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Schröder Nadja

Satanarchist13
21.06.2018

Content:

  • Schröder Nadja
  • Nadja Schröder
  • Top journals
  • Nadja Schroder. Doctorate. Professor. Universidade Federal do Rio Grande do Sul (UFRGS). Porto Alegre, Brazil. View All. mini profile avatar Nadja Schroder. Universidade Federal do Rio Grande do Sul (UFRGS). Porto Alegre, Brazil. Primary. View All. mini profile avatar Nadja Schroder. Overview · Bio · Network. Nadja Schröder, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS ), Faculdade de Biociências Department, Faculty Member. Studies Diritto.

    Schröder Nadja

    Vanessa Kappel da Silva K Matthew Lattal Peter Franz Riederer Methamphetamine mAMPH , when administered repeatedly to rodents or primates, is neurotoxic to some cortical neurons and to forebrain dopaminergic and serotonergic axon terminals. The aim of the … More. Rats implanted bilaterally with cannulae in the CA1 region of the dorsal hippocampus or in the amygdala were trained in one-trial step-down inhibitory passive avoidance using a 0.

    Although the gastrin-releasing peptide-preferring bombesin receptor GRPR has been implicated in memory formation, the underlying molecular events are poorly understood.

    Muscimol MUS -induced unilateral functional inactivation of the BLA prevented the enhancement of memory retention produced by posttraining infusion of TSA into the ipsilateral hippocampus. TSA did not affect IA extinction or reconsolidation. Reversion of age-related recognition memory impairment by iron chelation in rats more. Rescue of social behavior impairment by clozapine and alterations in the expression of neuronal receptors in a rat model of neurodevelopmental impairment induced by GRPR blockade more.

    We have previously shown that pharmacological blockade of the gastrin-releasing peptide receptor GRPR during the neonatal period in rats produces behavioral features of developmental neuropsychiatric disorders. Here, we show that social Here, we show that social interaction deficits in this model are reversed by the atypical antipsychotic clozapine given in the adulthood.

    In addition, we analyzed the mRNA expression of three neuronal receptors potentially involved in the etiology of disorders of the autism spectrum. One hour prior to the behavioral testing, rats were given a systemic injection of clozapine or saline. Rats given neonatal RC showed decreased social interaction and impaired object recognition memory. Clozapine rescued the social interaction impairment. The results contribute to further validate the novel rat model of neurodevelopmental disorders induced by GRPR blockade, and shows alterations in the expression of neuronal receptors in this model.

    Journal of Neural Transmission. Iron exposure modifies acetylcholinesterase activity in zebrafish Danio rerio tissues: Fish Physiology and Biochemistry. Selegiline protects against recognition memory impairment induced by neonatal iron treatment more. In the present study we demonstrate that propionic acid PA , a metabolite that accumulates in large amounts in propionic acidemia, is able to decrease in vitro incorporation of [32P]ATP into neurofilament subunits NF-M and NF-L and In the present study we demonstrate that propionic acid PA , a metabolite that accumulates in large amounts in propionic acidemia, is able to decrease in vitro incorporation of [32P]ATP into neurofilament subunits NF-M and NF-L and alpha- and beta-tubulin.

    In addition, we demonstrated that PA totally inhibited in vitro dephosphorylation of neurofilament subunits and tubulins mediated by PP1 in brain slices pretreated with the acid. This study suggests that PA at the same concentrations found in tissues from propionic acidemic children may alter phosphorylation of cytoskeletal proteins, which may contribute to the neurological dysfunction characteristic of propionic acidemia. Reversal of age-related deficits in object recognition memory in rats with l-deprenyl more.

    Differential neurobehavioral deficits induced by apomorphine and its oxidation product, 8-oxo-apomorphine-semiquinone, in rats more. Apomorphine is a potent dopamine receptor agonist, which has been used in the therapy of It has been proposed that apomorphine and other dopamine receptor agonists might induce neurotoxicity mediated by their quinone and semiquinone oxidation derivatives.

    The aim of the present study was to evaluate the possible neurobehavioral effects of apomorphine and its oxidation derivative, 8-oxo-apomorphine-semiquinone 8-OASQ. Adult female Wistar rats were treated with a systemic injection of apomorphine 0. Apomorphine and 8-OASQ induced differential impairing effects on short- and long-term retention of an inhibitory avoidance task.

    Apomorphine, but not 8-OASQ, dose-dependently impaired habituation to a novel environment. The memory-impairing effects could not be attributed to reduced nociception or other nonspecific behavioral alterations, since neither apomorphine nor 8-OASQ affected footshock reactivity or behavior during exploration of an open field.

    The results suggest that oxidation products of dopamine or dopamine receptor agonists might induce cognitive deficits. European Journal of Pharmacology. Desferoxamine reverses neonatal iron-induced recognition memory impairment in rats more. Recognition memory impairment and brain oxidative stress induced by postnatal iron administration more.

    Iron accumulation in the brain has been implicated in the pathogenesis of neurodegenerative disorders. It is known that iron catalyses the formation of highly reactive hydroxyl radicals.

    Recent studies have implicated oxidative damage in Recent studies have implicated oxidative damage in memory deficits in rats and humans. The purpose of the present study was to investigate the long-term effects of iron treatment in four different phases of the neonatal period on recognition memory in rats. Additionally, parameters of oxidative stress in cerebral regions related to memory formation were evaluated. Male Wistar rats received vehicle or Animals given iron at any phase of the neonatal period showed impairments in long-term retention of object recognition memory, although only the group given iron from postnatal days showed a complete memory blockade.

    Iron treatment induced oxidative damage in the brain as assessed by the thiobarbituric acid reactive species assay. Moreover, iron administration increased superoxide production in submitochondrial particles, suggesting impaired mitochondrial function; and there was an increase in superoxide dismutase activity in brain regions susceptible to iron administration.

    The results show that iron load in the early stages of life induces cognitive impairment possibly by inducing oxidative damage in the brain. These findings are consistent with the view that oxidative stress may be related to the cognitive decline observed in normal ageing.

    European Journal of Neuroscience. Differential effects of low and high doses of topiramate on consolidation and retrieval of novel object recognition memory in rats more.

    Maze learning and motor activity deficits in adult mice induced by iron exposure during a critical postnatal period more. Neonatal iron exposure induces oxidative stress in adult Wistar rat more. Agents that affect cAMP levels or protein kinase A activity modulate memory consolidation when injected into rat hippocampus but not amygdala more. Brazilian Journal of Medical and Biological Research. Methylmalonic acid reduces the in vitro phosphorylation of cytoskeletal proteins in the cerebral cortex of rats more.

    Differential involvement of hippocampal and amygdalar NMDA receptors in contextual and aversive aspects of inhibitory avoidance memory in rats more. Adult male rats bilaterally implanted with guide canullae aimed either at the dorsal hippocampus dHIP or the basolateral nucleus of the amygdala BLA were trained in a step-down inhibitory avoidance task IA and tested for retention Adult male rats bilaterally implanted with guide canullae aimed either at the dorsal hippocampus dHIP or the basolateral nucleus of the amygdala BLA were trained in a step-down inhibitory avoidance task IA and tested for retention 24 h after training.

    Both intrahippocampal and intraamygdala infusions of AP5 blocked IA retention. Preexposure to the training box, but not to a different environment 24 h prior to training prevented the impairing effect of intrahippocampal infusion of AP5 on retention.

    This article has been cited by other articles in PMC. Four Figures and Six Tables. Abstract Defects of ciliogenesis have been implicated in a wide range of human phenotypes and play a crucial role in signal transduction and cell-cycle coordination.

    Main Text Many key developmental processes are maintained by regulation of cell-signaling pathways. Open in a separate window. Radiographic Features of the Investigated Patients with SRPS Type Majewski Both affected individuals, from family 1 A—E and family 3 F—J , presented with severely shortened and horizontal ribs A, B, F, G , squared scapulae and elevated clavicles with lateral kinking A, F , normal vertebral column and pelvis and regular metaphyseal margins of the tubular bones, incompletely calcified and irregularly shaped metacarpal and metatarsal bones C, D, H, I , shortened humerus and femurs, and extreme shortening of the tibial bones.

    GlyAsp exon 82 missense, splice site C domain. I In contrast, P1 cell cilia are shortened, with a broad base and a thin tip. Acknowledgments We thank Frank Majewski for helpful discussion of the phenotype, the families for giving their consent for this study, and J. Supplemental Data Document S1. Four Figures and Six Tables: Click here to view.

    Patched1 regulates hedgehog signaling at the primary cilium. The dynamic cilium in human diseases. Overview of structure and function of mammalian cilia.

    Intraflagellar transport IFT role in ciliary assembly, resorption and signalling. Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways. PDGFRalphaalpha signaling is regulated through the primary cilium in fibroblasts.

    The primary cilium coordinates signaling pathways in cell cycle control and migration during development and tissue repair. The roles of cilia in developmental disorders and disease. When cilia go bad: Diagnostic dilemmas in the short rib-polydactyly syndrome group. Nosology and classification of genetic skeletal disorders: Ciliary abnormalities due to defects in the retrograde transport protein DYNC2H1 in short-rib polydactyly syndrome.

    Allegro, a new computer program for multipoint linkage analysis. Piecing together a ciliome. Gene prioritization through genomic data fusion. Identification and genetic mapping of a new polycystic kidney disease on mouse chromosome 8. The mammalian Nek1 kinase is involved in primary cilium formation. Clinical and pathologic findings in two new allelic murine models of polycystic kidney disease. Evidence of oligogenic inheritance in nephronophthisis. The oligogenic properties of Bardet-Biedl syndrome.

    Further support for digenic inheritance in Bardet-Biedl syndrome. Cilia and Hedgehog responsiveness in the mouse. Loss of the retrograde motor for IFT disrupts localization of Smo to cilia and prevents the expression of both activator and repressor functions of Gli. Mitotic regulation by NIMA-related kinases. Identification of proteins that interact with the central coiled-coil region of the human protein kinase NEK1.

    Nadja Schröder

    Nadja Schröder's 74 research works with citations and reads, including: Antiapoptotic effects of cannabidiol in an experimental model of cognitive. The latest Tweets from boutiquedababr3.xyzöder (@nadja_schrder): "Check out my photo of #ClumsyNinja for iPad! Try it for FREE! boutiquedababr3.xyz View the profiles of people named Nadja Schroder. Join Facebook to connect with Nadja Schroder and others you may know. Facebook gives people the power.

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    martin1995

    Nadja Schröder's 74 research works with citations and reads, including: Antiapoptotic effects of cannabidiol in an experimental model of cognitive.

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