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First Postnatal Week (first + postnatal_week)
Selected AbstractsPhagocyte activation in preterm infants following premature rupture of the membranes or chorioamnionitisACTA PAEDIATRICA, Issue 10 2000I Nupponen Phagocyte activation was studied in 48 preterm infants, gestational age 27.3 ± 0.3 wk, birthweight 968 ± 40 g, during the first postnatal week. Human neutrophil lipocalin as a marker of neutrophil activation was measured in plasma and tracheal aspirate fractions; and lysozyme, as a marker of monocyte and macrophage activation, in plasma. The concentration of plasma human neutrophil lipocalin was 69 (46,126) ,g/l (median and quartiles), tracheal aspirate fraction fluid 213 (71,433) (,g/l and plasma lysozyme 1337 (923,1764) ,g/l. Infants born to mothers with premature rupture of the membranes or clinical chorioamnionitis (group A, n 20) had significantly higher plasma [73 (58,151) vs 53 (38,108) ,g/l; p 0.027], and tracheal aspirate fraction human neutrophil lipocalin [319 (129,540) vs 190 (57,324) ,g/l; p= 0.019], and plasma lysozyme [1739 (1356,2021) vs 1140 (739,1557) ,g/l; p 0.0001] than did infants whose mothers had intact membranes and who had no suspicion of infection (Group B, n 28). In infants born to mothers receiving corticosteroids ante partum, correlations existed between time from treatment to delivery and plasma (r 0.322, p 0.0256) and tracheal aspirate fraction human neutrophil lipocalin (r= 0.314, p 0.0096). Infants born to mothers with at risk of infection are exposed to the potentially harmful effects of activated neutrophils. Premature rupture of the membranes, even without signs of clinical infection of the mother or the fetus, is associated with phagocyte activation that may begin already in utero. Corticosteroid treatment of the mother may cause transient inhibition of neutrophil activation in the newborn. [source] MMP-2 contributes to the development of the mouse ventral prostate by impacting epithelial growth and morphogenesisDEVELOPMENTAL DYNAMICS, Issue 9 2010Alexandre Bruni-Cardoso Abstract Epithelial growth, branching, and canalization are important morphogenetic events of the rodent ventral prostate (VP) that take place during the first postnatal week. In this study, we evaluated the effect of knocking out MMP-2 (MMP-2,/,), by examining developmental and structural aspects of the VP in MMP-2,/, mice. Neonate (day 6) MMP-2,/, mice showed fewer epithelial tips, a lower epithelial cell proliferation rate, and also reticulin fiber accumulation. The VP of adult MMP-2,/, mice showed lower relative weight, smaller epithelial and smooth-muscle cell volume, and a larger amount of thicker reticulin fibers. No differences in cell proliferation or apoptotic index were noted between adult MMP-2,/, and wild-type mice. MMP-9 was found in the adult MMP-2,/,, but not in the wild-type. In conclusion, MMP-2 function is essential for the epithelial morphogenesis of the mouse VP, and expression of MMP-9 is not sufficient for acquisition of the normal adult histology. Developmental Dynamics 239:2386,2392, 2010. © 2010 Wiley-Liss, Inc. [source] Influx of calcium through L-type calcium channels in early postnatal regulation of chloride transporters in the rat hippocampusDEVELOPMENTAL NEUROBIOLOGY, Issue 13 2009Jennifer G. Bray Abstract During the early postnatal period, GABAB receptor activation facilitates L-type calcium current in rat hippocampus. One developmental process that L-type current may regulate is the change in expression of the K+Cl, co-transporter (KCC2) and N+K+2Cl, co-transporter (NKCC1), which are involved in the maturation of the GABAergic system. The present study investigated the connection between L-type current, GABAB receptors, and expression of chloride transporters during development. The facilitation of L-type current by GABAB receptors is more prominent in the second week of development, with the highest percentage of cells exhibiting facilitation in cultures isolated from 7 day old rats (37.5%). The protein levels of KCC2 and NKCC1 were investigated to determine the developmental timecourse of expression as well as expression following treatment with an L-type channel antagonist and a GABAB receptor agonist. The time course of both chloride transporters in culture mimics that seen in hippocampal tissue isolated from various ages. KCC2 levels increased drastically in the first two postnatal weeks while NKCC1 remained relatively stable, suggesting that the ratio of the chloride transporters is important in mediating the developmental change in chloride reversal potential. Treatment of cultures with the L-type antagonist nimodipine did not affect protein levels of NKCC1, but significantly decreased the upregulation of KCC2 during the first postnatal week. In addition, calcium current facilitation occurs slightly before the large increase in KCC2 expression. These results suggest that the expression of KCC2 is regulated by calcium influx through L-type channels in the early postnatal period in hippocampal neurons. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009 [source] Differential development of body equilibrium among littermates in the newborn rabbitDEVELOPMENTAL PSYCHOBIOLOGY, Issue 1 2009Edith Muciño Abstract Interest is growing among psychobiologists and behavioral ecologists in the role of sibling relations in shaping individual development and life histories. In litters of domestic rabbits Oryctolagus cuniculus the heaviest pups at birth are more likely to survive the critical first postnatal week, they compete more effectively with littermates for milk and well-insulated positions in the litter huddle, and are the heaviest at weaning. Here we report that high birth weight pups are also better able to maintain body equilibrium. Testing pups' ability to maintain equilibrium when placed on a 15° ramp for 2 min each day during the first postnatal week, we found that pups showed a continual daily improvement in their ability to maintain balance while moving on the ramp, rarely lost balance by postnatal day 8, and that heavier pups could maintain balance better and earlier than their lighter littermates. Better ability to maintain body equilibrium, however achieved, may help explain heavier pups' advantage in competing for vital resources such as milk and in gaining access to better-insulated positions in the litter huddle. It also provides further support for the usefulness of birth weight, not only as an absolute measure but also relative to the weight of other littermates, as a predictor of different developmental trajectories, behavioral and physiological, among same-age siblings in this mammal. © 2008 Wiley Periodicals, Inc. Dev Psychobiol 51: 24,33, 2009 [source] Descending respiratory polysynaptic inputs to cervical and thoracic motoneurons diminish during early postnatal maturation in rat spinal cordEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2005Laurent Juvin Abstract Isolated brainstem-spinal cord preparations were used to explore the coexistence of a direct and an indirect descending drive from the brainstem respiratory centre to cervical and thoracic respiratory motoneurons in the neonatal Sprague,Dawley rat. Polysynaptic spinal relay pathways from the respiratory centre were suppressed by selectively perfusing the cord with mephenesin (1 mm) or a solution enriched with Ca2+ and Mg2+. At birth, both direct and spinally relayed pathways are functional and contribute equally to the global descending respiratory drive. However, during the first postnatal week, significant maturational changes appear in the way the respiratory centre controls its target respiratory motoneurons in the cervical and thoracic spinal cord, with the direct respiratory drive becoming progressively predominant with maturation (from 50% to around 75% of the global descending command). The relative contributions of the monosynaptic and the polysynaptic spinal pathways may therefore have important implications for effective respiratory control during early postnatal development. [source] Altered sensorimotor development in a transgenic mouse model of amyotrophic lateral sclerosisEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2004Julien Amendola Abstract Most neurodegenerative diseases become manifest at an adult age but abnormalities or pathological symptoms appear earlier. It is important to identify the initial mechanisms underlying such progressive neurodegenerative disease in both humans and animals. Transgenic mice expressing the familial amyotrophic lateral sclerosis (ALS)-linked mutation (G85R) in the enzyme superoxide dismutase 1 (SOD1) develop motor neuron disease at 8,10 months of age. We address the question of whether the mutation has an early impact on spinal motor networks in postnatal mutant mice. Behavioural tests showed a significant delay in righting and hind-paw grasping responses in mutant SOD1G85R mice during the first postnatal week, suggesting a transient motor deficit compared to wild-type mice. In addition, extracellular recordings from spinal ventral roots in an in vitro brainstem,spinal cord preparation demonstrated different pharmacologically induced motor activities between the two strains. Rhythmic motor activity was difficult to evoke with N -methyl- dl -aspartate and serotonin at the lumbar levels in SOD1G85R mice. In contrast to lumbar segments, rhythmic activity was similar in the sacral roots from the two strains. These results strongly support the fact that the G85R mutation may have altered lumbar spinal motor systems much earlier than previously recognized. [source] In vivo blockade of neural activity alters dendritic development of neonatal CA1 pyramidal cellsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2002Laurent Groc Abstract During development, neural activity has been proposed to promote neuronal growth. During the first postnatal week, the hippocampus is characterized by an oscillating neural network activity and a rapid neuronal growth. In the present study we tested in vivo, by injecting tetanus toxin into the hippocampus of P1 rats, whether this neural activity indeed promotes growth of pyramidal cells. We have previously shown that tetanus toxin injection leads to a strong reduction in the frequency of spontaneous GABA and glutamatergic synaptic currents, and to a complete blockade of the early neural network activity during the first postnatal week. Morphology of neurobiotin-filled CA1 pyramidal cells was analyzed at the end of the first postnatal week (P6,10). In activity-reduced neurons, the total length of basal dendritic tree was three times less than control. The number, but not the length, of basal dendritic branches was affected. The growth impairment was restricted to the basal dendrites. The apical dendrite, the axons, or the soma grew normally during activity deprivation. Thus, the in vivo neural activity in the neonate hippocampus seems to promote neuronal growth by initiating novel branches. [source] Postnatal maturation of Na+, K+, 2Cl, cotransporter expression and inhibitory synaptogenesis in the rat hippocampus: an immunocytochemical analysisEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2002Serge Marty Abstract GABA, a major inhibitory neurotransmitter, depolarizes hippocampal pyramidal neurons during the first postnatal week. These depolarizations result from an efflux of Cl, through GABAA -gated anion channels. The outward Cl, gradient that provides the driving force for Cl, efflux might be generated and maintained by the Na+, K+, 2Cl, cotransporter (NKCC) that keeps intracellular Cl, concentration above electrochemical equilibrium. The developmental pattern of expression of the cotransporter in the hippocampus is not known. We studied the postnatal distribution pattern of NKCC in the hippocampus using a monoclonal antibody (T4) against a conserved epitope in the C-terminus of the cotransporter molecule. We also examined the temporal relationships between the developmental pattern of NKCC expression and the formation of perisomatic GABAergic synapses. This study was aimed at determining, with antivesicular inhibitory amino acid transporter (VIAAT) antibodies, whether perisomatic GABAergic synapses are formed preferentially at the time when GABA is depolarizing. During the first postnatal week, NKCC immunolabelling was restricted to cell bodies in the pyramidal cell layer and in the strata oriens and radiatum. In contrast, at postnatal day 21 (P21) and in adult animals little or no labelling occurred in cell bodies; instead, a prominent dendritic labelling appeared in both pyramidal and nonpyramidal neurons. The ultrastructural immunogold study in P21 rat hippocampi corroborated the light-microscopy results. In addition, this study revealed that a portion of the silver-intensified colloidal gold particles were located on neuronal plasmalemma, as expected for a functional cotransporter. The formation of inhibitory synapses on perikarya of the pyramidal cell layer was a late process. The density of VIAAT-immunoreactive puncta in the stratum pyramidale at P21 reached four times the P7 value in CA3, and six times the P7 value in CA1. Electron microscopy revealed that the number of synapses per neuronal perikaryal profile in the stratum pyramidale of the CA3 area at P21 was three times higher than at P7, even if a concomitant 20% increase in the area of these neuronal perikaryal profiles occurred. It is concluded that, in hippocampal pyramidal cells, there is a developmental shift in the NKCC localization from a predominantly somatic to a predominantly dendritic location. The presence of NKCC during the first postnatal week is consistent with the hypothesis that this transporter might be involved in the depolarizing effects of GABA. The depolarizing effects of GABA may not be required for the establishment of the majority of GABAergic synapses in the stratum pyramidale, because their number increases after the first postnatal week, when GABA action becomes hyperpolarizing. [source] Developmental change and function of chondroitin sulfate deposited around cerebellar Purkinje cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2005Yumiko Shimazaki Abstract Chondroitin sulfate is a long sulfated polysaccharide with enormous structural heterogeneity that binds with various proteins, such as growth factors, in a structure-dependent manner. In this study, we analyzed the expression of chondroitin sulfate in the postnatally developing cerebellar cortex by using three monoclonal antibodies against chondroitin sulfate, MO-225, 2H6, and CS-56, which recognize different structural domains in this polysaccharide. During the first postnatal week, the patterns of immunohistochemical staining made by these antibodies were quite similar, and the molecular layer, the granule cell layer, and Bergmann glial fibers in the external granular layer were densely stained. After postnatal day 12 (P12), the expression of 2H6 epitopes was down-regulated in the molecular layer, and the expression of CS-56 epitopes in this layer was also reduced after P16. On the other hand, the strong expression of MO-225 epitopes, GlcA(2S),1,3GalNAc(6S) (D unit)-containing structures, remained until adulthood. These chondroitin sulfate epitopes were observed around Purkinje cells, including cell soma and dendrites. Detailed immunohistochemical analysis suggested that chondroitin sulfate was deposited between Purkinje cell surfaces and the processes of Bergmann glia. Furthermore, the amount of pleiotrophin, a heparin-binding growth factor, in the cultured cerebellar slices was remarkably diminished after treatment with chondroitinase ABC or D unit-rich chondroitin sulfate. With the previous findings that pleiotrophin binds to D unit-rich chondroitin sulfate, we suggest that the D-type structure is important for the signaling of pleiotrophin, which plays roles in Purkinje cell,Bergmann glia interaction, and that the structural changes of chondroitin sulfate regulate this signaling pathway. © 2005 Wiley-Liss, Inc. [source] Roles of Endothelial Cell Migration and Apoptosis in Vascular Remodeling during Development of the Central Nervous SystemMICROCIRCULATION, Issue 5 2000SUZANNE HUGHES ABSTRACT Objective: To examine the roles of apoptosis, macrophages, and endothelial cell migration in vascular remodeling during development of the central nervous system. Methods: The terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) technique was combined with Griffonia simplicifolia isolectin B4 histochemistry to detect apoptotic endothelial cells in retinal whole-mount preparations derived from rats at various stages of postnatal development as well as from rat pups exposed to hyperoxia. Macrophages were detected by immunohistochemistry with the monoclonal antibody ED1, and proliferating endothelial cells were identified by incorporation of bromodeoxyuridine. Results: Only small numbers of TUNEL-positive endothelial cells were detected during normal development of the retinal vasculature, with the apoptotic cell density in the inner plexus peaking during the first postnatal week and decreasing markedly during the second week, at a time when vessel retraction was widespread. Neither apoptotic endothelial cells nor macrophages were apparent at sites of initiation of vessel retraction. TUNEL-positive endothelial cells were observed in vessels destined to remain. Hyperoxia induced excessive vessel withdrawal, resulting in the generation of isolated vascular segments containing apoptotic endothelial cells. A topographical analysis showed low numbers of proliferating endothelial cells at sites of angiogenesis whereas vascular proliferation was increased in the adjacent inner plexus. Conclusions: Endothelial cell apoptosis and macrophages do not initiate vessel retraction, but rather contribute to the removal of redundant cells throughout the vasculature. We suggest that vessel retraction is mediated by endothelial cell migration and that endothelial cells derived from retracting vascular segments are redeployed in the formation of new vessels. Only when retraction results in compromised circulation and redeployment is not possible, does endothelial cell apoptosis occur. [source] Expression pattern of calcitonin gene-related peptide in the superior colliculus during postnatal development: Demonstration of its intrinsic nature and possible rolesTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 5 2006Inmaculada Gerrikagoitia Abstract Calcitonin gene-related peptide (CGRP) is a widespread neuropeptide with multiple central and peripheral targets. In an analysis on the expression of this peptide throughout the rat brain during postnatal development, we observed a discrepancy between results obtained by immunohistochemistry and by in situ hybridization. In the superior colliculus (SC), only the immunohistochemical signal could be detected (Terrado et al. [1997] Neuroscience 80:951,970). Here we focus our attention on this structure because the temporal pattern of CGRP immunoreactivity observed in the SC suggested the participation of this peptide in the postnatal maturation of the SC. In the present study, we describe in detail the postnatal development of collicular CGRP-immunoreactive structures and their spatiotemporal relationship with cholinergic modules and definitively demonstrate the local expression of CGRP in the SC. CGRP-immunopositive axons and neurons were distributed within the most ventral part of superficial strata and in the intermediate strata of the SC, showing a peak in staining intensity and density at the end of the first postnatal week. At P14, CGRPergic terminal fibers are arranged in small, clearly defined patches in a complementary manner with respect to the cholinergic modules, which start forming at this stage. By using Western blot and RT-PCR analyses, and by means of injections of antisense oligonucleotides, both the presence of CGRP peptide in the SC and the local expression of ,-CGRP transcripts in collicular neurons were demonstrated. A possible role of CGRP is discussed in the context of postnatal modular compartmentalization of collicular afferents. J. Comp. Neurol. 494:721,737, 2006. © 2005 Wiley-Liss, Inc. [source] Electrical and chemical synapses between relay neurons in developing thalamusTHE JOURNAL OF PHYSIOLOGY, Issue 13 2010Seung-Chan Lee Gap junction-mediated electrical synapses interconnect diverse types of neurons in the mammalian brain, and they may play important roles in the synchronization and development of neural circuits. Thalamic relay neurons are the major source of input to neocortex. Electrical synapses have not been directly observed between relay neurons in either developing or adult animals. We tested for electrical synapses by recording from pairs of relay neurons in acute slices of developing ventrobasal nucleus (VBN) of the thalamus from rats and mice. Electrical synapses were common between VBN relay neurons during the first postnatal week, and then declined sharply during the second week. Electrical coupling was reduced among cells of connexin36 (Cx36) knockout mice; however, some neuron pairs remained coupled. This implies that electrical synapses between the majority of coupled VBN neurons require Cx36 but that other gap junction proteins also contribute. The anatomical distribution of a ,-galactosidase reporter indicated that Cx36 was expressed in some VBN neurons during the first postnatal week and sharply declined over the second week, consistent with our physiological results. VBN relay neurons also communicated via chemical synapses. Rare pairs of relay neurons excited one another monosynaptically. Much more commonly, spikes in one relay neuron evoked disynaptic inhibition (via the thalamic reticular nucleus) in the same or a neighbouring relay neuron. Disynaptic inhibition between VBN cells emerged as electrical coupling was decreasing, during the second postnatal week. Our results demonstrate that thalamic relay neurons communicate primarily via electrical synapses during early postnatal development, and then lose their electrical coupling as a chemical synapse-mediated inhibitory circuit matures. [source] Expression of c-Met in developing rat hippocampus: evidence for HGF as a neurotrophic factor for calbindin D-expressing neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2000Laura Korhonen Abstract Hepatocyte growth factor-scatter factor (HGF) is expressed in different parts of the nervous system, and has been shown to exhibit neurotrophic activity. Here we show that c-Met, the receptor for HGF, is expressed in developing rat hippocampus, with the highest levels during the first postnatal weeks. To study the function of HGF, hippocampal neurons were prepared from embryonic rats and treated with different HGF concentrations. In these cultures, HGF increased the number of neurons expressing the 28-kDa calcium-binding protein (calbindin D) in a dose-dependent manner. The effect of HGF was larger than that observed with either brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3), and cotreatment of the cultures with HGF and the neurotrophins was additive with respect to calbindin D neurons. Besides affecting the number of neurons, HGF significantly increased the degree of sprouting of calbindin D-positive neurons, suggesting an influence on neuronal maturation. BDNF and NT-3 stimulated neurite outgrowth of calbindin D neurons to a much smaller degree. In contrast to calbindin D neurons, HGF did not significantly increase the number of neurons immunoreactive with the neurotransmitter ,-aminobutyric acid (GABA) in the hippocampal cultures. Immunohistochemical studies showed that c-Met-, calbindin D- and HGF-immunoreactive cells are all present in the dentate gyrus and partly colocalize within neurons. These results show that HGF acts on calbindin D-containing hippocampal neurons and increases their neurite outgrowth, suggesting that HGF plays an important role for the maturation and function of these neurons in the hippocampus. [source] | |||||||||||||