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PubMed2004

Effects of annexins II and V on survival of neurons and astrocytes in vitro.

AIM: To study the effects of annexins II and V on the survival and neurite outgrowth of primary cultured neurons and the survival of astrocytes after peroxide and hypoxia insults in vitro. METHODS: Annexins II and V proteins and/or corresponding antibodies were added to the medium of primary neocortical cultures. H(2)O(2) and NaN(3) were used to induce neuron injury, respectively. Lactate dehydrogenase (LDH) release was measured. RESULTS: Addition of annexin II or V into the culture medium did not affect the normal survival and neurite outgrowth of cortical neurons. However, when an antibody against annexin II or V was added to the culture, the survival and neurite outgrowth of these neurons markedly declined. Further, addition of the two annexins into cortical cultures after peroxide and hypoxia insults markedly reduced the LDH release and cell death. CONCLUSION: Annexins II and V are essential for the survival and neurite outgrowth of developing cortical neurons, the survival of glial cells, and protect neurons and glial cells against peroxide and hypoxia injuries.

Animals↗
PubMed2002

Laminar organization of the human fetal cerebrum revealed by histochemical markers and magnetic resonance imaging.

The developing human cerebrum displays age-specific changes in its patterns of lamination. Among these, the subplate zone is the most prominent transient compartment because growing major afferent systems temporarily reside in this zone, establish synapses and take part in cellular interactions that are crucial for subsequent cortical development. We explored the potential of magnetic resonance imaging (MRI) for tracing the developmental history of the most prominent cortical layer (the subplate zone) and other laminar compartments of the fetal cerebral wall between 15 and 36 weeks post-ovulation. We found that changes in the MRI lamination pattern of the human fetal cerebral wall are predominantly caused by changes in the subplate zone. Histochemical staining of the extracellular matrix (ECM) enables selective visualization of the subplate zone and correlation with an increase in MRI signal intensity in the subplate zone and ingrowth and accumulation of thalamocortical and corticocortical afferents and their subsequent relocation to the cortical plate. Thus, dynamic changes in the MRI appearance of the subplate zone and histochemical staining of its ECM can be used as indirect parameters for an assessment of normal versus disturbed unfolding of crucial histogenetic events that are involved in prenatal shaping of the human cerebral cortex.

Biomarkers↗
PubMed1996

Spatio-temporal pattern of N-methyl-D-aspartate receptor NR1 mRNA expression during postnatal development of visual structures of the rat brain.

N-methyl-D-aspartate (NMDA) excitatory amino acid receptors (NMDAR) play a pivotal role in various physiological and pathological responses of the central nervous system (CNS), including such phenomena of neuronal plasticity as cortical development. Hence, it could be suggested that expression of genes coding for NMDAR components can be differentially regulated throughout the development. To test this notion we analyzed with in situ hybridization mRNA levels of NMDAR subunit designated as NR1, during time of development (1-6 weeks postnatally) spanning the critical period of functional formation of major visual structures of the rat brain, namely visual cortex (VC), superior colliculus (SC), and lateral geniculate nucleus (LGN). The highest levels of NR1 mRNA were found in the VC and SC at the onset of the critical period, i.e., 21 days postnatally, whereas in the LGN a tendency toward a similar pattern of expression was observed. Analysis of spatial distribution of NR1 mRNA in the SC and VC revealed that an adult-like laminar pattern of expression was also achieved between 14 and 21 days postnatally. This pattern of expression corroborates with developmentally regulated changes in an overall density of cell bodies in these areas.

Animals↗
PubMed1978

Acute whisker removal reduces neuronal activity in barrels of mouse SmL cortex.

The autoradiographic 2-deoxy-D glucose (2-DG) method has been used to map relative changes in metabolic activity in the CNS during various functional states (Plum et al., '76). Here we describe the application of the 2-DG method to assay regional activity in the posteromedial barrel subfield (PMBSF) region of the mouse SmI cortex after acute removal of mystacial vibrissae. One day prior to isotope injection, various combinations of vibrissae (e.g., all vibrissae, row-C only, rows-B and -D only) were plucked from adult male Swiss Webster mice under anesthetic. The next day, 5 muCi of 14C-2-DG were injected into a tail vein, and the mice were allowed to actively explore an empty cage for 45 minutes. The animals were then sacrificed, the brains quickly removed, frozen, and sectioned either parallel or perpendicular to the pia at 80 mum in a cryostat. The sections were mounted, dried on coverslips, and were used to expose X-ray film, after which the sections were stained with thionin and the X-ray film developed. The tissue sections and matching autoradiograms were compared directly from photomicrographs of each. The autoradiograms showed areas of higher activity in barrels for which corresponding vibrissae were present and lower activity in barrels for which appropriate vibrissae were missing. In tangential sections from animals with all vibrissae intact, the PMBSF was uniformly and consistently higher in activity than in cases with all vibrissae missing. The removal of row-C or rows-B and -D resulted in strips of decreased activity in the corresponding PMBSF rows. The same patterns of increased or decreased activity were also seen in sections normal to the pia, but the changes in activity, while greatest in layer IV, extended through all layers of the cortex. Finally, in a number of the autoradiograms, density patterns could be recognized which later were shown to relate directly to sides of individual barrels. The results indicate: (1) Acute removal of the peripheral vibrissal hairs is sufficient to deprive the related contralateral cortical barrel neurons of normal activity. Thus in the mouse somatosensory system it may be possible to determine the relative importance of sensory deprivation and neonatal peripheral lesions in normal cortical development. (2) The barrels are part of a functional cortical columnar organization similar to that in other sensory systems. And, (3) the 14C-2-DG-X-ray technique is sufficiently sensitive to reveal parts of individual barrels in autoradiograms and thus, with some modification, may be suitable for the study of small populations of neurons.

Animals↗
PubMed2006

Mirror movements following cortical resection of polymicrogyria in a child with intractable epilepsy.

Mirror movements may be congenital or acquired. There are few reports of acquired mirror movements in pediatric patients. Further, mirror movements in children with epilepsy have rarely been reported. A 9-year old male, with intractable partial epilepsy resulting from polymicrogyria of the right hemisphere, underwent cortical resection of the right frontotemporoparietal region for a malformation of cortical development. He developed left hemiplegia and mirror movements in the left hand in the postoperative period. Four months after surgery, he remained seizure-free with mild residual left-sided hemiplegia and persistent mirror movements. Mechanisms postulated for mirror movements include aberrant pyramidal tract development and transcallosal inhibitory pathways. The latter mechanism might have contributed to the mirror movements observed in this child. This study is the first report of mirror movements following focal cortical resection for intractable epilepsy due to polymicrogyria.

Cerebral Cortex↗
PubMed1999

Fibroblast growth factor signaling regulates growth and morphogenesis at multiple steps during brain development.

The fibroblast growth factor (FGF) family comprises several members with distinct patterns of expression in the developing central nervous system. FGFs regulate the early specification and the subsequent growth of central nervous system regions. These different actions require the coordinated activation of distinct sets of target genes by FGFs at the appropriate stage of development. The role of FGF2 in the growth and morphogenesis of the cerebral cortex is reviewed in detail. The cellular and molecular mechanisms that underlie the action of FGF2 on cortical development are discussed.

Animals↗
PubMedDate not supplied

Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration.

Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.

Animals↗
PubMed2026

The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.

The extreme morphology and polarised architecture of neurons require the highly sophisticated microtubule transport system for both construction and lifelong survival. Genomic evidence from an expanding landscape of human mutations supports the essential role of the microtubule transport machinery. During neurodevelopment, mutations disrupt the proliferation and migration of neuronal precursors, as well as the initial establishment of polarity. In the mature nervous system, the reliance on microtubule transport shifts to the long-term maintenance of axon integrity and synaptic proteostasis. Across the motor proteins responsible for long distance transport in neurons, mutations highlight a specific vulnerability of long axons to transport failure in Hereditary Spastic Paraplegia (HSP), Charcot Marie Tooth disease Type 2 (CMT2), Spinal Muscular Atrophy (SMA), Perry Syndrome, and Amyotrophic Lateral Sclerosis (ALS) amongst others. Due to the role of microtubule motors in development and maintenance, there is frequently a phenotypic spectrum within a single gene of the microtubule transport system. For example, mutations in dynein motors are linked both to malformations of cortical development and specific motor neuron loss in SMA-LED (Spinal Muscular Atrophy with Lower Extremity Predominance). By synthesising genetic evidence, this review illustrates how specific molecular failures, ranging from motor-domain kinetics to cargo binding, can inform our understanding of neuronal homeostasis. Ultimately, we argue that microtubule transport is not merely a cellular utility, but a key determinant of neuronal longevity.

Humans↗
PubMed2005

The CC2D1A, a member of a new gene family with C2 domains, is involved in autosomal recessive non-syndromic mental retardation.

BACKGROUND: The molecular basis of autosomal recessive non-syndromic mental retardation (NSMR) is poorly understood, mostly owing to heterogeneity and absence of clinical criteria for grouping families for linkage analysis. Only two autosomal genes, the PRSS12 gene on chromosome 4q26 and the CRBN on chromosome 3p26, have been shown to cause autosomal recessive NSMR, each gene in only one family. OBJECTIVE: To identify the gene causing autosomal recessive NSMR on chromosome 19p13.12. RESULTS: The candidate region established by homozygosity mapping was narrowed down from 2.4 Mb to 0.9 Mb on chromosome 19p13.12. A protein truncating mutation was identified in the gene CC2D1A in nine consanguineous families with severe autosomal recessive NSMR. The absence of the wild type protein in the lymphoblastoid cells of the patients was confirmed. CC2D1A is a member of a previously uncharacterised gene family that carries two conserved motifs, a C2 domain and a DM14 domain. The C2 domain is found in proteins which function in calcium dependent phospholipid binding; the DM14 domain is unique to the CC2D1A protein family and its role is unknown. CC2D1A is a putative signal transducer participating in positive regulation of I-kappaB kinase/NFkappaB cascade. Expression of CC2D1A mRNA was shown in the embryonic ventricular zone and developing cortical plate in staged mouse embryos, persisting into adulthood, with highest expression in the cerebral cortex and hippocampus. CONCLUSIONS: A previously unknown signal transduction pathway is important in human cognitive development.

Adaptor Proteins, Signal Transducing↗
PubMed1991

Homology and evolutionary origins of the 'neocortex'.

The telencephalon of mammals is characterized by the presence of a hexalaminated structure on its external surface, with specific auditory, visual, somatosensory and motor regions. Due to its seeming unique presence in mammals, it is frequently designated as the neocortex. The evolutionary origins of the so-called neocortex have long puzzled comparative neuroanatomists, in view of the seeming absence of a neocortical-like anlage in nonmammalian amniotes. The resolution of this puzzle requires analysis of both adult and embryonic brains. Experimental neuroanatomical, physiological and behavioral methods applied to adult avian and reptilian brains have finally clarified several fundamental questions regarding the origins of 'neocortex' and have indicated that these origins can be viewed as consequent to two separate events: (1) The elaboration of constituent neuronal populations and their associated connections that are common to the telencephalae of both nonmammalian and mammalian amniotes. In mammals these populations are found within the so-called neocortex. In birds and reptiles, most of these neurons are found within the dorsal and dorsolateral ventricular ridges (DVR and DLVR). (2) In mammals, the components of the DVR and DLVR are incorporated into the thin overlying pallium to form a laminated 'neocortex'. Analysis of development in domestic chicks suggests that the DVR is one of several prosencephalic neuromeres ('Prosomeres') that contribute to the ontogeny of comparable structures in birds. Perhaps in mammals, as well, cortical development is consequent to incorporation of these several prosomeres into proliferative ependyma of the pallial mantle.

Animals↗
PubMed1999

Reorganization and movement of microtubules in axonal growth cones and developing interstitial branches.

Local changes in microtubule organization and distribution are required for the axon to grow and navigate appropriately; however, little is known about how microtubules (MTs) reorganize during directed axon outgrowth. We have used time-lapse digital imaging of developing cortical neurons microinjected with fluorescently labeled tubulin to follow the movements of individual MTs in two regions of the axon where directed growth occurs: the terminal growth cone and the developing interstitial branch. In both regions, transitions from quiescent to growth states were accompanied by reorganization of MTs from looped or bundled arrays to dispersed arrays and fragmentation of long MTs into short MTs. We also found that long-term redistribution of MTs accompanied the withdrawal of some axonal processes and the growth and stabilization of others. Individual MTs moved independently in both anterograde and retrograde directions to explore developing processes. Their velocities were inversely proportional to their lengths. Our results demonstrate directly that MTs move within axonal growth cones and developing interstitial branches. Our findings also provide the first direct evidence that similar reorganization and movement of individual MTs occur in the two regions of the axon where directed outgrowth occurs. These results suggest a model whereby short exploratory MTs could direct axonal growth cones and interstitial branches toward appropriate locations.

Animals↗
PubMed1988

Cell lineage in the cerebral cortex of the mouse studied in vivo and in vitro with a recombinant retrovirus.

To analyze cell lineage in the murine cerebral cortex, we infected progenitor cells with a recombinant retrovirus, then used the retroviral gene product to identify the descendants of infected cells. Cortices were infected on E12-E14 either in vivo or following dissociation and culture. In both cases, nearly all clones contained either neurons or glia, but not both. Thus, neuronal and glial lineages appear to diverge early in cortical development. To analyze the distribution of clonally related cells in vivo, clonal boundaries were reconstructed from serial sections. Perinatally (E18-PN0), clonally related cells were radially arrayed as they migrated to the cortical plate. Thus, clonal cohorts traverse a similar radial path. Following migration (PN7-PN23), neuronal clones generally remained radially arrayed, while glial clones were variable in orientation, suggesting that these two cell types accumulate in different ways. Neuronal clones sometimes spanned the full thickness of the cortex. Thus, a single progenitor can contribute neurons to several laminae.

Animals↗
PubMed2004

Histologic heterogeneity and intranodal shunt flow in lymph nodes from elderly subjects: a cadaveric study.

Gaps of the superficial cortex of the lymph node provide intranodal shunts that are more often the cause of skip metastasis than are collateral vessels. Examination of lymph nodes from cadavers of elderly subjects often revealed cortical gaps, especially in specific three-dimensional assembled cords; these cortical gaps were readily seen in para-aortic and pelvic nodes. This architecture seemed to be more appropriate for a systemic immune response than a local defense. Evidence of poorly developed cortices, anthracosis, and hyalinization also suggested impaired nodal function. We suspect that this histologic heterogeneity, perhaps a result of aging, affects the nodal trapping of colorimetric/isotopic tracers and metastatic cancer cells. This may have implications for lymphatic mapping of the sentinel lymph node in elderly patients with early-stage cancer.

Aged↗
PubMed2003

Immunocytochemical applications of specific antisera raised against synthetic fragment peptides of mummichog GtH subunits: examining seasonal variations of gonadotrophs (FSH cells and LH cells) in the mummichog and applications to other acanthopterygian fishes.

Two distinct types of gonadotrophs, FSH (GtH I) cells and LH (GtH II) cells, were immunocytochemically identified from mummichog (Fundulus heteroclitus; Cyprinodontiformes, Acanthopterygii) pituitary using antisera raised against synthetic fragment peptides of FSHbeta and LHbeta. Both cell types were abundant during the spawning period (spring and early summer) and decreased in number during the post-spawning immature period. The number of FSH cells increased again during the early phases of gonadal development (cortical alveoli accumulation in the oocytes and basal spermatogenesis) in early winter, whereas the number of LH cells did not. Only FSH cells were abundant during the latter phases of gonadal development (vitellogenesis and active spermatogenesis) in early spring. These observations suggest that both GtHs have important yet different roles for reproduction in this species. Antisera against the conservative region of the FSHbeta and the LHbeta subunits immunostained FSH cells and LH cells, respectively, also in red seabream (Pagrus major; Perciformes, Acanthopterygii) and small mouth bass (Micropterus dolomieu; Perciformes, Acanthopterygii), suggesting the possibility of their use for other acanthopterygian fishes.

Animals↗
PubMed1998

Meningeal cells stimulate and direct the migration of cerebellar external granule cells in vitro.

The external granular layer is a secondary proliferative zone that arises from the caudolateral margin of the cerebellar ventricular zone and then spreads beneath the pial surface, eventually covering the entire cerebellar anlage. Here, both a part of the Bergmann glia and granule cells are generated. Selective destruction of the leptomeningeal cell layer during development in vivo disrupts the subpial extension of the external granular layer and the laminar deposition of its descendant cells. The mechanisms by which meningeal fibroblasts exert their controlling influence on cortical development have remained unclear but could involve diffusible factors and/or interactions mediated by direct cellular contacts. In order to test these assumptions, we have co-cultivated cerebellar slice explants with meningeal cells with and without interposition of a microfilter barrier. In this setup, meningeal cells by a diffusible factor stimulated the emigration of immature neurons exclusively from the external granular layer. This effect could also be elicited by fibroblasts from other tissues but not by nonfibroblastic cells such as, e.g., astroglia. In the Boyden chamber assay, the migration of undifferentiated neurons isolated from the external granular layer was chemotactically oriented towards the source of meningeal cell conditioned media. In comparison, neurons from the internal granular layer did not respond to this stimulus. The attraction of immature neurons towards the pial surface could (1) represent a mechanism for the establishment of (subpial) secondary proliferative zones and (2) hypothetically also play a role in the outward-directed migration of postmitotic cells, e.g., in the isocortical anlage.

Animals↗
PubMed2003

[MRI of cerebral cortical dysgenesis].

PURPOSE: Cortical cerebral dysgenesis is a heterogeneous disorder of cortical development and organization. It is well known by neuropathologists and is becoming more important in the clinical setting, mainly due to MRI. Our purpose is to report the MRI features of cortical dysplasia in 30 patients and to propose a simple classification with review of the literature. PATIENTS AND METHODS: It is a retrospective study of the MRI features of 30 cases of cortical dysgenesis. All patients were evaluated by electroencephalography and brain MRI using T1 and T2 weighted, inversion recovery T1 weighted, FLAIR and MPR 3D sequences with multiplanar reformations. RESULTS: Twenty-nine patients were referred to the neurology department because of refractory epilepsy and one patient for mental retardation. Our patients were distributed in 4 groups: diffuse forms represented by agyria-pachygyria (4 cases), polymicrogyria (one case), and nodular heterotopias (5 cases), local bilateral forms represented by bilateral polymicrogyria (11 cases), unilateral forms represented by hemi-megalencephaly (one case), and focal cortical forms found in eight cases. CONCLUSION: Neuroblast migration disorders are better known, mainly due to high resolution MRI techniques that by the quality of multiplanar study and a better differentiation between gray and white matter, allow a more precise diagnosis.

Adolescent↗
PubMed1989

Cyclosporin A prevents the in vivo development of murine prothymocytes from uncommitted (Thy-1-) precursor cells.

Cyclosporin A (CsA) is known to cause atrophy of the thymic medulla in normal mice. We show that medullary regeneration in lethally irradiated animals reconstituted with syngeneic marrow is also inhibited. For such animals, thymic cortical development is apparently normal. However, if the marrow is depleted of either Thy-1+ or Lyt-1+ cells, thymic regeneration is severely inhibited by CsA. This is not a permanent process, since thymic regeneration proceeds normally if the drug is withdrawn. CsA is only effective at preventing thymic regeneration if it is given at the time of grafting; after a delay of 3 days it is ineffective. We conclude that CsA inhibits the development of prothymocytes (pre-T cells) from common stem cells in the marrow. The significance of these findings with reference to T-cell ontogeny and clinical bone marrow (BM) transplantation is discussed.

Animals↗
PubMedDate not supplied

Adult-onset neurologic dysfunction associated with cortical malformations.

BACKGROUND AND PURPOSE: Malformations of cerebral cortical development are common anomalies of the brain, typically causing developmental delay or seizures that are classically thought to begin in childhood. We present clinical and MR imaging data of 16 patients with cortical malformations in whom evidence of neurologic dysfunction was first noted in adulthood, and attempt to determine whether these malformations had any differentiating features from those presenting in childhood. METHODS: Imaging studies and clinical records of 16 patients with adult-onset neurologic dysfunction were reviewed retrospectively. The patients ranged in age from 17 to 64 years (mean age, 35 years) at the time of imaging. Imaging findings were correlated with seizure history. RESULTS: Fourteen patients had subependymal heterotopia (seven women, seven men), and two patients had closed-lip schizencephalies. Eleven patients had epilepsy, with age of onset ranging from 14 to 45 years (mean age, 22 years); four of them were successfully controlled by medication. The remaining five patients had no seizure disorder. All patients, except one, had normal intelligence. The bilaterality or multiplicity of location of heterotopias was not associated with the presence or absence of seizures, seizure frequency, or electroencephalographic results. CONCLUSION: Subependymal heterotopia and small closed-lip schizencephaly may have minor clinical manifestations that are not evident until adulthood, or may, occasionally, never cause neurologic signs or symptoms whatsoever.

Adolescent↗