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https://www.readbyqxmd.com/read/28924206/ephrin-a2-regulates-excitatory-neuron-differentiation-and-interneuron-migration-in-the-developing-neocortex
#1
Jihane Homman-Ludiye, William C Kwan, Mitchell J de Souza, Jennifer Rodger, James A Bourne
The development of the neocortex requires co-ordination between proliferation and differentiation, as well as the precise orchestration of neuronal migration. Eph/ephrin signaling is crucial in guiding neurons and their projections during embryonic development. In adult ephrin-A2 knockout mice we consistently observed focal patches of disorganized neocortical laminar architecture, ranging in severity from reduced neuronal density to a complete lack of neurons. Loss of ephrin-A2 in the pre-optic area of the diencephalon reduced the migration of neocortex-bound interneurons from this region...
September 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28923356/subcutaneous-injections-of-aluminum-at-vaccine-adjuvant-levels-activate-innate-immune-genes-in-mouse-brain-that-are-homologous-with-biomarkers-of-autism
#2
Dan Li, Lucija Tomljenovic, Yongling Li, Christopher A Shaw
Autism is a neurobehavioral disorder characterized by immune dysfunction. It is manifested in early childhood, during a window of early developmental vulnerability where the normal developmental trajectory is most susceptible to xenobiotic insults. Aluminum (Al) vaccine adjuvants are xenobiotics with immunostimulating and neurotoxic properties to which infants worldwide are routinely exposed. To investigate Al's immune and neurotoxic impact in vivo, we tested the expression of 17 genes which are implicated in both autism and innate immune response in brain samples of Al-injected mice in comparison to control mice...
September 5, 2017: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/28922833/the-knockout-of-synapsin-ii-in-mice-impairs-social-behavior-and-functional-connectivity-generating-an-asd-like-phenotype
#3
Caterina Michetti, Angela Caruso, Marco Pagani, Mara Sabbioni, Lucian Medrihan, Gergely David, Alberto Galbusera, Monica Morini, Alessandro Gozzi, Fabio Benfenati, Maria Luisa Scattoni
Autism spectrum disorders (ASD) and epilepsy are neurodevelopmental conditions that appear with high rate of co-occurrence, suggesting the possibility of a common genetic basis. Mutations in Synapsin (SYN) genes, particularly SYN1 and SYN2, have been recently associated with ASD and epilepsy in humans. Accordingly, mice lacking Syn1 or Syn2, but not Syn3, experience epileptic seizures and display autistic-like traits that precede the onset of seizures. Here, we analyzed social behavior and ultrasonic vocalizations emitted in 2 social contexts by SynI, SynII, or SynIII mutants and show that SynII mutants display the most severe ASD-like phenotype...
October 1, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/28922251/shank3-regulates-intestinal-barrier-function-through-modulating-zo-1-expression-through-the-pkc%C3%AE%C2%B5-dependent-pathway
#4
Shu-Chen Wei, Hsin-Fang Yang-Yen, Po-Nien Tsao, Meng-Tzu Weng, Chien-Chih Tung, Linda C H Yu, Liang-Chuan Lai, Jen-Hao Hsiao, Eric Y Chuang, Chia-Tung Shun, Yen-Hsuan Ni, Ramnik J Xavier, Daniel K Podolsky, Jeffery J Y Yen, Jau-Min Wong
BACKGROUND: The integrity of the gut barrier in patients with inflammatory bowel disease is known to be impaired but the exact mechanisms remain mostly unknown. SHANK3 mutations are associated with autism, and patients with autism are known to have higher proportions of inflammatory bowel disease. Here, we explore the role of SHANK3 in inflammatory bowel disease, both in vivo and in vitro. METHODS: Dextran sulfate sodium colitis was induced in SHANK3 knockout mice...
August 23, 2017: Inflammatory Bowel Diseases
https://www.readbyqxmd.com/read/28921757/the-neurobiological-bases-of-autism-spectrum-disorders-the-r451c-neuroligin-3-mutation-hampers-the-expression-of-long-term-synaptic-depression-in-the-dorsal-striatum
#5
Giuseppina Martella, Maria Meringolo, Laura Trobiani, Antonella De Jaco, Antonio Pisani, Paola Bonsi
Autism spectrum disorders (ASDs) comprise a heterogeneous group of disorders with a complex genetic etiology. Current theories on the pathogenesis of ASDs suggest that they might arise from an aberrant synaptic transmission affecting specific brain circuits and synapses. The striatum, which is part of the basal ganglia circuit, is one of the brain regions involved in ASDs. Mouse models of ASDs have provided evidence for an imbalance between excitatory and inhibitory neurotransmission. Here we investigated the expression of long-term synaptic plasticity at corticostriatal glutamatergic synapses in the dorsal striatum of the R451C-NL3 phenotypic mouse model of autism...
September 16, 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/28921675/altered-cav1-2-function-in-the-timothy-syndrome-mouse-model-produces-ascending-serotonergic-abnormalities
#6
Daniel G Ehlinger, Kathryn G Commons
Polymorphism in the gene CACNA1C, encoding the pore-forming subunit of Cav1.2 L-type calcium channels, has one of the strongest genetic linkages to schizophrenia, bipolar disorder, and major depressive disorder: psychopathologies in which serotonin signaling has been implicated. Additionally, a gain-of-function mutation in CACNA1C is responsible for the neurodevelopmental disorder Timothy Syndrome that presents with prominent behavioral features on the autism spectrum. Given an emerging role for serotonin in the etiology of autism spectrum disorders, we investigate the relationship between Cav1...
September 16, 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/28920075/of-mice-and-men-empirical-support-for-the-population-based-social-epistasis-amplification-model-a-comment-on
#7
Matthew Alexandar Sarraf, Michael Anthony Woodley Of Menie
This commentary article offers new perspective on recent research investigating the behavioral and social ecological effects of a mutation related to autism spectrum disorders in mice. The authors explain the consistency of this research on mice with predictions advanced by a theory of the role of mutations in altering interorganismal gene-gene interactions (social epistasis) in social species including humans, known as the social epistasis amplification model. The potential significance of the mouse research for understanding contemporary human behavioral trends is explored...
July 2017: ENeuro
https://www.readbyqxmd.com/read/28915148/adult-fmr1-knockout-mice-present-with-deficiencies-in-hippocampal-interleukin-6-and-tumor-necrosis-factor-%C3%AE-expression
#8
Samantha L Hodges, Suzanne O Nolan, Joseph H Taube, Joaquin N Lugo
Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by a single genetic mutation in the FMR1 gene. Mutations in the FMR1 gene are the largest monogenic cause of autism spectrum disorder (ASD), and thus both disorders share many of the same cognitive and behavioral impairments. There is increasing evidence suggesting that dysregulated immune responses play a role in the pathophysiology of ASD; however, the association between FXS and altered immunity requires further investigation. This study examined whether Fmr1 knockout (KO) and wild-type mice on a FVB/NJ background strain had altered cytokine expression at baseline levels in the hippocampus...
September 14, 2017: Neuroreport
https://www.readbyqxmd.com/read/28906292/shank3-regulates-intestinal-barrier-function-through-modulating-zo-1-expression-through-the-pkc%C3%AE%C2%B5-dependent-pathway
#9
Shu-Chen Wei, Hsin-Fang Yang-Yen, Po-Nien Tsao, Meng-Tzu Weng, Chien-Chih Tung, Linda C H Yu, Liang-Chuan Lai, Jen-Hao Hsiao, Eric Y Chuang, Chia-Tung Shun, Yen-Hsuan Ni, Ramnik J Xavier, Daniel K Podolsky, Jeffery J Y Yen, Jau-Min Wong
BACKGROUND: The integrity of the gut barrier in patients with inflammatory bowel disease is known to be impaired but the exact mechanisms remain mostly unknown. SHANK3 mutations are associated with autism, and patients with autism are known to have higher proportions of inflammatory bowel disease. Here, we explore the role of SHANK3 in inflammatory bowel disease, both in vivo and in vitro. METHODS: Dextran sulfate sodium colitis was induced in SHANK3 knockout mice...
October 2017: Inflammatory Bowel Diseases
https://www.readbyqxmd.com/read/28905926/pregnant-mice-illuminate-risk-factors-that-could-lead-to-autism
#10
EDITORIAL
(no author information available yet)
No abstract text is available yet for this article.
September 13, 2017: Nature
https://www.readbyqxmd.com/read/28902840/maternal-gut-bacteria-promote-neurodevelopmental-abnormalities-in-mouse-offspring
#11
Sangdoo Kim, Hyunju Kim, Yeong Shin Yim, Soyoung Ha, Koji Atarashi, Tze Guan Tan, Randy S Longman, Kenya Honda, Dan R Littman, Gloria B Choi, Jun R Huh
Maternal immune activation (MIA) contributes to behavioural abnormalities associated with neurodevelopmental disorders in both primate and rodent offspring. In humans, epidemiological studies suggest that exposure of fetuses to maternal inflammation increases the likelihood of developing autism spectrum disorder. In pregnant mice, interleukin-17a (IL-17a) produced by T helper 17 (TH17) cells (CD4(+) T helper effector cells involved in multiple inflammatory conditions) induces behavioural and cortical abnormalities in the offspring exposed to MIA...
September 13, 2017: Nature
https://www.readbyqxmd.com/read/28901633/response-to-mortazavi-s-comment
#12
Bellieni Carlo Valerio, Giuseppe Buonocore
Mortazavi's comment (1) on our letter (2) on whether electromagnetic fields (EMF) in incubators are a risk factor for autism contains several points that need to be corrected. First, we did not base our observations just on our previous papers as Mortazavi maintains. In fact, our observations were also based on several more papers about EMF in incubators, including the paper by Calvente et al, which was published in 2017 (3). Second, it is incorrect to write that a very simple intervention, such as changing the infants' sleep position, namely the position of the head and feet, can lead to a significant drop, as big as several orders of magnitude, in the infant's brain exposure (1), because in most incubators EMF levels are similar at all points of the mattress...
September 13, 2017: Acta Paediatrica
https://www.readbyqxmd.com/read/28899869/autism-like-behavior-caused-by-deletion-of-vaccinia-related-kinase-3-is-improved-by-trkb-stimulation
#13
Myung-Su Kang, Tae-Yong Choi, Hye Guk Ryu, Dohyun Lee, Seung-Hyun Lee, Se-Young Choi, Kyong-Tai Kim
Vaccinia-related kinases (VRKs) are multifaceted serine/threonine kinases that play essential roles in various aspects of cell signaling, cell cycle progression, apoptosis, and neuronal development and differentiation. However, the neuronal function of VRK3 is still unknown despite its etiological potential in human autism spectrum disorder (ASD). Here, we report that VRK3-deficient mice exhibit typical symptoms of autism-like behavior, including hyperactivity, stereotyped behaviors, reduced social interaction, and impaired context-dependent spatial memory...
September 12, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28888943/melanin-concentrating-hormone-modulates-oxytocin-mediated-marble-burying
#14
Nayna M Sanathara, Celia Garau, Amal Alachkar, Lien Wang, Zhiwei Wang, Katsuhiko Nishimori, Xiangmin Xu, Olivier Civelli
Repetitive and perseverative behaviors are common features of a number of neuropsychiatric diseases such as Angelman's syndrome, Tourette's syndrome, obsessive-compulsive disorder, and autism spectrum disorders. The oxytocin system has been linked to the regulation of repetitive behavior in both animal models and humans, but many of its downstream targets have still to be found. We report that the melanin-concentrating hormone (MCH) system is a target of the oxytocin system in regulating one repetitive behavior, marble burying...
September 6, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28884888/foxp1-haploinsufficiency-phenotypes-beyond-behavior-and-intellectual-disability
#15
Angela Myers, Christèle du Souich, Connie L Yang, Lior Borovik, Jill Mwenifumbo, Rosemarie Rupps, Causes Study, Anna Lehman, Cornelius F Boerkoel
The forkhead box (FOX) transcription factors have roles in development, carcinogenesis, metabolism, and immunity. In humans FOXP1 mutations have been associated with language and speech defects, intellectual disability, autism spectrum disorder, facial dysmorphisms, and congenital anomalies of the kidney and urinary tract. In mice, Foxp1 plays critical roles in development of the spinal motor neurons, lymphocytes, cardiomyocytes, foregut, and skeleton. We hypothesized therefore that mutations of FOXP1 affect additional tissues in some humans...
September 8, 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/28883881/zinc-and-copper-metabolism-and-risk-of-autism-a-reply-to-sayehmiri-et-al
#16
Keith Fluegge Ba
OBJECTIVE: Sayehmiri et al. recently conducted a meta-analysis to explore the relationship between zinc and copper metabolism and autism spectrum disorders (ASD). Recent reports have elucidated a full behavioral profile of mice exposed to prenatal zinc deficiency and documented a phenotype similar to that found in autism spectrum disorders (ASD). These studies suggest that significant alterations in Zn metabolism may be an important nutritional component in the development of ASD. MATERIALS & METHODS: The idea that prenatal zinc deficiency may be to blame is cursorily challenged...
2017: Iranian Journal of Child Neurology
https://www.readbyqxmd.com/read/28879198/complement-c3-expression-is-decreased-in-autism-spectrum-disorder-subjects-and-contributes-to-behavioral-deficits-in-rodents
#17
Kiley Fagan, Amanda Crider, Anthony O Ahmed, Anilkumar Pillai
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with hallmark symptoms including social deficits, communication deficits and repetitive behaviors. Accumulating evidence suggests a potential role of the immune system in the pathophysiology of ASD. The complement system represents one of the major effector mechanisms of the innate immune system, and regulates inflammation, and orchestrates defense against pathogens. However, the role of CNS complement system in ASD is not well understood. In the present study, we found a significant increase in C2, C5, and MASP1, but a decrease in C1q, C3, and C4 mRNA levels in the middle frontal gyrus of ASD subjects compared to controls...
July 2017: Molecular Neuropsychiatry
https://www.readbyqxmd.com/read/28867767/arid1b-haploinsufficiency-causes-abnormal-brain-gene-expression-and-autism-related-behaviors-in-mice
#18
Mihiro Shibutani, Takuro Horii, Hirotaka Shoji, Sumiyo Morita, Mika Kimura, Naomi Terawaki, Tsuyoshi Miyakawa, Izuho Hatada
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with core symptoms that include poor social communication, restricted interests, and repetitive behaviors. Several ASD mouse models exhibit impaired social interaction, anxiety-like behavior, and elevated perseveration. Large-scale whole exome sequencing studies identified many genes putatively associated with ASD. Like chromodomain helicase DNA binding protein 8 (CHD8), the most frequently mutated gene in individuals with ASD, the candidate gene AT-rich interaction domain 1B (ARID1B) encodes a chromatin remodeling factor...
August 30, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28855130/pten-deletion-increases-hippocampal-granule-cell-excitability-in-male-and-female-mice
#19
Victor R Santos, Raymund Y K Pun, Salwa R Arafa, Candi L LaSarge, Shane Rowley, Shadi Khademi, Tom Bouley, Katherine D Holland, Norberto Garcia-Cairasco, Steve C Danzer
Deletion of the mTOR pathway inhibitor PTEN from postnatally-generated hippocampal dentate granule cells causes epilepsy. Here, we conducted field potential, whole cell recording and single cell morphology studies to begin to elucidate the mechanisms by which granule cell-specific PTEN-loss produces disease. Cells from both male and female mice were recorded to identify sex-specific effects. PTEN knockout granule cells showed altered intrinsic excitability, evident as a tendency to fire in bursts. PTEN knockout granule cells also exhibited increased frequency of spontaneous excitatory synaptic currents (sEPSCs) and decreased frequency of inhibitory currents (sIPSCs), further indicative of a shift towards hyperexcitability...
September 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28851986/skeletal-site-specific-changes-in-bone-mass-in-a-genetic-mouse-model-for-human-15q11-13-duplication-seen-in-autism
#20
Kirsty E Lewis, Kunal Sharan, Toru Takumi, Vijay K Yadav
Children suffering from autism have been reported to have low bone mineral density and increased risk for fracture, yet the cellular origin of the bone phenotype remains unknown. Here we have utilized a mouse model of autism that duplicates 6.3 Mb region of chromosome 7 (Dp/+) corresponding to a region of chromosome 15q11-13, duplication of which is recurrent in humans to characterize the bone phenotype. Paternally inherited Dp/+ (patDp/+) mice showed expected increases in the gene expression in bone, normal postnatal growth and body weight acquisition compared to the littermate controls...
August 29, 2017: Scientific Reports
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