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[Postpartum amaurosis in patients with pre-eclampsia].

Cortical blindness without retinal changes is a rare complication in preeclampsia. We report two patients, both of whom developed cortical blindness one and two days post partum. In one of these patients, the blindness occurred following eclamptic seizure. In both patients the total blindness recovered fully after two and three days respectively following treatment for hypertension and cerebral edema. Spasm of small vessels in the occipital cortex is assumed to be the cause of this complication.

Adult↗
PubMed1996

Ocular dominance plasticity under metabotropic glutamate receptor blockade.

Occluding vision through one eye during a critical period in early life nearly abolishes responses to that eye in visual cortex. This phenomenon is mimicked by long-term depression of synaptic transmission in vitro, which may require metabotropic glutamate receptors (mGluRs) and is age-dependent. Peaks in mGluR expression and glutamate-stimulated phosphoinositide turnover during visual cortical development have been proposed as biochemical bases for the critical period. Pharmacological blockade of mGluRs specifically prevented synapse weakening in mouse visual cortical slices but did not alter kitten ocular dominance plasticity in vivo. Thus, a heightened mGluR response does not account for the critical period in development.

Animals↗
PubMed1992

Spontaneous synchronous synaptic calcium transients in cultured cortical neurons.

The firing pattern displayed by neuronal aggregates is thought to play a key role in cortical development and physiology. In this study, we have employed optical recording of intracellular calcium to monitor activity of multiple neurons simultaneously in primary cortical cultures. With this approach, we have observed spontaneous synchronous calcium transients among adjacent cortical neurons. These transients appear to be mediated by prominent spontaneous synaptic excitation, as they are enhanced by picrotoxin, a blocker of inhibitory GABAergic transmission, and reduced by antagonism of glutamate receptors or addition of TTX. After picrotoxin treatment, the calcium transients exhibit regular frequency and amplitude, and occur in synchrony with bursts of excitatory synaptic potentials every 10-20 sec. Using electrical stimulation, we have identified a relative refractory period, extending up to 5 sec after a synchronous burst, that may play a role in cell synchronization. NMDA receptor antagonists or reduced extracellular calcium levels lower the amplitude of the calcium transients yet fail to alter their frequency, suggesting that intracellular calcium levels may not be a major determinant of burst frequency. In contrast, mild depolarization with kainic acid (0.5-1 microM) increased burst frequency up to fivefold, suggesting a critical dependence of rhythmic activity on membrane potential. Chronic blockade of electrical activity with TTX beginning a few days after plating of cultures dampens the amplitude and significantly increases the frequency of calcium transients in mature cultures. These studies demonstrate that aggregates of cultured cortical neurons express synchronous firing activity in vitro and that this network activity is dependent in part on neuronal firing during development.

2-Amino-5-phosphonovalerate↗
PubMed2000

Netrin-1 promotes thalamic axon growth and is required for proper development of the thalamocortical projection.

The thalamocortical axon (TCA) projection originates in dorsal thalamus, conveys sensory input to the neocortex, and has a critical role in cortical development. We show that the secreted axon guidance molecule netrin-1 acts in vitro as an attractant and growth promoter for dorsal thalamic axons and is required for the proper development of the TCA projection in vivo. As TCAs approach the hypothalamus, they turn laterally into the ventral telencephalon and extend toward the cortex through a population of netrin-1-expressing cells. DCC and neogenin, receptors implicated in mediating the attractant effects of netrin-1, are expressed in dorsal thalamus, whereas unc5h2 and unc5h3, netrin-1 receptors implicated in repulsion, are not. In vitro, dorsal thalamic axons show biased growth toward a source of netrin-1, which can be abolished by netrin-1-blocking antibodies. Netrin-1 also enhances overall axon outgrowth from explants of dorsal thalamus. The biased growth of dorsal thalamic axons toward the internal capsule zone of ventral telencephalic explants is attenuated, but not significantly, by netrin-1-blocking antibodies, suggesting that it releases another attractant activity for TCAs in addition to netrin-1. Analyses of netrin-1 -/- mice reveal that the TCA projection through the ventral telencephalon is disorganized, their pathway is abnormally restricted, and fewer dorsal thalamic axons reach cortex. These findings demonstrate that netrin-1 promotes the growth of TCAs through the ventral telencephalon and cooperates with other guidance cues to control their pathfinding from dorsal thalamus to cortex.

Animals↗
PubMed1996

The equivalent source technique and cortical imaging.

As an equivalent source localisation technique, the radial dipole source has been chosen as the equivalent source of the actual neural source in the recently developed cortical imaging technique (CIT). In this short paper, the point current source is numerically tested as a new kind of equivalent source for implementing CIT. The results confirm the efficiency of the new equivalent source.

Cerebral Cortex↗
PubMed2005

Developmental mechanics of the primate cerebral cortex.

The idea that the brain is shaped through the interplay of predetermined ontogenetic factors and mechanisms of self-organization has a long tradition in biology, going back to the late-nineteenth century. Here we illustrate the substantial impact of mechanical forces on the development, morphology, and functioning of the primate cerebral cortex. Based on the analysis of quantitative structural data for prefrontal cortices of the adult rhesus monkey, we demonstrate that (1) the characteristic shape of cortical convolutions can be explained by the global minimization of axonal tension in corticocortical projections; (2) mechanical forces resulting from cortical folding have a significant impact on the relative and absolute thickness of cortical layers in gyri and sulci; (3) folding forces may affect the cellular migration during cortical development, resulting in a significantly larger number of neurons in gyral compared to non-gyral regions; and (4) mechanically induced variations of morphology at the cellular level may result in different modes of neuronal functioning in gyri and sulci. These results underscore the significant contribution of mechanical forces during the self-organization of the primate cerebral cortex. Taking such factors into account within a framework of developmental mechanics can lead to a better understanding of how genetic specification, the layout of connections, brain shape as well as brain function are linked in normal and pathologically transformed brains.

Animals↗
PubMed2006

A transgenic marker mouse line labels Cajal-Retzius cells from the cortical hem and thalamocortical axons.

Cajal-Retzius (CR) cells are among the earliest born cortical neurons and are required for normal cortical development in rodents and humans; however, their embryonic origin has been controversial. Recent genetic lineage studies and direct visualization of migration of CR cells have demonstrated multiple germinative sources for CR cells on the edges of the developing pallium. We generated transgenic mice using 5' untranslated regions of the Frizzled10 gene in order to mark the cortical hem (the most caudomedial edge of the telencephalic neuroepithelium) and found that these mice faithfully reproduce the previously described expression pattern of Frizzled10 mRNA in the cortical hem, dorsal thalamus and dorsal neural tube. In the cortical hem, expression of LacZ mRNA was confined to the ventricular zone and perdurance of LacZ protein served as lineage marker for CR cells derived from the hem during embryonic life. When these marker mice were crossed with FoxG1 (BF1) mutants, they confirmed the previous finding that in these mice the cortical hem is expanded leading to increased production of CR cells from the medial wall of the cortex.

Animals↗
PubMed2002

Pathologic characteristics of the cortical dysplasias.

The gross and microscopic features of cortical dysplasia (malformations caused by abnormalities of cortical development) are reviewed and illustrated in this article. The pathologic associations of neurocutaneous disorders, neoplasms, and hippocampal sclerosis with cortical dysplasia also are discussed.

Brain↗
PubMed2006

A century of progress in corticoneurogenesis: from silver impregnation to genetic engineering.

Within the past 125 years, we have witnessed great strides in understanding development and evolution of the cerebral cortex, arguably the structure that makes us human. Among the distinguishing features of cortical development are discoveries that its constituent neurons are not generated locally and that after assuming their proper areal, radial, and laminar position, they serve the individual throughout the lifespan. Although the basic cellular events and all major developmental phenomena have been discovered by the use of classical methods, advents of new, evermore sophisticated experimental methods that range from neuroimaging to molecular genetics enable elucidation of the molecular and cellular mechanisms underlying evolutionary elaboration of the cortex and opens the possibility for the prevention and treatment of congenital disorders of the highest cognitive functions in humans.

Animals↗
PubMed1993

Meeting report: Second International Rett Syndrome Workshop and Symposium.

Dawna Armstrong led off the summary session by reviewing the morphologic findings. Brain weights in Rett syndrome autopsy samples are 60% to 80% of expected values. Cerebral cortex has increased packing density, with decreased size of neurons and an apparently normal number of neurons, suggesting immature cortical development. Findings in the substantia nigra from Cheryl Kitt are similar. Dr Armstrong quantitated the dendritic tree in six cortical areas and found reduction in dendritic trees in all areas, with the most prominent being in the temporal lobe and the least prominent in the visual cortex. The reductions in dendritic branching do not differ with age, being the same from 4 to 35 years of age. Basal dendrites were more affected than apical dendrites, and neurons in layer 5 were more affected than those in layer 3. Dr Armstrong postulated that the increase in synaptic density from 28 weeks' gestation to birth occurred on schedule, but the secondary increase that occurs after 2 months, with a peak at 19 months, was disordered. Verne Caviness noted that these are the most informative data regarding Rett syndrome presented to date and can be summarized in three areas: (1) There is a morphologic disorder with a decrease in dendritic length, decrease in branching, and probably a decrease in the total number of synapses. He stressed that a morphologist requires a change of about 50% in the population to recognize a difference. (2) There is a dropout of certain histochemical variables, with a 93% reduction in the cholinergic system, and substantia nigra debris indicating cell death. (3) The phenomenon is generalized, with a 30% reduction volumetrically.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1975

The effect of in utero decapitation on the morphological and physiological development of the fetal rabbit lung.

A study has been made of the consequences of in utero decapitation on the morphological and physiological development of the fetal lung. Fetal rabbits were decapitated in situ at 22 days, without losing any amniotic fluid, and allowed to continue their development with their undamaged littermates as controls. Such decapitation, of course, removes the pituitary and so interferes with adrenal cortical development. Morphological studies showed an interference with lung development in that, although the number of alveolar saccules increased normally, their walls failed to thin. In the decapitated fetuses, a reduction in the number of lamellated bodies per Type II pneumonocyte was found at each age studied; while dense, homogeneous bodies were more numerous. The normal disappearance of glycogen in the Type II pneumonocytes of the decapitated fetuses was retarded. Physiological studies supported these findings. In control fetuses allowed to breathe for a while the Bubble Stability Ratio increased rapidly from day 26 to reach a maximum at 28 days; whereas, in the decapitated ones, bubble stability was not apparent before day 28 and by the 29th day had reached a maximum which was lower than that of the controls. In the control fetuses, lecithin was detected in lung fluid from 26 days on, and in stomach fluid from 29 days. It is argued that lung development must be, at least in part, under the control of the fetus' own pituitary-adrenal axis.

Animals↗
PubMed2004

Ndel1 operates in a common pathway with LIS1 and cytoplasmic dynein to regulate cortical neuronal positioning.

Correct neuronal migration and positioning during cortical development are essential for proper brain function. Mutations of the LIS1 gene result in human lissencephaly (smooth brain), which features misplaced cortical neurons and disarrayed cerebral lamination. However, the mechanism by which LIS1 regulates neuronal migration remains unknown. Using RNA interference (RNAi), we found that the binding partner of LIS1, NudE-like protein (Ndel1, formerly known as NUDEL), positively regulates dynein activity by facilitating the interaction between LIS1 and dynein. Loss of function of Ndel1, LIS1, or dynein in developing neocortex impairs neuronal positioning and causes the uncoupling of the centrosome and nucleus. Overexpression of LIS1 partially rescues the positioning defect caused by Ndel1 RNAi but not dynein RNAi, whereas overexpression of Ndel1 does not rescue the phenotype induced by LIS1 RNAi. These results provide strong evidence that Ndel1 interacts with LIS1 to sustain the function of dynein, which in turn impacts microtubule organization, nuclear translocation, and neuronal positioning.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1994

Development of the superior temporal neocortex is anomalous in trisomy 21.

Trisomy 21 (Down syndrome) is the most common inherited form of mental retardation in the United States, however, the basis of impaired cognition is unknown. We have used recently developed stereological cell counting techniques to quantitatively examine the pattern of neuronal migration and maturation in one neocortical area during gestation in normal development and in trisomy 21. Normal development of the cerebral cortex occurs in two general sequences: Beginning at approximately 7-8 weeks gestation, migration of cells destined to become neurons results in the accumulation of cells in the cortical mantle. This process is largely complete by 20-21 weeks. Over the next 7-10 weeks an "inside-out" differentiation into lamina of different neuronal densities occurs. Our data suggest that the second phase of cortical development, the emergence of lamination, is both delayed and disorganized in trisomy 21. The observed pattern of cortical maturation may reflect an abnormality in axonal and dendritic arborization that subsequently subserve the connectional and functional units underlying normal cognition.

Cell Movement↗
PubMed2000

Schizencephaly: clinical and imaging features in 30 infantile cases.

Schizencephaly is an uncommon structural disorder of cerebral cortical development, characterized by congenital clefts spanning the cerebral hemispheres from the pial surface to the lateral ventricles and lined by cortical gray matter. Either an antenatal environmental incident or a genetic origin could be responsible for this lesion which occurs between the third and fourth month of gestation. We report the clinical and cranial imaging features of 30 children, of whom 15 had unilateral and 15 had bilateral lesions. Their ages at the time of the first presentation ranged from 1 month to 10 years. They were thoroughly studied from clinical, epileptical, imaging and electroencephalographic (EEG) viewpoints. Five patients were investigated by cranial computed tomography (CT), eight by cranial magnetic resonance (MR) imaging, and 17 by both methods. The clinical features consisted of mild hemiparesis in 17 cases (57%), 12/17 were related to a unilateral phenotype (80% of all unilateral forms) and 5/17 to a bilateral phenotype. A tetraparesis was present in nine cases, all of which were due to a bilateral cleft. Bilateral forms were significantly associated with tetraparesis, whereas unilateral forms were associated with hemiparesis. Mental retardation was observed in 17 cases (57%), and was observed significantly more often in bilateral clefts (80%). When both hemispheres are involved, an absence of reorganization of the brain function between the two hemispheres leads to severe mental deficits, in addition to the cerebral anomaly itself. Eleven patients had seizures (seven from unilateral and three from bilateral forms). The degree of malformation was not related to the severity of epilepsy. Migration disorders, such as dysplasia or heterotopia, were observed in 30% of cases and are also important etiopathogenetic factors. The septum pellucidum was absent in 13 cases (43%), with septo-optical dysplasia in two cases. Corpus callosum dysgenesis was noted in 30% of cases. Four cases of mega cisterna magna were noted. Although familial cases and environmental factors have been previously reported, schizencephaly appears to be, in the majority of cases, sporadic.

Adolescent↗
PubMed2001

Early-generated preplate neurons in the developing telencephalon: inward migration into the developing striatum.

Specialized subsets of early-generated neurons provide the cellular cues that are necessary for the establishment of characteristic cell and fiber interactions in each brain region. During the development of the mammalian cerebral cortex, the early-generated cells line up in the most superficial part of the telencephalic pallium forming the preplate. It has been generally thought that the preplate derivatives are exclusively located in the cortical region and govern the early histogenetic phase of cortical development. However, we here disclose an unexpected evidence that a subset of early-generated neurons of the piriform preplate migrate inward into and disperse within the subcortical structure striatum during the embryonic stage. Their migratory route is unique and its direction is opposite to the ordinary migration of neuronal precursors directed outward from the periventricular germinal zone. After immigrating into the developing striatum, these early-generated cells are closely associated with the intrastriatal fascicules of axons. The majority of these cells are eliminated by apoptotic cell death during the early postnatal stage. Based on these findings, we propose a new concept: the preplate neurons may not only direct cortical histogenesis but also change their location to play a role in the development of subcortical structures.

Animals↗
PubMed1999

Cortical atrophy detected by computed tomography in gasoline station attendants.

BACKGROUND: To evaluate the contribution of leaded gasoline in the presence of abnormal calcifications or cortical atrophy seen in computed tomographies (CT) of the head of occupationally exposed professionals working in the centre of Athens. METHODS: One hundred and twenty-two head CTs from gas station employees and traffic-exposed professionals (taxi and bus drivers) were analyzed for evidence of cortical atrophy or abnormal calcifications. Blood lead level (BLL) of these lead occupationally exposed groups was compared with 37 non-exposed subjects. RESULTS: All three occupationally exposed-to-lead groups had similar blood lead levels compared to the non-exposed group and within the currently accepted norms for lead. No abnormal calcifications were found. Cortical atrophy was more frequently seen in the gas station employees group using univariate and multivariate analysis. In the logistic regression model gas station employment had a stronger impact in developing cortical atrophy [odds ratio of 6.43 (1.46-28.3, 95% CI)] than BLL [odds ratio of 1.4 (1.01-2.05, 95% CI)]. CONCLUSIONS: These results show that employment in gasoline stations may be associated with detectable cortical atrophy in imaging studies and suggest the contribution of a leaded gasoline to its development.

Adult↗
PubMed1998

Meningeal cells stimulate neuronal migration and the formation of radial glial fascicles from the cerebellar external granular layer.

The cerebellar granule cell layer and partly the Bergmann glial scaffold arise from a secondary subpial proliferative zone, the external granular layer. Their development can be disrupted by selective destruction of meningeal cells. In order to clarify the mechanisms of meningeal control of cortical development, we have investigated the development of early postnatal rat cerebellar slice explants in different coculture set-ups with meningeal cells and other fibroblasts. Fibroblasts of various sources (1) stimulate migration of undifferentiated neurons from the explants by a diffusible factor and (2) trigger the development of a radial phenotype in glial cells by contact-mediated mechanisms involving basal lamina constituents. These data provide further evidence for the involvement of mesenchymal-epithelial interactions in the development of the cerebellar cortex.

Animals↗
PubMed2006

Childhood onset schizophrenia: cortical brain abnormalities as young adults.

BACKGROUND: Childhood onset schizophrenia (COS) is a rare but severe form of the adult onset disorder. While structural brain imaging studies show robust, widespread, and progressive gray matter loss in COS during adolescence, there have been no longitudinal studies of sufficient duration to examine comparability with the more common adult onset illness. METHODS: Neuro-anatomic magnetic resonance scans were obtained prospectively from ages 7 through 26 in 70 children diagnosed with COS and age and sex matched healthy controls. Cortical thickness was measured at 40,962 points across the cerebral hemispheres using a novel, fully automated, validated method. Patterns of patient-control differences in cortical development were compared over a 19-year period. RESULTS: Throughout the age range, the COS group had significantly smaller mean cortical thickness compared to controls. However, the COS brain developmental trajectory appeared to normalize in posterior (parietal) regions, and remained divergent in the anterior regions (frontal and temporal) regions, and the pattern of loss became more like that seen in adults. CONCLUSIONS: Cortical thickness loss in COS appears to localize with age to prefrontal and temporal regions that are seen for both medication naïve and medicated adult onset patients.

Adolescent↗