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PubMed1986

Dendritic development of cortical neurons of mice subjected to total asphyxia: a Golgi-Cox study.

The effect of total asphyxia on dendritic development of the pyramidal cells in the mouse cerebrum was investigated using the Golgi-Cox method. Although neonatal asphyxia did not alter the number of basal dendrites arising from the cell bodies, the dendrites in the 20-day-old treated animals were significantly shorter than those in the controls. Even at 60 days, the number of longer dendrites in the treated mice was significantly less than that in the controls.

Animals↗
PubMed1999

Activity-dependent development of cortical axon terminations in the spinal cord and brain stem.

Corticospinal (CS) axon terminations in several species are widespread early in development but are subsequently refined into a spatially more restricted distribution. We studied the role of neural activity in sensorimotor cortex in shaping postnatal development of CS terminations in cats. We continuously infused muscimol unilaterally into sensorimotor cortex to silence neurons during the postnatal CS refinement period (weeks 3-7). Using anterograde transport of WGA-HRP, we examined the laterality of terminations from the muscimol-infused (i.e., silenced) and active sides in the spinal cord, as well as in the cuneate nucleus and red nucleus. We found that CS terminations from the muscimol-infused cortex were very sparse and limited to the contralateral side, while those from the active cortex maintained an immature bilateral topography. Controls (saline infusion, noninfusion) had dense, predominantly contralateral, CS terminations. There was a substantial decrease in the spinal gray matter area occupied by terminations from the side receiving the blockade and a concomitant increase in the area occupied by ipsilateral terminations from the active cortex. Optical density measurements of HRP reaction product from the active cortex in muscimol-infused animals showed substantial increases over controls in the ratio of ipsilateral to contralateral CS terminations for all laminae examined (IV-V, VI, VII). Our findings suggest that ipsilateral dorsal horn terminations reflect new axon growth during the refinement period because they are not present there earlier in development. Those in the ventral horn are present earlier in development and thus could reflect maintenance of transient terminations. Increased ipsilateral terminations from active cortex were due to recrossing of CS axons in lamina X and not to an increase in labeled CS axons in the ipsilateral white matter. Examination of brain stem terminations suggested that, between postnatal weeks 3 and 7, development of corticocuneate terminations also is activity-dependent but that development of corticorubral terminations is not. Activity-dependent CS development is a plausible mechanism by which early motor experiences could shape the anatomical and functional organization of the motor systems during a critical postnatal period.

Aging↗
PubMed2005

Brain abnormalities in a case of malonyl-CoA decarboxylase deficiency.

Malonyl-CoA decarboxylase (MCD) deficiency is an extremely rare inborn error of metabolism that presents with metabolic acidosis, hypoglycemia, and/or cardiomyopathy. Patients also show neurological signs and symptoms that have been infrequently reported. We describe a girl with MCD deficiency, whose brain MRI shows white matter abnormalities and additionally diffuse pachygyria and periventricular heterotopia, consistent with a malformation of cortical development. MLYCD-gene sequence analysis shows normal genomic sequence but no messenger product, suggesting an abnormality of transcription regulation. Our patient has strikingly low appetite, which is interesting in the light of the proposed role of malonyl-CoA in the regulation of feeding control, but this remains to be confirmed in other patients. Considering the incomplete understanding of the role of metabolic pathways in brain development, patients with MCD deficiency should be evaluated with brain MRI and unexplained malformations of cortical development should be reason for metabolic screening.

Agenesis of Corpus Callosum↗
PubMed1987

Development of cortical circuitry and cognitive function.

Recent functional and anatomical studies in nonhuman primates have elucidated the basic neural circuitry underlying delayed-response function in adult nonhuman primates. Thus circuitry includes connections of the principal sulcus with other areas of parietal association and limbic cortex and projections to the caudate nucleus, superior colliculus, and other premotor centers. Anatomical tracing in primate fetuses and in monkeys at various stages of postnatal development indicates that these various classes of cortical connections begin to form by the second trimester of pregnancy. Electromicroscopic studies of the principal sulcus and other areas of cerebral cortex show that the number and density of synapses in the cortex increase rapidly, reaching and maintaining higher than normal adult values between 2 and 4 months postnatally, before slowly declining over a period of years to stable adult levels. The capacity to perform delayed-response and/or AB at short delays emerges around 4 months of age, coinciding with the end of the period of highest synaptic density in the principal sulcus. These findings suggest that a critical mass of cortical synapses is important for the emergence of this cognitive function, and that fully mature capacity may depend upon the elimination of excess synapses that occurs during adolescence and young adulthood. Knowledge of the neural basis of normal cognitive development may prove useful both to social and educational purposes as well as to understanding developmental disorders of cognition.

Animals↗
PubMed2006

The quantitative assessment of MHC II on thymic epithelium: implications in cortical thymocyte development.

The dynamics of MHC II expression in various thymic stromal compartments was investigated. By including MHC II in flow cytometry in addition to the cortical CDR1, medullary UEA-1 and pan-epithelial G8.8 markers, thymic stromal compartments were subdivided into at least six different populations. The total level of surface and cytoplasmic MHC II from fresh cortical thymic epithelial cells (cTECs) of normal mouse was as high as MHC II levels in medullary thymic epithelial cells (mTECs). MHC II levels as well as the percentages and cycling status of thymic epithelial cell populations expressing MHC II were not static during post-natal development, suggesting quantitative flexibility in presenting signals to the developing thymocytes. Although there was no evidence found for regulation of surface MHC II levels by TCR or by IFN-gamma, the absence of class II transactivator reduced both the level of MHC II expression and the number of MHC II+ cells. Surprisingly, MHC II molecules were found to form distinct focal aggregates on the surface of cTEC but not mTEC using high-resolution analysis by confocal microscopy. Moreover, these aggregates were formed independent of TCR or TCR-bearing cells in the thymus. These aggregates could potentially generate a functional unit containing a much higher local MHC II concentration to yield a higher avidity interaction. We discuss possible mechanisms for positive selection by weak interactions in the presence of such preformed MHC II aggregate units in cTEC.

Animals↗
PubMed2003

Development of the human cerebral cortex: a histochemical study.

In recent years, improvement in diagnostic techniques has led to better recognition of "disorders of cortical development". These disorders constitute a significant cause of epilepsy, mental retardation, developmental delay and neurological deficits in childhood, and may also contribute to the pathogenesis of psychological and neurodegenerative diseases in adults. Hitherto, however, few systematic studies of the human fetal cortex have been performed, and little is known about the ontogenetic processes of the neocortex in man. The aim of the study is to establish an understanding of the developmental events that occur in the second and third trimesters of gestation, by investigating the biochemical patterns of development of the human neocortex during this period. The temporal and spatial patterns of expression of the neuronal markers gamma-aminobutyric acid (GABA), choline acetyltransferase (ChAT), dopamine beta hydroxylase (DBH), dopamine receptor DR1 and synaptophysin, as well as the glial cell markers glial fibrillary acidic protein (GFAP), S100B and excitatory amino acid transporter protein GLT-1 are delineated in the fetal cortex using immunohistochemistry. Results of this study showed that different neuronal and glial cell proteins follow different developmental patterns and many show inter- or intra-regional variations in expression. Details of these patterns are described and discussed. The early expression of these proteins suggests that they play important roles in the developmental processes of cell proliferation, migration and differentiation. Both neurotransmitters and glial cell proteins probably function outside the confines of synapses in the fetal brain, as paracrine/autocrine factors. Early developmental events seem to be dictated by an innate programme, whereas late events may be more susceptible to extrinsic influences. It is hoped that knowledge of the normal developmental process can lead to better understanding of the causes and mechanisms of "disorders of cortical development", and to better treatments.

Acetylcholine↗
PubMed2003

Reelin and disabled-1 expression in developing and mature human cortical neurons.

In developing mammalian (mouse) brain, Reelin (Reln) is secreted by the Cajal-Retzius (CR) neurons in the marginal zone, binds apolipoprotein E receptor 2 (ApoER2) and very low density lipoprotein receptor (Vldlr), and induces the phosphorylation of the downstream cytoplasmic molecule disabled-1 (Dab1) in cortical plate neurons. Although this is a well-characterized signaling pathway in mice, it has not been well defined in human brain. In this paper we examined the expression of RELN, APOER2, VLDLR, and DAB1 in the developing human brain by RT-PCR. We further determined the cellular expression of the proteins RELN and DAB1 in 50 human brains ranging in age from 10 gestational weeks (GW) to 62 years using immunochemistry. We found that the pattern of expression of RELN and DAB1 in the human brain isnot identical to that observed in the mouse brain. In particular, we report the novel finding that human DAB1and RELN are coexpressed in CR neurons during cortical development and in cortical pyramidal neurons after neuronal migration is complete. Thus, in the human brain, the whole RELN signaling pathway is present within selected populations of cortical neurons throughout life. We speculate that RELN and DAB1 coexpression in these neurons is necessary for both normal cortical development and mature function.

Adolescent↗
PubMed2007

Development of cortical maps: perspectives from the barrel cortex.

One approach to examining how higher sensory, motor, and cognitive faculties emerge in the neocortex is to elucidate the underlying wiring principles of the brain during development. The mammalian neocortex is a layered structure generated from a sheet of proliferating ventricular cells that progressively divide to form specific functional areas, such as the primary somatosensory (S1) and motor (M1) cortices. The basic wiring pattern in each of these functional areas is based on a similar framework, but is distinct in detail. Functional specialization in each area derives from a combination of molecular cues within the cortex and neuronal activity-dependent cues provided by innervating axons from the thalamus. One salient feature of neocortical development is the establishment of topographic maps in which neighboring neurons receive input relayed from neighboring sensory afferents. Barrels, which are prominent sensory units in the somatosensory cortex of rodents, have been examined in detail, and data suggest that the initial, gross formation of the barrel map relies on molecular cues, but the refinement of this topography depends on neuronal activity. Several excellent reviews have been published on the patterning and plasticity of the barrel cortex and the precise targeting of ventrobasal thalamic axons. In this review, the authors will focus on the formation and functional maturation of synapses between thalamocortical axons and cortical neurons, an event that coincides with the formation of the barrel map. They will briefly review cortical patterning and the initial targeting of thalamic axons, with an emphasis on recent findings. The rest of the review will be devoted to summarizing their understanding of the cellular and molecular mechanisms underlying thalamocortical synapse maturation and its role in barrel map formation.

Animals↗
PubMed2005

Taylor-type focal cortical dysplasia in infants: some MRI lesions almost disappear with maturation of myelination.

Identification of focal cortical dysplasia (FCD) on magnetic resonance (MR) images of young children with refractory focal epilepsy is important, as surgical resection may offer improvement of seizure control and subsequent developmental progress. However, the MR appearances of malformations of cortical development may change during brain maturation. We report 4 children with refractory focal epilepsy, whose MR images in infancy showed localized cortical and subcortical signal abnormalities (hypointense on T(2)-weighted and hyperintense on T(1)-weighted images), suggestive of abnormal cortical development. The visibility of these lesions was significantly reduced on later MR images. Subtle blurring of the gray-white matter junction in these areas was the only indicator of cortical abnormality in 3 patients, which was recognized only after comparison with earlier images. Taylor-type FCD was subsequently confirmed in all patients, following surgical cortical resection of the lesions. MR images performed early within the first year of life in children with epilepsy are important to identify areas of FCD. The appearances of FCD on later scans can be very subtle escaping recognition, and conclusions may be misleading with respect to diagnosis and appropriateness of surgical treatment.

Age Factors↗
PubMed2005

The cells of cajal-retzius: still a mystery one century after.

Cajal-Retzius (CR) cells are an enigmatic class of neurons located at the surface of the cerebral cortex, playing a major role in cortical development. In this review, we discuss several distinct features of these neurons and the mechanisms by which they regulate cortical development. Many CR cells likely have extracortical origin and undergo cell death during development. Recent genetic studies report unique patterns of gene expression in CR cells, which may help to explain the developmental processes in which they participate. Moreover, a number of studies indicate that CR cells, and their secreted gene product, reelin, are involved in neuronal migration by acting on two key partners, migrating neurons and radial glial cells. Emerging data show that these neurons are a critical part of an early and complex network of neural activity in layer I, supporting the notion that CR cells modulate cortical maturation. Given these key and complex developmental properties, it is therefore conceivable for CR cells to be implicated in the pathogenesis of a variety of neurological disorders.

Animals↗
PubMed2000

Cortical plasticity and the development of behavior after early frontal cortical injury.

It has been known for over 100 years that frontal lobe injury in children is often associated with considerably more functional recovery than after similar injury in adulthood. Systematic study of frontal cortical injury in laboratory animals has shown that this recovery is tightly tied to developmental age: There is a brief window of time during cortical development during which the brain is able to compensate. Simply being young is not sufficient because injury prior to this critical period leads to miserable behavioral outcomes. For humans, the least favorable time for cortical injury is likely at the end of the gestational period, perhaps including the 1st month or so of life whereas the most favorable time is around 1 to 2 years of age. In addition to age, the extent of behavioral recovery is influenced by age at assessment, the nature of the behavioral assessment, sex, and lesion size. Anatomical studies have shown that functional recovery following early cortical injury is correlated with a reorganization of remaining cortical circuitry, including increased dendritic arborization and increased spine density. Recovery, and the compensatory anatomical changes, can also be potentiated by application of different treatments including behavioral therapy, trophic factors, and neuromodulators. Finally, there is preliminary evidence in laboratory animals to suggest that it may be possible to induce neural regeneration in the injured brain and that the regenerated brain functions to support functional recovery.

Adult↗
PubMed2005

Surgery for epilepsy due to cortical malformations: ten-year follow-up.

Children with malformations of cortical development represent a significant proportion of pediatric epilepsy surgery candidates. From a cohort of 40 children operated on between 1980 and 1992 with malformation of cortical development, 38 were alive and had data 10 years after surgery. Age at surgery ranged from 6 months to 18 years (mean, 9.6 years). Thirty-six had partial seizures, and two had infantile spasms; 20 were nonlesional. Pathologic diagnoses were cortical dysplasia (n = 31) and developmental tumor (n = 7). At 10-year follow-up, 15 (40%) were seizure free, 10 (26%) had >90% seizure reduction, and 13 (34%) were improved or unchanged. Children seizure free at two-year follow-up were likely to remain seizure free. Ten-year seizure freedom was 72% in children with developmental tumors and 32% in the cortical dysplasia group. Complete resection was statistically significant for favorable outcome, and no patient with an incomplete resection was seizure free.

Adolescent↗
PubMed1998

Infantile epileptic encephalopathy (Ohtahara syndrome) and migrational disorder.

A case of early infantile epileptic encephalopathy (EIEE) with suppression-bursts (Ohtahara syndrome) associated with a diffuse cerebral migrational and maturation disorder evident on microscopic examination is reported. Although virtually all reported cases of EIEE are secondary to a congenital or acquired structural malformation of cortical development, EIEE is sometimes identified only by detailed neuropathologic examination, as confirmed by this case report. In addition to the malformation of cortical development, the patient demonstrated an absence of gamma-aminobutyric acid in the cerebrospinal fluid. All children with EIEE should be thoroughly examined by magnetic resonance imaging, cerebrospinal fluid amino acid level determination, and detailed postmortem neuropathologic examination.

Amygdala↗
PubMedDate not supplied

[Electroencephalographic analysis of the functional development of cortical regions of the brain in children under 1 month of age].

Reorganization of background electric activity of newborns brain under the action of rhythmic photostimulation was studied in children of the first month of life in a state of quiet alertness by the method of age transversal slides (I, II, III-IV weeks of life). At the age of III-IV weeks, the repeated rhythmic light stimulation elicits a stable reorganization of the background activity in the theta-frequency range in the central areas at 5 Hz stimulation and in delta-frequency range in the occipital areas at 2 Hz stimulation. Characteristics of spatial manifestation of background activity reorganization in various cortical areas reflect frequency-specific character of newborns' cerebral cortex reactivity, appearing to the end of the first month of postnatal development.

Cerebral Cortex↗
PubMed2004

Long-term outcome after epilepsy surgery for focal cortical dysplasia.

OBJECT: Reports of outcomes for surgical treatment of cortical dysplasia associated with epilepsy are conflicting due to the inclusion of patients with a wide range of malformations of cortical development. The authors report their experience and the long-term outcome for a subgroup of patients with the histopathological diagnosis of focal cortical dysplasia of Taylor. METHODS: The records of 22 patients with focal cortical dysplasia of Taylor (15 with the balloon-cell type and seven with the nonballoon-cell type) were reviewed. There were 11 female and 11 male patients whose mean age was 26 +/- 17.6 years (mean +/- standard deviation [SD]) at surgery. The details of their epilepsy evaluation and resection were analyzed. Extent of resection was preoperatively planned using information obtained from long-term intracranial monitoring (15 patients) and/or more definitively determined by histopathologically proven clear margins during resection when feasible (12 patients). The mean duration of follow up was 6.3 +/- 5.1 years (mean +/- SD, range 0.5-15.6 years). Risk factors for epilepsy were trauma (seven patients) or meningoencephalitis (one patient); 14 patients (64%) had no obvious risk factors. The mean age at seizure onset was 9.2 years and the mean duration of their epilepsy was 16.1 +/- 9 years. In two patients there were no adverse findings on magnetic resonance (MR) imaging. In 15 patients (68%), the epileptogenic zone identified on long-term intracranial monitoring extended beyond the abnormality observed on MR images. Focal resection (lesion plus margins) was performed in 14 patients (64%), whereas eight (36%) underwent partial/tailored lobectomy. Two patients underwent multiple subpial transections in addition to partial lesionectomy because their lesions involved the sensorimotor cortex. In these two, functional MR imaging confirmed a normal functional anatomy despite the presence of the cortical dysplasia. Eleven (92%) of 12 patients who underwent resection guided by histopathologically proven clear margins and three (43%) of seven patients who underwent histopathologically proven subtotal resection have remained seizure free. Evidence of clear margins was significantly associated with an improved seizure outcome (p = 0.003). Postoperatively, expected deficits included nondisabling visual field defects, which occurred in three patients (14%), and transient sensorimotor deficits, which appeared in five (23%). Two patients had meningitis, which was successfully treated with antibiotics. Overall, 16 patients (73%) are either seizure free (13 patients), have rare nondisabling partial seizures (one patient), or had one seizure after their medication was changed (two patients). Thirteen patients (59%) have discontinued anticonvulsant medications or are being maintained on monotherapy. Of five patients (23%), two have had rare disabling seizures or significant reduction in their seizure frequency (three patients). One patient's seizures have remained the same. CONCLUSIONS: Focal cortical dysplasias are a distinct subgroup of malformations of cortical development and have a favorable outcome after resection. The epileptogenic zone often extends beyond the abnormality found on neuroimaging. Resection of the epileptogenic zone guided by histopathologically proven clear margins is associated with an improved seizure outcome.

Adolescent↗
PubMed2002

A reciprocal relationship between reliability and responsiveness in developing visual cortical neurons.

As the visual cortex matures, developmental modifications change the visually evoked firing patterns of single neurons. To explore the relationship between these developmental changes and the fidelity with which neurons transmit information, we measured the reliability of neuronal responses during postnatal development. Infant neurons have lower variability and higher dependence of transmitted information on firing rate than adult cells. Fewer spikes are needed by the infant cortex to convey the same amount of information. The increase in firing rates that occurs during development is largely offset, therefore, by a decrease in the reliability of responses. We propose that these changes are a consequence of the increasing ability of cortical cells to encode rapid changes in the visual environment.

Animals↗
PubMed2004

Genetics and cell biology of lysophosphatidic acid receptor-mediated signaling during cortical neurogenesis.

Lysophosphatidic acid (LPA) is a small lysophospholipid that signals through G-protein coupled receptors (GPCRs) to mediate diverse cellular responses. Two LPA receptors, LPA(1) and LPA(2), show gene expression profiles in mouse embryonic cerebral cortex, suggesting roles for LPA signaling in cerebral cortical development. Here, we review loss-of-function and gain-of-function models that have been used to examine LPA signaling. Genetic deletion of lpa(1) or both lpa(1) and lpa(2) in mice results in 50-65% neonatal lethality, but not obvious cortical phenotypes in survivors, suggesting that compensatory signaling systems exist for regulating cortical development. A gain-of-function model, approached by increasing receptor activation through exogenous delivery of LPA, shows that LPA signaling regulates cerebral cortical growth and anatomy by affecting proliferation, differentiation and cell survival during embryonic development.

Animals↗