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PubMed1990

Microglia and cell death in the developing mouse cerebellum.

The appearance and distribution of microglia in the developing cerebellum has been examined with the aid of a peroxidase-conjugated lectin derived from Griffonia simplicifolia. This distribution has in turn been correlated with that of pyknotic figures in the same Nissl-counterstained sections, in order to gain an understanding of the role of microglial in the developing cerebellum. Round and ameboid microglia may be recognised in the fetal cerebellum as early as E11. Numbers of microglia increase steadily from that time, with initial concentrations in the region of the dorsal and ventricular surfaces. By P1, concentrations of both pyknotic figures and ameboid microglia begin to appear in the region of the future cerebellar medulla. Ameboid microglia are recognisable in the cerebellar medulla until P10, with particular concentrations where folia branch and in the rostral cerebellar peduncles. After this time only resting microglia are found in the cerebellum. Concentrations of microglia largely match the positions of pyknotic figures throughout development, except at P10 and P14, when cell death is found in the external granular layer without an accompanying concentration of microglia. Electron microscopic examination of the phagosomes of ameboid microglia at P5 and P6 indicates that these cells are mainly concerned with the phagocytosis of entire cells rather than axons. Cell death in the cerebellar medulla may serve to clear pathways for developing cortical afferents and efferents, or to increase the mechanical plasticity of the medulla during cortical folding.

Animals↗
PubMed1995

Neonatal infraorbital nerve transection and blockade of axoplasmic transport reduce expression of acetylcholinesterase by thalamocortical axons.

Acetylcholinesterase (AChE) is transiently expressed by ventrobasal thalamic neurons and their axons in the primary somatosensory cortex and this enzyme has been used as a marker for these axons in studies concerned with cortical development and plasticity. The present experiment evaluated the effects of both peripheral nerve transection and blockade of axoplasmic transport upon the expression of AChE in thalamic axon terminals in the primary somatosensory cortex. Both manipulations resulted in marked reductions in the density of AChE in thalamocortical axons and less dramatic decreases in the density of this enzyme in thalamic neurons. These results indicate that AChE may not invariably provide unequivocal information about the distribution of somatosensory thalamocortical axon terminals in developing rodents.

Acetylcholinesterase↗
PubMed1995

Neural pattern formation via a competitive Hebbian mechanism.

In this contribution we investigate a simple pattern formation process [9,10] based on Hebbian learning and competitive interactions within cortex. This process generates spatial representations of afferent (sensory) information which strongly resemble patterns of response properties of neurons commonly called brain maps. For one of the most thoroughly studied phenomena in cortical development, the formation of topographic maps, orientation and ocular dominance columns in macaque striate cortex, the process, for example, generates the observed patterns of receptive field properties including the recently described correlations between orientation preference and ocular dominance. Competitive Hebbian learning has not only proven to be a useful concept in the understanding of development and plasticity in several brain areas, but the underlying principles have have been successfully applied to problems in machine learning [22]. The model's universality, simplicity, predictive power, and usefulness warrants a closer investigation.

Animals↗
PubMed1979

Early histogenesis in the mouse cerebral cortex: a Golgi study.

The early histogenesis in the cerebral cortex of the mouse was studied with a modification of the rapid Golgi method. Three stages can be distinguished first, a period during which the telencephalon is exclusively populated with neuroepithelial cells (till E12); secondly the transient stage of the primordial cortical organization, characterized by the presence, in the outer part of the neural tube, of a loose network of primitive horizontal nerve cells and third, the appearance of the early cortical plate (E14) which contains closely packed, radial bipolar nerve cells. In addition to some salient morphological features of the various cell types, the technique also reveals the importance of efferent fibers from the cortex during the early cortical development.

Animals↗
PubMed1988

Ontogeny of neurotensin receptor binding sites in the rat visual cortex.

The ontogeny of neurotensin receptor binding sites in the rat visual cortex was examined by in situ receptor autoradiography. Binding sites were present in the embryonic cortex and showed extremely high densities at birth and in early postnatal life. Their densities began a gradual decline in the second postnatal week to reach very low levels in adult animals. These results suggest that neurotensin receptor binding sites may play a role in cortical development.

Animals↗
PubMed1992

Monoclonal antibodies reveal molecular differences between terminal fields in the rat dentate gyrus.

We have derived a number of monoclonal antibodies which detect molecular differences correlating with the afferent inputs to the molecular layer of the adult rat hippocampal dentate gyrus. One group, dubbed OM-1 to OM-4, strongly stain the outer zone of the molecular layer, which receives its major innervation from the ipsilateral entorhinal cortex. A second group, IM-1 and IM-2, show a complementary pattern and preferentially stain the inner molecular layer, which receives inputs from the ipsilateral and contralateral hippocampus. These antigens are not, however, restricted to these layers, being found outside the hippocampus in several other areas of neuropil in the adult brain. In the developing brain the IM-1 antigen appears ubiquitously from the earliest age studied, embryonic day 12. Within the dentate gyrus, its restriction to the inner terminal field of the molecular layer only occurs during the second postnatal week. In contrast, OM staining appears only sparsely and late in the prenatal brain, appearing in developing cortical white matter between embryonic days 18 and 20. The outer dentate molecular layer becomes OM-positive from birth onwards, corresponding to the time of arrival of entorhinal axons during the first postnatal week. These two groups of monoclonal antibodies recognize a number of different glycoproteins. Ultrastructural immunohistochemistry shows they are cell surface molecules, and as such may be involved in the recognition events required for the establishment of specific patterns of neuronal connectivity.

Animals↗
PubMed1994

Developmentally regulated expression of a brain specific species of chondroitin sulfate proteoglycan, neurocan, identified with a monoclonal antibody IG2 in the rat cerebrum.

The mammalian brain contains many species of proteoglycan. To identify each proteoglycan species, we have raised monoclonal antibodies against soluble chondroitin sulfate proteoglycans purified from 10-day-old rat brains. One monoclonal antibody, named monoclonal antibody 1G2, recognized two proteoglycan species with 220,000 and 150,000 mol. wt core glycoproteins (chondroitin sulfate proteoglycan-220 and chondroitin sulfate proteoglycan-150). Partial amino acid sequences of N-termini of their core proteins coincided with those of neurocan, a brain-unique chondroitin sulfate proteoglycan species, whose complete coding sequence was recently reported [Rauch et al. (1992) J. biol. Chem. 269, 19,536-19,547]. Western blots revealed that chondroitin sulfate proteoglycan-220 became detectable in the rat cerebrum on embryonic day 14, and that it disappeared from the brain around postnatal day 30. In contrast, a fairly large amount of chondroitin sulfate proteoglycan-150 remained in the mature brain. Immunohistochemical studies revealed that 1G2 antigen was first localized in the preplate zone, then both in the marginal zone and in the subplate of the rat cerebrum on embryonic day 16, prior to arrival of the first thalamic afferents at the cortex. On embryonic day 20, immunolabeling with monoclonal antibody 1G2 began to spread from the subplate into the developing cortical plate. On postnatal day 10, the neuropil of the cerebrum, except for the barrel field, was diffusely stained with the antibody, intensely in the hippocampus and superficial layers (I-III) of the cerebral cortex and weakly elsewhere. The barrel hollows were stained very weakly compared with the barrel walls at this stage. The immunoreactivity in the hippocampus and superficial cortical layers was weakened in the mature brain, so that no particular staining pattern, but weak and diffuse staining was observed in the adult rat cerebrum. The 1G2 antigen was immunohistochemically associated largely with glial fibrillary acidic protein-positive cells in primary cultures of the neonatal rat cerebrum. Both chondroitin sulfate proteoglycan-220 and chondroitin sulfate proteoglycan-150 were detected in the conditioned media not only of highly enriched cultures of fetal rat cortical neurons but also of pure cultures of mature astrocytes; more (12- to 20-fold) in the astrocyte conditioned media. Astrocytes, in addition to neurons, may be a cellular source of neurocan in brain at least under certain physiological conditions. The spaciotemporal expression pattern of 1G2 epitope-bearing proteoglycan, or neurocan, suggests that this proteoglycan species plays some roles at least in forming the elongation pathway for early cortical afferent fibers as well as the functional barrel structure in the somatosensory cortex.

Amino Acid Sequence↗
PubMed1995

The neuroprotective effects of MK-801 on the induction of microgyria by freezing injury to the newborn rat neocortex.

Four-layered microgyria is associated with many developmental disorders, including mental retardation, epilepsy, and developmental dyslexia. Freezing lesions to the newborn rodent neocortex result in the formation of four-layered microgyria. Previous research had suggested this type of injury acts as an hypoxic/ischemic event to the developing cortical plate. The current study examines the effectiveness of the non-competitive N-methyl-D-aspartate receptor antagonist dizocilpine (MK-801) in protecting against freezing injury to the newborn rat cortical plate. Three groups of rats received freezing injury to the cortical plate on the first day of life (postnatal day 1). Two groups were treated with MK-801 (1 or 2 mg/kg) 0.5 h before the lesion and 6 and 14 h after, while one group received saline injections. A fourth group received MK-801 injections, but did not have a freezing lesion. The volume of neocortical abnormality was determined for all three groups in rats killed after postnatal day 7. Treatment with the higher dose of MK-801 (3 x 2 mg/kg) dramatically reduced the effects of freezing injury but also resulted in over 50% mortality in both lesioned and unlesioned groups. Animals in the lesioned group, however, had a decreased volume of abnormal cortex, and there were fewer animals with microsulci than in the untreated group. This is the first demonstration of a significant anatomical neuroprotective effect in newborns leading to a reduction of cortical malformation.

Animals↗
PubMed1991

Control of postsynaptic Ca2+ influx in developing neocortex by excitatory and inhibitory neurotransmitters.

We assessed the pathways by which excitatory and inhibitory neurotransmitters elicit postsynaptic changes in [Ca2+]i in brain slices of developing rat and cat neocortex, using fura 2. Glutamate, NMDA, and quisqualate transiently elevated [Ca2%]i in all neurons. While the quisqualate response relied exclusively on voltage-gated Ca2+ channels, almost all of the NMDA-induced Ca2+ influx was via the NMDA ionophore itself, rather than through voltage-gated Ca2+ channels. Glutamate itself altered [Ca2+]i almost exclusively via the NMDA receptor. Furthermore, synaptically induced Ca2+ entry relied almost completely on NMDA receptor activation, even with low-frequency stimulation. The inhibitory neurotransmitter GABA also increased [Ca2+]i, probably via voltage-sensitive Ca2+ channels, whereas the neuromodulator acetylcholine caused Ca2+ release from intracellular stores via a muscarinic receptor. Low concentrations of these agonists produced nonperiodic [Ca2+]i oscillations, which were temporally correlated in neighbouring cells. Optical recording with Ca2(+)-sensitive indicators may thus permit the visualization of functional networks in developing cortical circuits.

Acetylcholine↗
PubMed2005

Pterygium, pinguecula, and 5-year incidence of cataract.

PURPOSE: To assess longitudinal associations between pterygium, pinguecula, and 5-year incident cataract. DESIGN: Population-based cohort study. METHODS: The Blue Mountains Eye Study examined 3,654 residents aged > or =49 years during 1992 to 1994 and reexamined 2,335 (75.1% of survivors) 5 years later. Slit-lamp examination recorded pterygium and pinguecula. Cataract was assessed using masked grading of lens photographs. Incidence was assessed in participants without cataract at baseline. Eye-specific data were analyzed using generalized estimating equation models, adjusting for age, sex, smoking, diabetes, and corticosteroid use. RESULTS: Pinguecula was associated with a borderline-significant, increased risk of developing cortical cataract (adjusted odds ratio, 1.3; 95% confidence interval, 1.0 to 1.7). We found no significant association between baseline pterygium and the incidence of cortical, nuclear, or posterior subcapsular cataract. CONCLUSIONS: Longitudinal data from the same study population provide weak support for cross-sectional associations between pinguecula and cortical cataract previously reported from our study.

Cataract↗
PubMed2026

Understanding septo-optic dysplasia: Endocrine implications and ophthalmic consequences.

Septo-optic dysplasia (SOD) is a heterogeneous neurodevelopmental disorder classically defined by optic nerve hypoplasia, hypothalamo-pituitary dysfunction, and midline brain abnormalities, although the full triad is not consistently present. This review synthesises current evidence on the developmental, endocrine, ophthalmic, and neuroradiological dimensions of the SOD/optic nerve hypoplasia spectrum. Shared embryological origins of the optic pathways, hypothalamus, and pituitary, together with disruption of inductive signalling pathways and pathogenic variants in developmental regulators including SOX2, HESX1, SOX3, and OTX2, provide a mechanistic basis for combined ocular and pituitary phenotypes. Clinically, affected children may present with nystagmus, strabismus, visual impairment, neonatal hypoglycaemia, or evolving pituitary hormone deficiencies, and remain at risk of neurodevelopmental morbidity. Neuroradiological studies have expanded the phenotype beyond classical midline defects to include malformations of cortical development and SOD-plus presentations. Current evidence supports longitudinal endocrine surveillance, detailed ophthalmic assessment, and multidisciplinary care, including timely hormone replacement and developmental support where indicated.

developmental genetics↗
PubMed2005

Factors of morbidity in hemispherectomies: surgical technique x pathology.

OBJECTIVE: The objective of this paper is to evaluate factors of surgical morbidity from different techniques of hemispherectomy with emphasis on causative pathology. PATIENTS AND METHODS: Thirty patients underwent hemispherectomy in our institution from 1987 to 2003, two presented with Sturge-Weber Syndrome (SWS), sixteen with Rasmussen's Syndrome (RS), eight with established hemispheric lesions (EHL), and four with cortical development malformations (CDM). Six surgeons operated on three patients using anatomical hemispherectomies (AH), 11 patients using functional hemispherectomy (FH), and 16 patients employing hemispherotomy (HT). Surgical technique and causative pathology were studied independently as factors of morbidity in hemispherectomy. RESULTS: Overall mean surgical time was 11:50+/-3:20 h and increased proportionately in pathologies with larger hemispheres. Blood transfusion was particularly influenced by the approach adopted by our team of anesthesiologists, independently of technique or pathology. Pathology was the most important factor related to hydrocephalus as two out of four patients with CDM needed ventriculoperitoneal shunt whilst none with EHL or SWS. Four patients undergoing HT and one FH presented residual bridges connecting the hemispheres, three were reoperated and are seizure free. Two patients with CDM did not improve their seizures worthwhile with surgery and other two (one with RS and other with CDM) were waiting a second procedure due to incomplete inter-hemispheric disconnection. Five patients presented infection and one died after developing meningoencephalitis. CONCLUSION: Hemispherectomies are procedures where pathology and surgical technique interact narrowly. Therefore, in order to study surgical morbidity or outcome, both pathology and technique have to be analyzed independently.

Adolescent↗
PubMed2006

A patient with simplified gyral pattern followed by progressive brain atrophy.

We present the case of a three-year-old boy who suffered from intractable epilepsy from birth, and who displayed microcephaly and severe developmental delay. Neuroradiological examination revealed the presence of simplified gyri of the cerebral cortex, and increased signal intensity changes in the cerebral white matter on T2-weighted magnetic resonance imaging. A tentative diagnosis of congenital cortical malformation was made, but unexpectedly, the cerebrum, cerebellum, and pons showed a progressive atrophy during the follow-up period. The basal ganglia and thalamus were relatively spared. Investigations could find no evidence of leukodystrophies, metabolic disorders, hereditary brain anomalies, or congenital central nervous infections. This case may represent a novel type of neurodegenerative disease with malformation of cortical development.

Atrophy↗
PubMed2006

A 3D model of Reelin subrepeat regions predicts Reelin binding to carbohydrates.

Reelin is a large molecule of the extracellular matrix (ECM) which regulates neuronal positioning during the early stages of cortical development in vertebrate species. The Reelin molecule can be subdivided into a smaller N-terminal domain, showing homology with F-spondin, and a larger C-terminal region containing 8 EGF-like repeats. The localization of Reelin in the ECM, its large dimensions and the modular organization of its primary structure led us to suppose a structure of its modules similar to domains commonly found in ECM proteins such as Agrin, laminins and thrombospondins. We therefore performed a sequence alignment and molecular modeling analysis to study the three-dimensional fold of the Reelin subrepeat regions. Our analysis produces a tentative model of the core region of the Reelin subrepeat sequences and suggests the presence in this 3D model of structural features common to polysaccharide-binding modules which are often found on proteoglycans of the ECM. These findings provide a conceptual framework for further experiments aimed at testing the functions of the EGF-like repeat regions of Reelin.

Amino Acid Sequence↗
PubMed2005

The nuclear receptor COUP-TFI represses differentiation of Cajal-Retzius cells.

The cellular diversity of neurons located in the marginal zone (MZ) of the cortex has a crucial role in cortical development. However, little is known about the molecular mechanisms involved in how these different neuronal cell types are specified. Here, we show that in the MZ, the nuclear receptor COUP-TFI is localized in calbindin-positive cells and not in reelin-positive cells. High expression of COUP-TFI has been detected in preplate (PP) and subplate (SP) cells, suggesting that this nuclear receptor is down-regulated during preplate differentiation towards the Cajal-Retzius (CR) cell lineage. By maintaining high ectopic expression of COUP-TFI in preplate cells, we show that COUP-TFI represses the CR cell markers reelin and calretinin, and with lower efficiency the transcription factor Tbr1. Furthermore, general differentiation is not affected, strongly suggesting that COUP-TFI represses differentiation of CR cells.

Animals↗
PubMed2006

A population based study of epilepsy in children from a Swedish county.

BACKGROUND: Epidemiological studies of childhood epilepsy are of importance to compare incidence and prevalence rates, age distribution, inheritance, seizure types, epilepsy syndromes and treatment strategies. AIM: To perform an epidemiological study on children with epilepsy in a Swedish county using current ILAE classifications and a recent proposal. METHODS: A population-based study was performed using the hospital data register to select children aged 1 month to 16 years with the diagnosis 'convulsions' or 'epilepsy' recognized between January 1996 and December 2000. Only patients with active epilepsy were included. RESULTS: Two hundred and five children met the study criteria on the prevalence day 31st December, 2000. The total prevalence rate was 3.4/1,000 with a peak prevalence in the age group 8-11 years. The incidence year 2000 was 40/100,000. Additional neuroimpairments were registered in 47.3%. A majority of the patients, 54.0%, had focal or focal plus secondarily generalized seizures. A named syndrome could be diagnosed in 49.4%. The most common syndrome was rolandic epilepsy occurring in 17.0%. Childhood absence epilepsy occurred in 5.9%. Different disorders associated with epilepsy were found in 31.7%. The most common associated phenomenon was malformation of cortical development. Antiepileptic drug treatment was used in 81.0%, the most common first choice being valproate. CONCLUSIONS: The prevalence and incidence rates in this strictly delineated study are lower than those found in other epidemiological studies. Together with many divergences between reported studies concerning frequencies of different items, the results apparently depend on design, e.g. differences in age groups included, inclusion criteria used, and general methodology.

Adolescent↗
PubMed2003

Gene expression profile analyses of cortical dysplasia by cDNA arrays.

Cortical dysplasia (CD) is a well-recognized cause of intractable epilepsy, especially in children and is characterized histologically by derangements in cortical development and organization. The objective of this study was to expand the current knowledge of altered gene expression in CD as a first step towards in the identification of additional genes operative in the evolution of CD. Surgical specimens were obtained from eight patients (4 males and 4 females; age range 2-38 years; mean 15 years) with a pathologic diagnosis of CD. Nondysplastic temporal neocortex was obtained from a 2-year-old boy with intractable epilepsy and medial temporal lobe ganglioglioma. After total RNA isolation from frozen brain tissues, we carried out gene expression profiling using a cDNA expression array. Differences in gene expressions between CD and the nondysplastic neocortex were confirmed by semi-quantitative conventional reverse transcription-PCR. Three genes (recombination activating gene 1 (RAG1), heat shock 60 kDa protein 1 (HSP-60), and transforming growth factor beta1 (TGF beta1)) were found to be up-regulated more than two-fold in CD, whereas four genes (phosphoinositide-3-kinase regulatory subunit polypeptide 1 [p85 alpha] (PI3K), frizzled homolog 2 [Drosophila], Bcl-2/adenovirus E1B 19 kDa interacting protein (NIP3), and glia maturation factor beta (GMF beta)) were down-regulated to less than 50% of their normal levels. Interestingly, the majority of genes showing altered expression were associated with apoptosis. Our study demonstrates diverse changes in gene expression in CD. However, it remains to be shown which of these are causally related to the evolution of CD.

Adolescent↗
PubMed2004

Electroclinical and magnetoencephalographic studies in epilepsy patients with polymicrogyria.

RATIONALE: Malformations of cortical development (MCDs) are increasingly recognized as important causes of developmental delay, epilepsy, and other neurological disorders. Polymicrogyria, a type of MCD, is characterized by many small microgyria separated by shallow sulci, a slightly thick cortex, neuronal heterotopia and often enlarged ventricles. The present descriptive study analysis the electroclinical and magnetoencephalographic findings of patients with epilepsy and polymicrogyria without schizencephaly. METHODS: We studied six patients; mean age was 27 years, who had evidence of polymicrogyria in neuroimaging studies. A single equivalent-current dipole (ECD) model was used to estimate the location of epileptiform spike dipole sources. Analysis was performed on selected data segments containing MEG spikes. MEG results were combined with MRI to create magnetic source images (MSI). RESULTS: In all cases we present results of MRI, MEG, Video-EEG monitoring, and other functional neuroimaging studies if performed. CONCLUSIONS: MSI can be used to accurately localize sources of epileptiform discharges. As such MSI can play a role of directly determining the functional epileptogenic significance of abnormalities depicted in imaging.

Adolescent↗