and specification of corticospinal motor neurons. Neuron 47 (6), 817-831; Chen, B., Schaevitz, L.R., McConnell, S.K., 2005. Fez1 regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex. Proc. Natl. Acad. Sci. U.S.A. 102 (47), 17184-17189]. These genes outline the numerous subtypes of pyramidal cells and are increasingly refining our previous classifications. They also indicate specific developmental programs operate in cell fate decisions. This review will describe the progress made on the correlation of these markers to each other within a specific subtype of layer V neurons with identified, stereotypic projections. Further work is needed to link these data with observations on somatodendritic morphology and physiological properties. The integrated molecular, anatomical and physiological characterisation of pyramidal neurons will lead to a much better appreciation of functional cortical circuits.

Animals↗
PubMed2003

A morphogenetic role for acetylcholine in mouse cerebral neocortex.

Recently, cholinergic afferents to cerebral cortex have met renewed attention regarding the regulation of plasticity as well as cognitive processing. My laboratory has developed a mouse neonatal basal forebrain lesion paradigm that has contributed considerably to the understanding of cholinergic mechanisms in cortical development. We have shown that transient cholinergic deafferentation, beginning at birth, precipitates alterations in neuronal differentiation and synaptic connectivity that persist into maturity, and contribute to altered cognitive behavior. These data are in general agreement with studies in rats in which the cholinergic basal forebrain is lesioned very early in development but contrast with effects of later developmental lesions. Moreover, in mouse, both morphological and behavioral consequences of the lesion are sex dependent. Studies of receptors and secondary messengers that are instrumental in morphogenesis and plasticity suggest that sex dependent molecular alterations occur within days if not hours following cortical cholinergic deafferentation.

Acetylcholine↗
PubMed1993

The fates of cells in the developing cerebral cortex of normal and methylazoxymethanol acetate-lesioned mice.

We are interested in the mechanisms that generate the mature cerebral cortex. We used bromodeoxyuridine (BrdU) to label cortical cells as they were being born. We followed the fates of specific sets of cortical precursors in normal mice and in mice in which other groups of cortical progenitors had been destroyed with the antimitotic agent methylazoxymethanol acetate (MAM Ac). In normal mice, most cells destined for the cerebral cortex were produced from embryonic day 12 (E12) to E16 in the expected inside-to-outside sequence (deep layers first, superficial layers last). Injection of MAM Ac at E13 killed cells that would normally have contributed to the deep cortical layers. As a consequence, the cortex was thinned by approximately 25% at postnatal day 21 (P21). However, all laminae were present and had normal connections with subcortical structures, although all were proportionately thinner. BrdU injected on E16 labelled a normally sized complement of cells that spanned a larger proportion of the depth of the thinned cortex. Thus, the deep cortical layers comprised many cells that were born several days later than normal. At embryonic ages prior to E12, a transient set of cells is produced in the early telencephalon. After injection with MAM Ac at E10, the cortex appeared histologically and histochemically normal at P21. However, many cells that would normally have contributed to superficial cortex (born on E15) were significantly deeper than normal. These results suggest that, during the early stages of cortical development, the nervous system is sufficiently plastic to compensate to some extent for the destruction of specific precursor cells by altering the fates of neurons born later. They indicate that the embryonic date on which a cortical cell is born does not necessarily determine its eventual phenotype.

Animals↗
PubMed2000

[Cortical dysgenesis. Current views on pathogenesis and pathophysiology].

Cortical dysgenesia are a heterogenous group of genetic or acquired disturbances of cortical development which, due to the enormous progress in modern neuroimaging techniques, are increasingly recognized in association with a variety of clinical disorders. The spectrum of clinical manifestations, depending on type and extent of the alterations, includes severe mental retardation and epilepsy as well as neuropsychological deficits and some psychiatric disorders. Although pathogenesis and pathophysiology of cortical dysgenesis are still not fully understood, the recent discovery of responsible genes, growth factors, neurotransmitters, and exogenous factors sheds light on elementary mechanisms. The development of animal models mimicking different types of human cortical malformations helped to increase further the understanding of functional consequences of focal cortical dysgenesis. Several studies on these models reveal widespread alterations of cortical connectivity and excitability which are probably of crucial importance in different clinical disorders.

Animals↗
PubMed1995

Distribution of a brain-specific proteoglycan, neurocan, and the corresponding mRNA during the formation of barrels in the rat somatosensory cortex.

Neurocan is a developmentally regulated chondroitin sulphate proteoglycan in the rat brain. In the present study, spatiotemporal patterns of expression of neurocan and the corresponding mRNA were examined in the developing cortical barrel field of the rat brain by using a monoclonal antibody that was highly specific to neurocan and a riboprobe for a portion of the mRNA. Immunohistochemical analysis revealed that neurocan was distributed throughout the cerebral cortex during early postnatal development but was excluded from the centres of cortical barrels at the time of entry and arborization of thalamocortical axons. At this developmental stage, expression of neurocan mRNA was shown by in situ hybridization to be down-regulated in the barrel centres. When a row of whisker follicles was laser-cauterized on postnatal day 1, the pattern of expression of neurocan was disturbed in the row of barrels that corresponded to the lesioned whisker follicles in the contralateral somatosensory cortex. From these observations, it appears that neuronal stimuli through early thalamocortical fibres from the sensory periphery cause reduced expression of neurocan mRNA in neurocan-producing cells in the presumptive barrel centres. Our findings also suggest that the pattern of distribution of neurocan in early postnatal barrel fields may be due mainly to the down-regulation of expression of neurocan mRNA.

Animals↗
PubMed2005

Areal and laminar variations in the vascularity of the visual, auditory, and entorhinal cortices of the developing rat brain.

Understanding of place-specific cortical cerebrovascular changes after insult and injury depends on the detailed knowledge of the areal and laminar variations in cortical vascularity. The present study examines comparatively the developmental changes of the total vascular density and the density of capillaries and medium- and large-sized vessels in the primary visual cortex (Oc1), the primary auditory cortex (Te1), and the lateral entorhinal cortex (EntL) of the developing rat brain. Vascular networks in the three cortical areas were marked after transcardial perfusion of India ink and quantified with an image analysis system. Parameters examined exhibited (i) peculiar developmental time course within individual cortical layers and (ii) area- and age-dependent variations. Angioarchitecture in Te1 layers was stabilized earlier than that in Oc1 layers and the period of postnatal development of the vascularity of neocortical sensory areas Oc1 and Te1 appeared to be more protracted compared to that of the phylogenetically older entorhinal cortex. By the end of the first postnatal month, vascular densities in the three cortical areas established a dorsoventral gradient (Oc1 > Te1 > EntL). Finally, in all areas, layer IV was the first layer to obtain adult values of capillary density.

Aging↗
PubMed2002

Transmantle dysplasia in tuberous sclerosis: clinical features and surgical outcome in four children.

In the literature, several malformations of cortical development have been described as additional lesions in tuberous sclerosis complex. Among these lesions, a very large focal cortical dysplasia has peculiar magnetic resonance imaging features: a signal abnormality that extends radially inward toward the lateral ventricle from the pachygyric cortical surface plus a homogeneous clinical picture. Affected patients have early-onset drug-resistant epilepsy and severe developmental delay. We describe the clinical, genetic, neurophysiologic, and neuroradiologic characteristics of four patients affected by tuberous sclerosis and this type of cortical dysplasia these patients are of special interest because they have been operated on for their dysplastic lesions. Total control of seizures has been achieved in the three children who underwent a complete lesionectomy. This result cannot be permanent, however, because of the presence of other cortical tubers which could become epileptogenic. All things considered, our choice was to give these children at least temporary relief from severe epilepsy and possibly support for developmental progression.

Adolescent↗