Kooperativer Bibliotheksverbund

Berlin Brandenburg


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  • 1
    New York: Academic Press
    Description: xvii, 631 p.
    Description: Proceedings of a conference sponsored by the Clinical Research Branch, National Institute of Mental Health, and held at Airlie House, Va., Apr. 26-29, 1977
    Description: Includes bibliographies and index
    Keywords: Neuropsychology--Congresses ; Evoked Potentials (Electrophysiology)--Congresses ; Brain--Diseases--Diagnosis--Congresses
    ISBN: 0121551504
    ISBN: 9780121551506
    E-ISSN: 97803231
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  • 2
    In: Neuropsychopharmacology, 2011, Vol.37(4), p.929
    Description: Prenatal exposure to restraint stress causes long-lasting changes in neuroplasticity that likely reflect pathological modifications triggered by early-life stress. We found that the offspring of dams exposed to repeated episodes of restraint stress during pregnancy (here named 'prenatal restraint stress mice' or 'PRS mice') developed a schizophrenia-like phenotype, characterized by a decreased expression of brain-derived neurotrophic factor and glutamic acid decarboxylase 67, an increased expression of type-1 DNA methyl transferase (DNMT1) in the frontal cortex, and a deficit in social interaction, locomotor activity, and prepulse inhibition. PRS mice also showed a marked decrease in metabotropic glutamate 2 (mGlu2) and mGlu3 receptor mRNA and protein levels in the frontal cortex, which was manifested at birth and persisted in adult life. This decrease was associated with an increased binding of DNMT1 to CpG-rich regions of mGlu2 and mGlu3 receptor promoters and an increased binding of MeCP2 to the mGlu2 receptor promoter. Systemic treatment with the selective mGlu2/3 receptor agonist LY379268 (0.5 mg/kg, i.p., twice daily for 5 days), corrected all the biochemical and behavioral abnormalities shown in PRS mice. Our data show for the first time that PRS induces a schizophrenia-like phenotype in mice, and suggest that epigenetic changes in mGlu2 and mGlu3 receptors lie at the core of the pathological programming induced by early-life stress.
    Keywords: Medicine ; Pharmacy, Therapeutics, & Pharmacology ; Anatomy & Physiology;
    ISSN: 0893-133X
    E-ISSN: 1740634X
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  • 3
    Language: English
    In: Biological Psychiatry, 15 March 2015, Vol.77(6), pp.589-596
    Description: Prenatal stress (PRS) is considered a risk factor for several neurodevelopmental disorders including schizophrenia (SZ). An animal model involving restraint stress of pregnant mice suggests that PRS induces epigenetic changes in specific GABAergic and glutamatergic genes likely to be implicated in SZ, including the gene for brain-derived neurotrophic factor (BDNF). Studying adult offspring of pregnant mice subjected to PRS, we explored the long-term effects of PRS on behavior and on the expression of key chromatin remodeling factors including DNA methyltransferase 1, ten-eleven-translocation hydroxylases, methyl CpG binding protein 2, histone deacetylases, and histone methyltransferases and demethylase in the frontal cortex and hippocampus. We also measured the expression of BDNF. Adult PRS offspring demonstrate behavioral abnormalities suggestive of SZ and molecular changes similar to changes seen in postmortem brains of patients with SZ. This includes a significant increase in DNA methyltransferase 1 and ten-eleven-translocation hydroxylase 1 in the frontal cortex and hippocampus but not in cerebellum; no changes in histone deacetylases, histone methyltransferases and demethylases, or methyl CpG binding protein 2, and a significant decrease in messenger RNA variants. The decrease of the corresponding transcript level was accompanied by an enrichment of 5-methylcytosine and 5-hydroxymethylcytosine at gene regulatory regions. In addition, the expression of transcripts (IV and IX) correlated positively with social approach in both PRS mice and nonstressed mice. Because patients with psychosis and PRS mice show similar epigenetic signature, PRS mice may be a suitable model for understanding the behavioral and molecular epigenetic changes observed in patients with SZ.
    Keywords: Bdnf ; DNA Methylation ; Dnmt ; Prenatal Stress ; Schizophrenia ; Tet ; Medicine ; Biology ; Chemistry
    ISSN: 0006-3223
    E-ISSN: 1873-2402
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  • 4
    In: NeuroReport, 2010, Vol.21(8), pp.543-548
    Description: Schizophrenia postmortem brain is characterized by γ aminobutyric acid downregulation and by decreased dendritic spine density in frontal cortex. Protracted L-methionine treatment exacerbates schizophrenia symptoms, and our earlier work (Tremolizzo et al. and Dong et al.) has shown that L-methionine decreases reelin and GAD67 transcription in mice which is prevented by co-administration of valproate. In this study, we observed a decrease in spine density following L-methionine treatment, which was prevented by co-administration of valproate. Together with our earlier findings conducted under the same experimental conditions, we suggest that downregulation of spine density in L-methionine-treated mice may be because of the decreased expression of reelin and that valproate may prevent spine downregulation by inhibiting the methylation induced decrease in reelin.
    Keywords: Dendritic Spines -- Drug Effects ; Frontal Lobe -- Drug Effects ; Methionine -- Toxicity ; Schizophrenia -- Pathology;
    ISSN: 0959-4965
    E-ISSN: 1473558X
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  • 5
    Language: English
    In: Progress in molecular biology and translational science, 2014, Vol.128, pp.89-101
    Description: Based on postmortem brain studies, our overarching epigenetic hypothesis is that chronic schizophrenia (SZ) is a psychopathological condition involving dysregulation of the dynamic equilibrium among DNA methylation/demethylation network components and the expression of SZ target genes, including GABAergic and glutamatergic genes. SZ has a natural course, starting with a prodromal phase, a first episode that occurs in adolescents or in young adults, and later deterioration over the adult years. Hence, the epigenetic status at each neurodevelopmental stage of the disease cannot be studied just in postmortem brain of chronic SZ patients, but requires the use of neurodevelopmental animal models. We have directed the focus of our research toward studying the epigenetic signature of the SZ brain in the offspring of dams stressed during pregnancy (PRS mice). Adult PRS mice have behavioral deficits reminiscent of behaviors observed in psychotic patients. The adult PRS brain, like that of postmortem chronic SZ patients, is characterized by a significant increase in DNA methyltransferase 1, Tet methylcytosine dioxygenase 1 (TET1), 5-methylcytosine, and 5-hydroxymethylcytosine at SZ candidate gene promoters and a reduction in the expression of glutamatergic and GABAergic genes. In PRS mice, measurements of epigenetic biomarkers for SZ can be assessed at different stages of development with the goal of further elucidating the pathophysiology of this disease and predicting treatment responses at specific stages of the illness, with particular attention to early detection and possibly early intervention.
    Keywords: Bdnf ; Clozapine ; DNA Demethylase ; DNA Methyltransferase ; Gad1 ; Prenatally Stressed Mice ; Reln ; S-Adenosylmethionine ; Schizophrenia ; Valproic Acid ; Disease Models, Animal ; Epigenesis, Genetic ; Prenatal Exposure Delayed Effects -- Genetics ; Psychotic Disorders -- Genetics ; Stress, Psychological -- Genetics
    E-ISSN: 1878-0814
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 6
    Language: English
    In: Current Opinion in Psychiatry, 1991, Vol.4(1), pp.7-11
    ISSN: 0951-7367
    Source: Wolters Kluwer - Ovid - Lippincott Williams & Wilkins (via CrossRef)
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  • 7
    Language: English
    In: Neuropharmacology, May 2013, Vol.68, pp.184-194
    Description: Human studies suggest that a variety of prenatal stressors are related to high risk for cognitive and behavioral abnormalities associated with psychiatric illness ( ). Recently, a downregulation in the expression of GABAergic genes (i.e., glutamic acid decarboxylase 67 and reelin) associated with DNA methyltransferase (DNMT) overexpression in GABAergic neurons has been regarded as a characteristic phenotypic component of the neuropathology of psychotic disorders ( ). Here, we characterized mice exposed to prenatal restraint stress (PRS) in order to study neurochemical and behavioral abnormalities related to development of schizophrenia in the adult. Offspring born from non-stressed mothers (control mice) showed high levels of DNMT1 and 3a mRNA expression in the frontal cortex at birth, but these levels progressively decreased at post-natal days (PND) 7, 14, and 60. Offspring born from stressed mothers (PRS mice) showed increased levels of DNMTs compared to controls at all time-points studied including at birth and at PND 60. Using GAD67-GFP transgenic mice, we established that, in both control and PRS mice, high levels of DNMT1 and 3a were preferentially expressed in GABAergic neurons of frontal cortex and hippocampus. Importantly, the overexpression of DNMT in GABAergic neurons was associated with a decrease in reelin and GAD67 expression in PRS mice in early and adult life. PRS mice also showed an increased binding of DNMT1 and MeCP2, and an increase in 5-methylcytosine and 5-hydroxymethylcytosine in specific CpG-rich regions of the reelin and GAD67 promoters. Thus, the epigenetic changes in PRS mice are similar to changes observed in the post-mortem brains of psychiatric patients. Behaviorally, adult PRS mice showed hyperactivity and deficits in social interaction, prepulse inhibition, and fear conditioning that were corrected by administration of valproic acid (a histone deacetylase inhibitor) or clozapine (an atypical antipsychotic with DNA-demethylation activity). Taken together, these data show that prenatal stress in mice induces abnormalities in the DNA methylation network and in behaviors indicative of a schizophrenia-like phenotype. Thus, PRS mice may be a valid model for the investigation of new drugs for schizophrenia treatment targeting DNA methylation. This article is part of the Special Issue entitled ‘Neurodevelopmental Disorders’. ► Prenatal restraint stress (PRS) in mice as a model of schizophrenia. ► Epigenetic alterations of DNMT1 and 3a, reelin and GAD67 in PRS mice. ► DNMT1 and 3a were preferentially expressed in GABAergic interneurons. ► Schizophrenia-like behavioral abnormalities in adult PRS mice.
    Keywords: Schizophrenia ; DNA Methyltransferase ; Prenatal Stress ; Epigenetic ; Antipsychotic ; Valproic Acid ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 8
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 22 December 1998, Vol.95(26), pp.15718-15723
    Description: Postmortem prefrontal cortices (PFC) (Brodmann's areas 10 and 46), temporal cortices (Brodmann's area 22), hippocampi, caudate nuclei, and cerebella of schizophrenia patients and their matched nonpsychiatric subjects were compared for reelin (RELN) mRNA and reelin (RELN) protein content. In all of the brain areas studied, RELN and its mRNA were significantly reduced (≈ 50%) in patients with schizophrenia; this decrease was similar in patients affected by undifferentiated or paranoid schizophrenia. To exclude possible artifacts caused by postmortem mRNA degradation, we measured the mRNAs in the same PFC extracts from γ -aminobutyric acid (GABA) A receptors α 1 and α 5 and nicotinic acetylcholine receptor α 7 subunits. Whereas the expression of the α 7 nicotinic acetylcholine receptor subunit was normal, that of the α 1 and α 5 receptor subunits of GABA A was increased when schizophrenia was present. RELN mRNA was preferentially expressed in GABAergic interneurons of PFC, temporal cortex, hippocampus, and glutamatergic granule cells of cerebellum. A protein putatively functioning as an intracellular target for the signal-transduction cascade triggered by RELN protein released into the extracellular matrix is termed mouse disabled-1 (DAB1) and is expressed at comparable levels in the neuroplasm of the PFC and hippocampal pyramidal neurons, cerebellar Purkinje neurons of schizophrenia patients, and nonpsychiatric subjects; these three types of neurons do not express RELN protein. In the same samples of temporal cortex, we found a decrease in RELN protein of ≈ 50% but no changes in DAB1 protein expression. We also observed a large (up to 70%) decrease of GAD67 but only a small decrease of GAD65 protein content. These findings are interpreted within a neurodevelopmental/vulnerability ``two-hit'' model for the etiology of schizophrenia.
    Keywords: Behavioral sciences -- Psychology -- Clinical psychology ; Physical sciences -- Chemistry -- Chemical compounds ; Biological sciences -- Biology -- Cytology ; Biological sciences -- Biology -- Anatomy ; Health sciences -- Medical sciences -- Immunology ; Biological sciences -- Biology -- Cytology ; Physical sciences -- Chemistry -- Chemical compounds ; Physical sciences -- Chemistry -- Chemical compounds ; Applied sciences -- Laboratory techniques -- Nucleic acid amplification techniques ; Physical sciences -- Chemistry -- Chemical compounds
    ISSN: 00278424
    E-ISSN: 10916490
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  • 9
    Language: English
    In: Science, 17 March 1967, Vol.155(3768), pp.1436-1439
    Description: The waveform of evoked responses recorded from human scalp is not determined solely by the physical eliciting stimulus, but also varies as a function of the effective information provided by the stimulus. There is a positive component whose latency is determined by the point in time at which ambiguity is reduced, and whose shape and amplitude are influenced by whether it is the presence or absence of an external event which delivers the information.
    Keywords: Physical sciences -- Physics -- Mechanics ; Biological sciences -- Biology -- Neuroscience ; Philosophy -- Epistemology -- Ambiguity ; Physical sciences -- Physics -- Mechanics
    ISSN: 00368075
    E-ISSN: 10959203
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  • 10
    Language: English
    In: British Journal of Psychiatry, 02/1982, Vol.140(2), pp.192-198
    Description: Platelet monoamine oxidase (MAO) activity was studied in 33 in-patients with bipolar and schizoaffective disorder who were treated with lithium. Platelet MAO activity was found to increase following 10-41 dys of lithium treatment compared to a prior drug free period, and the increase was positively correlated with the duration of lithium treatment. The increase in platelet MAO activity was not correlated wtih clinical improvement as measured by the Brief Psychiatric Rating Scale (BPRS) and the Global Assessment Scale (GAS). The number of platelets per unit of blood was also significantly correlated with the number of days of lithium treatment. However, the increase in the number of platelets in lithium-treated patients was not correlated with the increase in MAO activity and thus appears not to account for it. These results indicate that studies relating platelet MAO activity to psychiatric diagnosis should be interpreted cautiously if patients are receiving lithium carbonate.
    Keywords: Medicine;
    ISSN: 0007-1250
    E-ISSN: 1472-1465
    Source: CrossRef
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