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https://www.readbyqxmd.com/read/28089559/microglia-derived-neuregulin-expression-in-psychiatric-disorders
#1
Daisuke Ikawa, Manabu Makinodan, Keiko Iwata, Masahiro Ohgidani, Takahiro A Kato, Yasunori Yamashita, Kazuhiko Yamamuro, Sohei Kimoto, Michihiro Toritsuka, Takahira Yamauchi, Shin-Ichi Fukami, Hiroki Yoshino, Kazuki Okumura, Tatsuhide Tanaka, Akio Wanaka, Yuji Owada, Masatsugu Tsujii, Toshiro Sugiyama, Kenji Tsuchiya, Norio Mori, Ryota Hashimoto, Hideo Matsuzaki, Shigenobu Kanba, Toshifumi Kishimoto
Several studies have revealed that neuregulins (NRGs) are involved in brain function and psychiatric disorders. While NRGs have been regarded as neuron- or astrocyte-derived molecules, our research has revealed that microglia also express NRGs, levels of which are markedly increased in activated microglia. Previous studies have indicated that microglia are activated in the brains of individuals with autism spectrum disorders (ASD). Therefore, we investigated microglial NRG mRNA expression in multiple lines of mice considered models of ASD...
January 9, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28087836/neuropathological-consequences-of-gestational-exposure-to-concentrated-ambient-fine-and-ultrafine-particles-in-the-mouse
#2
Carolyn Klocke, Joshua L Allen, Marissa Sobolewski, Margot Mayer-Pröschel, Jason L Blum, Dana Lauterstein, Judith T Zelikoff, Deborah A Cory-Slechta
Increasing evidence indicates that the central nervous system (CNS) is a target of air pollution. We previously reported that postnatal exposure of mice to concentrated ambient ultrafine particles (UFP; ≤100nm) via the University of Rochester HUCAPS system during a critical developmental window of CNS development, equivalent to human 3(rd) trimester, produced male-predominant neuropathological and behavioral characteristics common to multiple neurodevelopmental disorders, including autism spectrum disorder (ASD), in humans...
January 13, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28077511/altered-connectivity-and-synapse-maturation-of-the-hippocampal-mossy-fiber-pathway-in-a-mouse-model-of-the-fragile-x-syndrome
#3
F Scharkowski, Michael Frotscher, David Lutz, Martin Korte, Kristin Michaelsen-Preusse
The Fragile X syndrome (FXS) as the most common monogenetic cause of cognitive impairment and autism indicates how tightly the dysregulation of synapse development is linked to cognitive deficits. Symptoms of FXS include excessive adherence to patterns that point to compromised hippocampal network formation. Surprisingly, one of the most complex hippocampal synapses connecting the dentate gyrus (DG) to CA3 pyramidal neurons has not been analyzed in FXS yet. Intriguingly, we found altered synaptic function between DG and CA3 in a mouse model of FXS (fmr1 knockout [KO]) demonstrated by increased mossy fiber-dependent miniature excitatory postsynaptic current (mEPSC) frequency at CA3 pyramidal neurons together with increased connectivity between granule cells and CA3 neurons...
January 10, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/28063882/mice-lacking-grip1-2-show-increased-social-interactions-and-enhanced-phosphorylation-at-glua2-s880
#4
Mei Han, Rebeca Mejias, Shu-Ling Chiu, Rebecca Rose, Abby Adamczyk, Richard Huganir, Tao Wang
Glutamate receptor interacting proteins 1 and 2 (GRIP1/2) play an important role in regulating synaptic trafficking of AMPA receptor 2/3 (GluA2/3) and synaptic strength. Gain-of-function GRIP1 mutations are implicated in social behavioral deficits in autism. To study mechanisms of Grip1/2-mediated AMPA signaling in the regulation of social behaviors, we performed social behavioral testing on neuron-specific Grip1/2-double knockout (DKO) and wild type (WT) mice that are matched for age, sex, and strain background...
January 4, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28045139/chrna7-deficient-mice-manifest-no-consistent-neuropsychiatric-and-behavioral-phenotypes
#5
Jiani Yin, Wu Chen, Hongxing Yang, Mingshan Xue, Christian P Schaaf
The alpha7 nicotinic acetylcholine receptor, encoded by the CHRNA7 gene, has been implicated in various psychiatric and behavioral disorders, including schizophrenia, bipolar disorder, epilepsy, autism, Alzheimer's disease, and Parkinson's disease, and is considered a potential target for therapeutic intervention. 15q13.3 microdeletion syndrome is a rare genetic disorder, caused by submicroscopic deletions on chromosome 15q. CHRNA7 is the only gene in this locus that has been deleted entirely in cases involving the smallest microdeletions...
January 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28035928/consecutive-analysis-of-bace1-function-on-developing-and-developed-neuronal-cells
#6
Yuji Kamikubo, Nobumasa Takasugi, Kazue Niisato, Yoshie Hashimoto, Takashi Sakurai
The amyloid-β protein precursor (AβPP) is cleaved by a transmembrane protease termed β-site AβPP cleavage enzyme (BACE1), which is being explored as a target for therapy and prevention of Alzheimer's disease (AD). Although genetic deletion of BACE1 results in abolished amyloid pathology in AD model mice, it also results in neurodevelopmental phenotypes such as hypomyelination and synaptic loss, observed in schizophrenia and autism-like phenotype. These lines of evidence indicate that the inhibition of BACE1 causes adverse side effects during the neurodevelopmental stage...
December 30, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28025742/loss-of-function-of-ptpr-%C3%AE-and-%C3%AE-observed-in-sporadic-schizophrenia-causes-brain-region-specific-deregulation-of-monoamine-levels-and-altered-behavior-in-mice
#7
Arnaud Cressant, Veronique Dubreuil, Jing Kong, Thorsten Manfred Kranz, Francoise Lazarini, Jean-Marie Launay, Jacques Callebert, Jan Sap, Dolores Malaspina, Sylvie Granon, Sheila Harroch
RATIONALE: The receptor protein tyrosine phosphatase PTPRG has been genetically associated with psychiatric disorders and is a ligand for members of the contactin family, which are themselves linked to autism spectrum disorders. OBJECTIVE: Based on our finding of a phosphatase-null de novo mutation in PTPRG associated with a case of sporadic schizophrenia, we used PTPRG knockout (KO) mice to model the effect of a loss-of-function mutation. We compared the results with loss-of-function in its close paralogue PTPRZ, previously associated with schizophrenia...
December 26, 2016: Psychopharmacology
https://www.readbyqxmd.com/read/28018171/association-of-cell-adhesion-molecules-contactin-6-and-latrophilin-1-regulates-neuronal-apoptosis
#8
Amila Zuko, Asami Oguro-Ando, Harm Post, Renske L R E Taggenbrock, Roland E van Dijk, A F Maarten Altelaar, Albert J R Heck, Alexander G Petrenko, Bert van der Zwaag, Yasushi Shimoda, R J Pasterkamp, J P H Burbach
In view of important neurobiological functions of the cell adhesion molecule contactin-6 (Cntn6) that have emerged from studies on null-mutant mice and autism spectrum disorders patients, we set out to examine pathways underlying functions of Cntn6 using a proteomics approach. We identified the cell adhesion GPCR latrophilin-1 (Lphn1, a.k.a. CIRL1/CL, ADGRL1) as a binding partner for Cntn6 forming together a heteromeric cis-complex. Lphn1 expression in cultured neurons caused reduction in neurite outgrowth and increase in apoptosis, which was rescued by coexpression of Cntn6...
2016: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28012946/impaired-gabaergic-inhibition-in-the-hippocampus-of-fmr1-knockout-mice
#9
Victor Sabanov, Sien Braat, Laura D'Andrea, Rob Willemsen, Shimriet Zeidler, Liesbeth Rooms, Claudia Bagni, R Frank Kooy, Detlef Balschun
Many clinical and molecular features of the fragile X syndrome, a common form of intellectual disability and autism, can be modeled by deletion of the Fmr1 protein (Fmrp) in mice. Previous studies showed a decreased expression of several components of the GABAergic system in Fmr1 knockout mice. Here, we used this mouse model to investigate the functional consequences of Fmrp deletion on hippocampal GABAergic inhibition in the CA1-region of the hippocampus. Whole-cell patch-clamp recordings demonstrated a significantly reduced amplitude of evoked inhibitory postsynaptic currents (eIPSCs) and a decrease in the amplitude and frequency of spontaneous IPSCs...
December 21, 2016: Neuropharmacology
https://www.readbyqxmd.com/read/28009282/beyond-epilepsy-and-autism-disruption-of-gabrb3-causes-ocular-hypopigmentation
#10
Ryan J Delahanty, Yanfeng Zhang, Terry Jo Bichell, Wangzhen Shen, Kelienne Verdier, Robert L Macdonald, Lili Xu, Kelli Boyd, Janice Williams, Jing-Qiong Kang
Reduced ocular pigmentation is common in Angelman syndrome (AS) and Prader-Willi syndrome (PWS) and is long thought to be caused by OCA2 deletion. GABRB3 is located in the 15q11-13 region flanked by UBE3A, GABRA5, GABRG3, and OCA2. Mutations in GABRB3 have frequently been associated with epilepsy and autism, consistent with its role in neurodevelopment. We report here a robust phenotype in the mouse in which deletion of Gabrb3 alone causes nearly complete loss of retinal pigmentation due to atrophied melanosomes, as evidenced by electron microscopy...
December 20, 2016: Cell Reports
https://www.readbyqxmd.com/read/28007538/adenosine-a2a-receptor-deletion-affects-social-behaviors-and-anxiety-in-mice-involvement-of-anterior-cingulate-cortex-and-amygdala
#11
Laura López-Cruz, Maria Carbó-Gas, Marta Pardo, Pilar Bayarri, Olga Valverde, Catherine Ledent, John D Salamone, Mercè Correa
Blockade of adenosine A2A receptors can potentiate motivation to work for natural reinforcers such as food. Conspecific interaction is a potent natural reinforcer in social animals that can be manifested as preference for social exploration versus other sources of novel stimulation. Deficiencies in this type of motivated behavior (social withdrawal) have been seen in several pathologies such as autism and depression. However, the role of A2A receptors in motivation for social interaction has not been widely explored...
December 19, 2016: Behavioural Brain Research
https://www.readbyqxmd.com/read/27984743/misregulation-of-an-activity-dependent-splicing-network-as-a-common-mechanism-underlying-autism-spectrum-disorders
#12
Mathieu Quesnel-Vallières, Zahra Dargaei, Manuel Irimia, Thomas Gonatopoulos-Pournatzis, Joanna Y Ip, Mingkun Wu, Timothy Sterne-Weiler, Shinichi Nakagawa, Melanie A Woodin, Benjamin J Blencowe, Sabine P Cordes
A key challenge in understanding and ultimately treating autism is to identify common molecular mechanisms underlying this genetically heterogeneous disorder. Transcriptomic profiling of autistic brains has revealed correlated misregulation of the neuronal splicing regulator nSR100/SRRM4 and its target microexon splicing program in more than one-third of analyzed individuals. To investigate whether nSR100 misregulation is causally linked to autism, we generated mutant mice with reduced levels of this protein and its target splicing program...
December 15, 2016: Molecular Cell
https://www.readbyqxmd.com/read/27920144/methyl-cpg-binding-protein-mbd1-regulates-neuronal-lineage-commitment-through-maintaining-adult-neural-stem-cell-identity
#13
Emily M Jobe, Yu Gao, Brian E Eisinger, Janessa K Mladucky, Charles C Giuliani, Laurel E Kelnhofer, Xinyu Zhao
: MBD1 belongs to a family of methyl-CpG binding proteins that are epigenetic "readers", linking DNA methylation to transcriptional regulation. MBD1 is expressed in neural stem cells residing in the dentate gyrus of the adult hippocampus (aNSCs), and MBD1 deficiency leads to reduced neuronal differentiation, impaired neurogenesis, learning deficits, and autism-like behaviors in mice; however the precise function of MBD1 in aNSCs remains unexplored. Here, we show that MBD1 is important for maintaining the integrity and stemness of NSCs, which is critical for their ability to generate neurons...
December 5, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27916453/shank3-deficiency-impairs-heat-hyperalgesia-and-trpv1-signaling-in-primary-sensory-neurons
#14
Qingjian Han, Yong Ho Kim, Xiaoming Wang, Di Liu, Zhi-Jun Zhang, Alexandra L Bey, Mark Lay, Wonseok Chang, Temugin Berta, Yan Zhang, Yong-Hui Jiang, Ru-Rong Ji
Abnormal pain sensitivity is commonly associated with autism spectrum disorders (ASDs) and affects the life quality of ASD individuals. SHANK3 deficiency was implicated in ASD and pain dysregulation. Here, we report functional expression of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic terminals. Homozygous and heterozygous Shank3 complete knockout (Δe4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. Specific deletion of Shank3 in Nav1...
December 21, 2016: Neuron
https://www.readbyqxmd.com/read/27912058/impaired-amino-acid-transport-at-the-blood-brain-barrier-is-a-cause-of-autism-spectrum-disorder
#15
Dora C Tărlungeanu, Elena Deliu, Christoph P Dotter, Majdi Kara, Philipp Christoph Janiesch, Mariafrancesca Scalise, Michele Galluccio, Mateja Tesulov, Emanuela Morelli, Fatma Mujgan Sonmez, Kaya Bilguvar, Ryuichi Ohgaki, Yoshikatsu Kanai, Anide Johansen, Seham Esharif, Tawfeg Ben-Omran, Meral Topcu, Avner Schlessinger, Cesare Indiveri, Kent E Duncan, Ahmet Okay Caglayan, Murat Gunel, Joseph G Gleeson, Gaia Novarino
Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping with other neurological conditions. We previously described abnormalities in the branched-chain amino acid (BCAA) catabolic pathway as a cause of ASD. Here, we show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter localized at the blood brain barrier (BBB), has an essential role in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation, and severe neurological abnormalities...
December 1, 2016: Cell
https://www.readbyqxmd.com/read/27903723/cerebellar-shank2-regulates-excitatory-synapse-density-motor-coordination-and-specific-repetitive-and-anxiety-like-behaviors
#16
Seungmin Ha, Dongwon Lee, Yi Sul Cho, Changuk Chung, Ye-Eun Yoo, Jihye Kim, Jiseok Lee, Woohyun Kim, Hyosang Kim, Yong Chul Bae, Keiko Tanaka-Yamamoto, Eunjoon Kim
: Shank2 is a multidomain scaffolding protein implicated in the structural and functional coordination of multiprotein complexes at excitatory postsynaptic sites as well as in psychiatric disorders, including autism spectrum disorders. While Shank2 is strongly expressed in the cerebellum, whether Shank2 regulates cerebellar excitatory synapses, or contributes to the behavioral abnormalities observed in Shank2(-/-) mice, remains unexplored. Here we show that Shank2(-/-) mice show reduced excitatory synapse density in cerebellar Purkinje cells in association with reduced levels of excitatory postsynaptic proteins, including GluD2 and PSD-93, and impaired motor coordination in the Erasmus test...
November 30, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27900342/cacna1c-protecting-young-hippocampal-neurons-in-the-adult-brain
#17
Héctor De Jesús-Cortés, Anjali M Rajadhyaksha, Andrew A Pieper
Neuropsychiatric disease is the leading cause of disability in the United States, and fourth worldwide.(1,2) Not surprisingly, human genetic studies have revealed a common genetic predisposition for many forms of neuropsychiatric disease, potentially explaining why overlapping symptoms are commonly observed across multiple diagnostic categories. For example, the CACNA1C gene was recently identified in the largest human genome-wide association study to date as a risk loci held in common across 5 major forms of neuropsychiatric disease: bipolar disorder, schizophrenia, major depressive disorder (MDD), autism spectrum disorder and attention deficit-hyperactivity disorder...
2016: Neurogenesis (Austin, Tex.)
https://www.readbyqxmd.com/read/27889489/the-drug-candidate-adx71441-is-a-novel-potent-and-selective-positive-allosteric-modulator-of-the-gabab-receptor-with-a-potential-for-treatment-of-anxiety-pain-and-spasticity
#18
Mikhail Kalinichev, Françoise Girard, Hasnaà Haddouk, Mélanie Rouillier, Eric Riguet, Isabelle Royer-Urios, Vincent Mutel, Robert Lütjens, Sonia Poli
Positive allosteric modulation of the GABAB receptor is a promising alternative to direct activation of the receptor as a therapeutic approach for treatment of addiction, chronic pain, anxiety, epilepsy, autism, Fragile X syndrome, and psychosis. Here we describe in vitro and in vivo characterization of a novel, potent and selective GABAB positive allosteric modulator (PAM) N-(5-(4-(4-chloro-3-fluorobenzyl)-6-methoxy-3,5-dioxo-4,5-dihydro-1,2,4-triazin-2(3H)-yl)-2-fluorophenyl)acetamide (ADX71441). In vitro, Schild plot and reversibility tests at the target confirmed PAM properties of the compound...
March 1, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/27881780/negative-allosteric-modulation-of-mglur5-partially-corrects-pathophysiology-in-a-mouse-model-of-rett-syndrome
#19
Jifang Tao, Hao Wu, Amanda A Coronado, Elizabeth de Laittre, Emily K Osterweil, Yi Zhang, Mark F Bear
: Rett syndrome (RTT) is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MECP2), an epigenetic regulator of mRNA transcription. Here, we report a test of the hypothesis of shared pathophysiology of RTT and fragile X, another monogenic cause of autism and intellectual disability. In fragile X, the loss of the mRNA translational repressor FMRP leads to exaggerated protein synthesis downstream of metabotropic glutamate receptor 5 (mGluR5). We found that mGluR5- and protein-synthesis-dependent synaptic plasticity were similarly altered in area CA1 of Mecp2 KO mice...
November 23, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27881779/allergic-inflammation-leads-to-neuropathic-pain-via-glial-cell-activation
#20
Ryo Yamasaki, Takayuki Fujii, Bing Wang, Katsuhisa Masaki, Mizuho A Kido, Mari Yoshida, Takuya Matsushita, Jun-Ichi Kira
: Allergic and atopic disorders have increased over the past few decades and have been associated with neuropsychiatric conditions, such as autism spectrum disorder and asthmatic amyotrophy. Myelitis presenting with neuropathic pain can occur in patients with atopic disorder; however, the relationship between allergic inflammation and neuropathic pain, and the underlying mechanism, remains to be established. We studied whether allergic inflammation affects the spinal nociceptive system...
November 23, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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