OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).
OBM Neurobiology publishes research articles, technical reports and invited topical reviews. Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.
Indexing: DOAJ-Directory of Open Access Journals.
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Rapid publication: manuscripts are undertaken in 7.5 days from acceptance to publication (median values for papers published in this journal in the first half of 2020, 1-2 days of FREE language polishing time is also included in this period).
On the Role of Early-life Neuroinflammation in Neuropsychiatric Disorders
Submission Deadline: December 30, 2018 (Open)
Jenny Berrío, MD, MSc
PPG-Ciências da reabilitação, Universidade Federal de Ciências da Saúde de Porto Alegre, Rua Sarmento Leite, 245, Porto Alegre, Brazil
Research Interests: Behavior; Cognition: Models, animal, Neurodegenerative diseases; Neuronal plasticity; neuro-immune interactions
Bart Ellenbroek, PhD
Professor and Deputy Head of School, School of Psychology, Victoria University of Wellington, PO Box 600, Wellington 6140, New Zealand
Website | E-Mail
Research Interests: animal models; schizophrenia; gene-environment interactions; drug addiction; autism; dopamine; serotonin; behavior
About This Topic
Immune homeostasis within the brain is of special importance for its adequate functioning, thus not surprisingly, any breach of this balance can lead to impaired brain activity. Recent research has identified dysregulated neuroinflammation as a contributing factor in the vulnerability to and development of several neuropsychiatric disorders. In addition to autism and schizophrenia, anxiety and depression, as well as dementia, have now been linked to excessive inflammation of the brain. Particularly, an inappropriate inflammatory response during early-life has been consistently associated with an elevated susceptibility. It has long been known that early-life experiences have the capacity to alter brain development. By changing the long-term function of the immune system, which in turn influences brain function, early-life events have the potential to modify, in the long-term, how the brain is shaped and how it responds to other environmental challenges. The aim of this special issue is to publish up-to-date scientific literature on the topic, deepening the understanding of the complex mechanisms through which this brain-immune connection stresses out our mental health. Original research reports, review articles, communications, and perspectives are welcome in all areas pertinent to the topic. All accepted papers will be published totally free of charge.
Title: Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction
Authors: Gina Sizemore1, Brandon Lucke-Wold2, Charles Rosen2, James W. Simpkins3, Sanjay Bhatia2, Dandan Sun4
1.Department of Clinical and Translational Science, West Virginia School of Medicine, Morgantown, WV
2.Department of Neurosurgery, West Virginia School of Medicine, Morgantown, WV
3.Center for Basic and Translational Stroke Research, West Virginia School of Medicine, Morgantown, WV
4.Department of Neurology, University of Pittsburgh, Pittsburgh, PA
Title: Possible roles of transglutaminase 2 in the molecular mechanisms responsible for human neuropsychiatric disorders.
Authors: Nicola Gaetano Gatta, Elenamaria Fioretti and Vittorio Gentile*
Affiliation: Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, via Costantinopoli 16, 80138 Naples, Italy.
Abstract: Transglutaminases are a family of Ca2+-dependent enzymes which catalyze post-translational modifications of proteins. The main activity of these enzymes is the cross-linking of glutaminyl residues of a protein/peptide substrate to lysyl residues of a protein/peptide co-substrate. In addition to lysyl residues, other second nucleophilic co-substrates may include monoamines or polyamines (to form mono- or bi-substituted/crosslinked adducts) or –OH groups (to form ester linkages). In absence of co-substrates, the nucleophile may be water, resulting in the net deamidation of the glutaminyl residue. Transglutaminase activity has been suggested to be involved in molecular mechanisms responsible for both physiological and pathological processes, including inflammation. In particular, transglutaminase 2, a member of the transglutaminase family, has been shown to be responsible for human autoimmune diseases, and Celiac Disease is just one of them. Interestingly, neurodegenerative diseases, such as Alzheimer’s Diseases, Parkinson’s Diseases, supranuclear palsy, Huntington’s Diseases and other polyglutamine diseases, are characterized in part by aberrant cerebral transglutaminase activity and by increased cross-linked proteins in affected brains. In this review we will focus on the possible molecular mechanisms by which this enzyme could be responsible for such diseases and the possible use of transglutaminase inhibitors for patients with neuropsychiatric diseases characterized by aberrant transglutaminase activity.
Title: Vascular plasticity involving AT1 receptors in the amphetamine-induced inflammatory scenario: relevance to animal models of psychiatric disorders.
Authors: Natalia Andrea Marchese 1, Victoria Belén Occhieppo 1, Osvaldo Martin Basmadjian 1, Ana De Paul 2, Gustavo Baiardi 3 and Claudia Bregonzio 1,*
1. Instituto de Farmacología Experimental Córdoba (IFEC-CONICET) Departamento de Farmacología. Facultad de Ciencias Químicas Universidad Nacional de Córdoba. Córdoba, Argentina
2. Instituto de Investigaciones en Ciencias de la Salud (INICSA- CONICET). Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba. Córdoba, Argentina
3. Laboratorio de Neurofarmacología, (IIBYT-CONICET) Universidad Nacional de Córdoba Facultad de Ciencias Químicas, Universidad Católica de Córdoba, Córdoba, Argentina
Amphetamine exposure is validated as a pharmacological tool to model several psychiatric diseases, such as the dopaminergic/glutamatergic imbalance in schizophrenia and mania. However, its effects extend beyond neurotransmission, as psychostimulant exposure has been associated to brain vascular damage and neuroinflammation. AT1 receptors (AT1-R) are implicated in brain micro-vascular physiological responses; whereas their over-expression is related to inflammatory mediators release, oxidative damage, and endothelial dysfunction in pathological conditions. In the present work, we aimed to evaluate amphetamine effects in main brain arteries, and to elucidate AT1-R role in amphetamine-induce alterations in brain micro-vessels. Male adult Wistar rats received amphetamine (2.5mg/kg-i.p., 5 days) and one week later main brain arteries and cerebral-spinal fluid were sampled to assess inflammatory markers. To evaluate AT1-R involvement in amphetamine-induced alterations in brain micro-vessels, AT1-R antagonist (Candesartan; 3mg/kg-p.o., days 1–5) was administered previous to amphetamine administration (days 6–10). One week later (day 17) AT1-R expression at basal conditions and cellular stress after a challenge (angiotensin-II or cold) were assessed. Two-way-ANOVA and Bonferroni test were used. Amphetamine modified carotid structure and increased AT1-R and intercellular-adhesion-molecule-1 expression in middle cerebral artery. Moreover, in cerebral-spinal fluid TNF-α and IL-6 levels were increased after a challenge. In brain micro-vessels, amphetamine increased AT1-R expression and exacerbated heat-shock-protein-70 levels after a challenge. AT1-R blockade prevented AT1-R up-regulation and the sensitized cellular stress responses. Our results stand out vascular plasticity, involving AT1-R, under amphetamine-induced pro-inflammatory conditions.
Title: Does early compositional changes to microflora promote central neuroinflammation in autism?
Authors: Daniel K Goyal 1, Anton Emmanuel 2
1. Neurosciences Department, University of Manchester, Manchester, England
2. Neurogastroenterology (TBC), University College London, London, United Kingdom
Title: Inflammation in neuronally derived exosomes on psychological outcomes following traumatic brain injury
Authors: Cassandra L Pattinson 1, André van der Merwe 2, Sara Lippa 2, Leighton Chan 2,3,†, Jessica M Gill 1,3,†
1. National Institute of Nursing Research, National Institutes of Health, Bethesda, MD
2. National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD
3. Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University, Bethesda, MD.
† Co-senior authors
Title: Autoantibodies against cerebellar neurons and phosphatidylethanolamine binding protein-1 in a paediatric patient with stiff-person syndrome and autoimmune polyendocrinopathy type 1
Authors: Carmen Schröder, Natalie Bachmaier, Timothy Howell, Heinz Lauffer, Roman Legrand, Philippe Chan, David Vaudry, Maria Hamze-Sinno, Marie François, Pierre Déchelotte, Tomas Hökfelt, Sergueï O. Fetissov
Stiff-person-syndrome (SPS) is commonly related to autoantibodies against glutamic acid decarboxylase (GAD). Here, putative brain autoantibody targets were studied in GAD autoantibody negative 11-years-old boy with SPS and autoimmune polyendocrine syndrome type 1. We found that at the peak of SPS symptoms, IgG from both patient’s serum and cerebrospinal fluid immunostained cerebellar Golgi cells and neuronal fibers. Using proteomics, phosphatidylethanolamine-binding protein-1 has been identified as the putative autoantigen in the cerebellum. These results show that an unusual case of SPS can be associated with autoimmunity against phosphatidylethanolamine-binding protein-1 and specific brain targets.
Title: Childhood Metabolic and Immune Diseases Determine the Onset of Mood Disorders
Authors: Diana Manzano, Inés Corraliza
Affiliation: Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, University of Extremadura, Cáceres, Spain
Daniel Goyal, Fatma Mansab, James Neil, Jaleel Miyan
Received: March 05, 2019; Published: June 28, 2019; doi:10.21926/obm.neurobiol.1902031
Ekta Kumari, Fernando J. Velloso, Steven W. Levison
Received: February 13, 2019; Published: May 13, 2019; doi:10.21926/obm.neurobiol.1902027
Minako Ito, Tanakorn Srirat, Toshihiro Nakamura, Kyoko Komai, Akihiko Yoshimura
Received: January 13, 2019; Published: March 27, 2019; doi:10.21926/obm.neurobiol.1901023