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Schizophrenia CA1

Lin Cui, Wei Sun, Ming Yu, Nan Li, Li Guo, Huating Gu, Yu Zhou
Disrupted-in-schizophrenia 1(DISC1) is a promising candidate susceptibility gene for a spectrum of psychiatric illnesses that share cognitive impairments in common, including schizophrenia, bipolar disorder and major depression. Here we report that DISC1 L100P homozygous mutant shows normal anxiety- and depression-like behavior, but impaired object recognition which is prevented by administration of atypical antipsychotic drug clozapine. Ca(2+) image analysis reveals suppression of glutamate-evoked elevation of cytoplasmic [Ca(2+)] in L100P hippocampal slices...
October 12, 2016: Molecular Brain
P Piyabhan, S Wannasiri, J Naowaboot
Reduced vesicular glutamate transporter 1 (VGLUT1) and 2 (VGLUT2) indicate glutamatergic hypofunction leading to cognitive impairment in schizophrenia. However, VGLUT3 involvement in cognitive dysfunction has not been reported in schizophrenia. Brahmi (Bacopa monnieri) might be new treatment and prevention for cognitive deficit in schizophrenia by affecting on cerebral VGLUT3 density. We aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition and cerebral VGLUT3 immunodensity in sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia...
August 25, 2016: Clinical and Experimental Pharmacology & Physiology
Dayton J Goodell, Tim A Benke, K Ulrich Bayer
The Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a major mediator of long-term potentiation (LTP) and depression (LTD), two opposing forms of synaptic plasticity underlying learning, memory and cognition. The heterozygous CaMKIIα isoform ko (CaMKIIα(+/-)) mice have a schizophrenia-related phenotype, including impaired working memory. Here, we examined synaptic strength and plasticity in two brain areas implicated in working memory, hippocampus CA1 and medial prefrontal cortex (mPFC). Young CaMKIIα(+/-) mice (postnatal day 12-16; corresponding to a developmental stage well before schizophrenia manifestation in humans) showed impaired hippocampal CA1 LTP...
August 17, 2016: Journal of Neurophysiology
Jing Li, Brent Wilkinson, Veronica A Clementel, Junjie Hou, Thomas J O'Dell, Marcelo P Coba
The postsynaptic site of neurons is composed of more than 1500 proteins arranged in protein-protein interaction complexes, the composition of which is modulated by protein phosphorylation through the actions of complex signaling networks. Components of these networks function as key regulators of synaptic plasticity, in particular hippocampal long-term potentiation (LTP). The postsynaptic density (PSD) is a complex multicomponent structure that includes receptors, enzymes, scaffold proteins, and structural proteins...
2016: Science Signaling
Mona E Hervig, Morten S Thomsen, Imre Kalló, Jens D Mikkelsen
Dysfunction of N-Methyl-d-aspartate receptors (NMDARs) is believed to underlie some of the symptoms in schizophrenia, and non-competitive NMDAR antagonists (including phencyclidine (PCP)) are widely used as pharmacological schizophrenia models. Furthermore, mounting evidence suggests that impaired γ-aminobutyric acid (GABA) neurotransmission contributes to the cognitive deficits in schizophrenia. Thus alterations in GABAergic interneurons have been observed in schizophrenia patients and animal models. Acute systemic administration of PCP increases levels of c-Fos in several cortical and subcortical areas, but whether such induction occurs in specific populations of GABAergic interneuron subtypes still remains to be established...
July 29, 2016: Neuroscience
Natalie Matosin, Francesca Fernandez-Enright, Jeremy S Lum, Martin Engel, Jessica L Andrews, Nils C Gassen, Klaus V Wagner, Mathias V Schmidt, Kelly A Newell
Alterations of postsynaptic density (PSD)95-complex proteins in schizophrenia ostensibly induce deficits in synaptic plasticity, the molecular process underlying cognitive functions. Although some PSD95-complex proteins have been previously examined in the hippocampus in schizophrenia, the status of other equally important molecules is unclear. This is especially true in the cornu ammonis (CA)1 hippocampal subfield, a region that is critically involved in the pathophysiology of the illness. We thus performed a quantitative immunoblot experiment to examine PSD95 and several of its associated proteins in the CA1 region, using post mortem brain samples derived from schizophrenia subjects with age-, sex-, and post mortem interval-matched controls (n=20/group)...
2016: NPJ Schizophrenia
Wei Yang, Chunyan Zhu, Yan Shen, Qi Xu
DTNBP1, which encodes dysbindin-1, is associated with cognitive impairment. Genetic evidence indicates that the C allele of rs117610176 leads to an increase in DTNBP-1b mRNA splicing in patients with paranoid schizophrenia. In addition, dysbindin-1B, rather than dysbindin-1A/C, exhibits a tendency toward toxic aggregation. In postmortem brains, dysbindin-1B not only aggregates with itself, it also co-aggregates with proteins that interact with it. However, the pathogenic mechanism underlying dysbindin-1B toxic aggregation remains unknown...
October 1, 2016: Neuroscience
Camila Mauricio Santos, Fernanda Fiel Peres, Mariana Cepollaro Diana, Veronica Justi, Mayra Akimi Suiama, Marcela Gonçalves Santana, Vanessa Costhek Abílio
Schizophrenia is a highly disabling mental disorder, in which genetics and environmental factors interact culminating in the disease. The treatment of negative symptoms and cognitive deficits with antipsychotics is currently inefficient and is an important field of research. Environmental enrichment (EE) has been suggested to improve some cognitive deficits in animal models of various psychiatric disorders. In this study, we aimed to evaluate a possible beneficial effect of early and long-term exposure to EE on an animal model of schizophrenia, the SHR strain...
October 2016: Schizophrenia Research
Hongyan Yu, Haisan Zhang, Yongfeng Yang, Wenqiang Li, Hongxing Zhang, Ge Yang, Luxian Lü
OBJECTIVE: To investigate the potential association of carbonic anhydrase I (CA1) anterior pharynx-defective 1A ( APH1A), neurodevelopment protein 1-like 1 (NDEL1) and serine racemase (SRR) gene polymorphisms with the susceptibility of schizophrenia (SZ). METHODS: A case-control study was performed to identify polymorphisms of the CA1, APH1A, NDEL1 and SRR gene that may confer susceptibility to SZ in the Han Chinese population. Five single nucleotide polymorphisms (SNPs) were genotyped in 516 paranoid SZ patients and 516 control subjects by real time quantitative polymerase chain reaction...
December 15, 2015: Zhonghua Yi Xue za Zhi [Chinese medical journal]
Jia Tian, Fei Geng, Feng Gao, Yi-Hua Chen, Ji-Hong Liu, Jian-Lin Wu, Yu-Jie Lan, Yuan-Ning Zeng, Xiao-Wen Li, Jian-Ming Yang, Tian-Ming Gao
Hippocampal function is important for learning and memory, and dysfunction of the hippocampus has been linked to the pathophysiology of neuropsychiatric diseases such as schizophrenia. Neuregulin1 (NRG1) and ErbB4, two susceptibility genes for schizophrenia, reportedly modulate long-term potentiation (LTP) at hippocampal Schaffer collateral (SC)-CA1 synapses. However, little is known regarding the contribution of hippocampal NRG1/ErbB4 signaling to learning and memory function. Here, quantitative real-time PCR and Western blotting were used to assess the mRNA and protein levels of NRG1 and ErbB4...
June 13, 2016: Molecular Neurobiology
Hongsheng Zhang, Eunchai Kang, Yaqing Wang, Chaojuan Yang, Hui Yu, Qin Wang, Zheyu Chen, Chen Zhang, Kimberly M Christian, Hongjun Song, Guo-Li Ming, Zhiheng Xu
Several genome- and proteome-wide studies have associated transcription and translation changes of CRMP2 (collapsing response mediator protein 2) with psychiatric disorders, yet little is known about its function in the developing or adult mammalian brain in vivo. Here we show that brain-specific Crmp2 knockout (cKO) mice display molecular, cellular, structural and behavioural deficits, many of which are reminiscent of neural features and symptoms associated with schizophrenia. cKO mice exhibit enlarged ventricles and impaired social behaviour, locomotor activity, and learning and memory...
June 1, 2016: Nature Communications
Ronald K Freund, Sharon Graw, Kevin S Choo, Karen E Stevens, Sherry Leonard, Mark L Dell'Acqua
Reduced α7 nicotinic acetylcholine receptor (nAChR) function is linked to impaired hippocampal-dependent sensory processing and learning and memory in schizophrenia. While knockout of the Chrna7 gene encoding the α7nAChR on a C57/Bl6 background results in changes in cognitive measures, prior studies found little impact on hippocampal synaptic plasticity in these mice. However, schizophrenia is a multi-genic disorder where complex interactions between specific genetic mutations and overall genetic background may play a prominent role in determining phenotypic penetrance...
August 3, 2016: Neuroscience Letters
Siriluk Veerasakul, Samur Thanoi, Gavin P Reynolds, Sutisa Nudmamud-Thanoi
Methamphetamine (METH) is a psychostimulant drug with potent effects on the central nervous system that can cause psychotic symptoms similar to those of schizophrenia. Specific alterations in GABAergic neuronal markers have been reported in schizophrenia and animal models of psychotic illness. The aim of this study was to determine whether there are changes in subpopulations of GABAergic neurons, defined by the presence of calcium binding proteins (CBPs), in animal models of METH abuse. Rats received acute (Binge) doses of 4 × 6 mg/kg, a chronic escalating dose regime (0...
October 2016: Neurotoxicity Research
T K Alshammari, M A Alshammari, M N Nenov, E Hoxha, M Cambiaghi, A Marcinno, T F James, P Singh, D Labate, J Li, H Y Meltzer, B Sacchetti, F Tempia, F Laezza
Cognitive processing is highly dependent on the functional integrity of gamma-amino-butyric acid (GABA) interneurons in the brain. These cells regulate excitability and synaptic plasticity of principal neurons balancing the excitatory/inhibitory tone of cortical networks. Reduced function of parvalbumin (PV) interneurons and disruption of GABAergic synapses in the cortical circuitry result in desynchronized network activity associated with cognitive impairment across many psychiatric disorders, including schizophrenia...
2016: Translational Psychiatry
James L Butler, Philipe R F Mendonça, Hugh P C Robinson, Ole Paulsen
UNLABELLED: Gamma oscillations (30-120 Hz) are thought to be important for various cognitive functions, including perception and working memory, and disruption of these oscillations has been implicated in brain disorders, such as schizophrenia and Alzheimer's disease. The cornu ammonis area 1 (CA1) of the hippocampus receives gamma frequency inputs from upstream regions (cornu ammonis area 3 and medial entorhinal cortex) and generates itself a faster gamma oscillation. The exact nature and origin of the intrinsic CA1 gamma oscillation is still under debate...
April 13, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Peter Falkai, Johann Steiner, Berend Malchow, Jawid Shariati, Andreas Knaus, Hans-Gert Bernstein, Thomas Schneider-Axmann, Theo Kraus, Alkomiet Hasan, Bernhard Bogerts, Andrea Schmitt
In schizophrenia, previous stereological post-mortem investigations of anterior, posterior, and total hippocampal subfields showed no alterations in total neuron number but did show decreased oligodendrocyte numbers in CA4, an area that corresponds to the polymorph layer of the dentate gyrus (DG). However, these investigations identified oligodendrocytes only on the basis of morphological criteria in Nissl staining and did not assess alterations of interneurons with immunohistochemical markers. Moreover, the association of findings in the posterior hippocampus with cognitive deficits remains unknown...
2016: Frontiers in Cellular Neuroscience
Jennifer A Honeycutt, Kevin M Keary Iii, Vanessa M Kania, James J Chrobak
Local circuit GABAergic neurons, including parvalbumin (PV)-containing basket cells, likely play a key role in the development, physiology, and pathology of neocortical circuits. Regionally selective and well-defined decreases in PV have been described in human postmortem schizophrenic brain tissue in both the hippocampus and prefrontal cortex. Animal models of schizophreniform dysfunction following acute and/or chronic ketamine treatment have also demonstrated decreases in PV expression. Conflicting reports with respect to PV immunoreactivity following acute and chronic ketamine treatments in rodents question the utility of using PV as a biological marker of pathology-related dysfunction...
2016: Developmental Neuroscience
Johann Steiner, Ralf Brisch, Kolja Schiltz, Henrik Dobrowolny, Christian Mawrin, Marta Krzyżanowska, Hans-Gert Bernstein, Zbigniew Jankowski, Katharina Braun, Andrea Schmitt, Bernhard Bogerts, Tomasz Gos
BACKGROUND: Glutamic acid decarboxylase (GAD) is a key enzyme in GABA synthesis and alterations in GABAergic neurotransmission related to glial abnormalities are thought to play a crucial role in the pathophysiology of schizophrenia. This study aimed to identify potential differences regarding the neuropil expression of GAD between paranoid and residual schizophrenia. METHODS: GAD65/67 immunostained histological sections were evaluated by quantitative densitometric analysis of GAD-immunoreactive (ir) neuropil...
February 24, 2016: Schizophrenia Research
G V Carr, J Chen, F Yang, M Ren, P Yuan, Q Tian, A Bebensee, G Y Zhang, J Du, P Glineburg, R Xun, O Akhile, D Akuma, J Pickel, J C Barrow, F Papaleo, D R Weinberger
Overexpression in humans of KCNH2-3.1, which encodes a primate-specific and brain-selective isoform of the human ether-a-go-go-related potassium channel, is associated with impaired cognition, inefficient neural processing and schizophrenia. Here, we describe a new mouse model that incorporates the KCNH2-3.1 molecular phenotype. KCNH2-3.1 transgenic mice are viable and display normal sensorimotor behaviors. However, they show alterations in neuronal structure and microcircuit function in the hippocampus and prefrontal cortex, areas affected in schizophrenia...
February 9, 2016: Molecular Psychiatry
Ming Teng Koh, Yi Shao, Andrew Sherwood, Dani R Smith
The hippocampus of patients with schizophrenia displays aberrant excess neuronal activity which affects cognitive function. Animal models of the illness have recapitulated the overactivity in the hippocampus, with a corresponding regionally localized reduction of inhibitory interneurons, consistent with that observed in patients. To better understand whether cognitive function is similarly affected in these models of hippocampal overactivity, we tested a ketamine mouse model of schizophrenia for cognitive performance in hippocampal- and medial prefrontal cortex (mPFC)-dependent tasks...
March 2016: Schizophrenia Research
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