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Glutamatergic dysregulation

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https://www.readbyqxmd.com/read/28100738/mir-142-3p-is-a-key-regulator-of-il-1%C3%AE-dependent-synaptopathy-in-neuroinflammation
#1
Georgia Mandolesi, Francesca De Vito, Alessandra Musella, Antonietta Gentile, Silvia Bullitta, Diego Fresegna, Helena Sepman, Claudio Di Sanza, Nabila Haji, Francesco Mori, Fabio Buttari, Emerald Perlas, Maria Teresa Ciotti, Eran Hornstein, Irene Bozzoni, Carlo Presutti, Diego Centonze
: MicroRNAs (miRNA) play an important role in post-transcriptional gene regulation of several physiological and pathological processes. In multiple sclerosis (MS), a chronic inflammatory and degenerative disease of the CNS, and in its mouse model, the experimental autoimmune encephalomyelitis (EAE), miRNA dysregulation has been mainly related to immune system dysfunction and white matter (WM) pathology. However, little is known about their role in gray matter pathology. Here, we explored miRNA involvement in the inflammation-driven alterations of synaptic structure and function, collectively known as synaptopathy, a neuropathological process contributing to excitotoxic neurodegeneration in MS/EAE...
January 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28074534/depolarizing-gaba-contributes-to-glutamatergic-network-rewiring-in-epilepsy
#2
Nazim Kourdougli, Christophe Pellegrino, Juho-Matti Renko, Stanislav Khirug, Geneviève Chazal, Tiina-Kaisa Kukko-Lukjanov, Sari E Lauri, Jean-Luc Gaiarsa, Liang Zhou, Angélique Peret, Eero Castrén, Raimo Kalevi Tuominen, Valérie Crépel, Claudio Rivera
OBJECTIVE: Rewiring of excitatory glutamatergic neuronal circuits is a major abnormality in epilepsy. Besides the rewiring of excitatory circuit, an abnormal depolarizing GABAergic drive has been hypothesized to participate in the epileptogenic processes. However, a remaining clinically relevant question is whether early post Status Epilepticus (SE) evoked chloride dysregulation is important for the remodeling of aberrant glutamatergic neuronal circuit. METHODS: Osmotic mini-pumps were used to infuse intracerebrally a specific inhibitor of depolarizing GABAergic transmission as well as a functionally blocking antibody towards the pan-neurotrophin receptor p75 (p75(NTR) )...
January 11, 2017: Annals of Neurology
https://www.readbyqxmd.com/read/28029335/enhanced-susceptibility-of-ca3-hippocampus-to-prenatal-nicotine-exposure
#3
O O Kalejaiye, M C Gondré-Lewis
The brain is highly susceptible to adverse effects of drugs of abuse during early phases of life. Prenatal nicotine exposure (PNE), a preventable cause of gestational and infant mortality, can alter neuron wiring and induce sustained deficits in attention and learning. Here, a rat model of PNE (embryonic days 7-21) was used to examine the maturing hippocampus, which encodes new memories and processes emotional memory. Components of synaptic signaling were evaluated at postnatal day 14 (P14), a period of prolific synaptogenesis in rats, to determine if glutamatergic transmission-associated molecules are regulated in subregions of hippocampus as early as P14...
December 28, 2016: Journal of Developmental Origins of Health and Disease
https://www.readbyqxmd.com/read/28012058/glutamate-and-brain-glutaminases-in-drug-addiction
#4
Javier Márquez, José A Campos-Sandoval, Ana Peñalver, José M Matés, Juan A Segura, Eduardo Blanco, Francisco J Alonso, Fernando Rodríguez de Fonseca
Glutamate is the principal excitatory neurotransmitter in the central nervous system and its actions are related to the behavioral effects of psychostimulant drugs. In the last two decades, basic neuroscience research and preclinical studies with animal models are suggesting a critical role for glutamate transmission in drug reward, reinforcement, and relapse. Although most of the interest has been centered in post-synaptic glutamate receptors, the presynaptic synthesis of glutamate through brain glutaminases may also contribute to imbalances in glutamate homeostasis, a key feature of the glutamatergic hypothesis of addiction...
December 23, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/28007910/neuronal-pentraxin-1-depletion-delays-neurodegeneration-and-extends-life-in-sandhoff-disease-mice
#5
Alexander W M Hooper, Javier F A González, Rosemarie E Venier, Deda C Gillespie, Suleiman A Igdoura
GM2 gangliosidoses are a group of lysosomal storage disorders which include Sandhoff disease and Tay-Sachs disease. Dysregulation of glutamate receptors has been recently postulated in the pathology of Sandhoff disease. Glutamate receptor association with neuronal pentraxins 1 and 2, and the neuronal pentraxin receptor facilitates receptor potentiation and synaptic shaping. In this study, we have observed an upregulation of a novel form of neuronal pentraxin 1 (NP1-38) in the brains of a mouse model of Sandhoff disease and Tay-Sachs disease...
December 22, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27973969/hyperactivity-and-impulsivity-in-adult-attention-deficit-hyperactivity-disorder-is-related-to-glutamatergic-dysfunction-in-the-anterior-cingulate-cortex
#6
Jochen Bauer, Anne Werner, Waldemar Kohl, Harald Kugel, Anna Shushakova, Anya Pedersen, Patricia Ohrmann
OBJECTIVES: Attention-deficit/hyperactivity disorder (ADHD) is closely linked to the dysregulation of dopaminergic and noradrenergic neurotransmission in the fronto-striatal neural network, including the anterior cingulate cortex (ACC) and the dorsolateral prefrontal cortex (DLPFC). Additionally, increasing evidence supports the involvement of the glutamatergic system in the pathophysiology of ADHD. Impulsivity, a core symptom in patients with ADHD, has been repeatedly associated with glutamatergic neurotransmission, and pharmacological treatment of ADHD has been shown to reduce glutamate levels in the prefrontal cortex...
December 15, 2016: World Journal of Biological Psychiatry
https://www.readbyqxmd.com/read/27920149/mir-142-3p-is-a-key-regulator-of-il-1%C3%AE-dependent-synaptopathy-in-neuroinflammation
#7
Georgia Mandolesi, Francesca De Vito, Alessandra Musella, Antonietta Gentile, Silvia Bullitta, Diego Fresegna, Helena Sepman, Claudio Di Sanza, Nabila Haji, Francesco Mori, Fabio Buttari, Emerald Perlas, Maria Teresa Ciotti, Eran Hornstein, Irene Bozzoni, Carlo Presutti, Diego Centonze
: MicroRNAs (miRNA) play an important role in posttranscriptional gene regulation of several physiological and pathological processes. In multiple sclerosis (MS), a chronic inflammatory and degenerative disease of the CNS, and in its mouse model, the experimental autoimmune encephalomyelitis (EAE), miRNA dysregulation has been mainly related to immune system dysfunction and white matter pathology. However, little is known about their role in grey matter pathology. Here, we explored miRNA involvement in the inflammation-driven alterations of synaptic structure and function, collectively known as synaptopathy, a neuropathological process contributing to excitotoxic neurodegeneration in MS/EAE...
December 5, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27917473/maternal-deprivation-alters-expression-of-neural-maturation-gene-tbr1-in-the-amygdala-paralaminar-nucleus-in-infant-female-macaques
#8
Danielle M de Campo, Judy L Cameron, Joseph M Miano, David A Lewis, Karoly Mirnics, Julie L Fudge
Early parental loss is associated with social-emotional dysregulation and amygdala physiologic changes. Previously, we examined whole amygdala gene expression in infant monkeys exposed to early maternal deprivation. Here, we focus on an amygdala region with immature neurons at birth: the paralaminar nucleus (PL). We hypothesized that 1) the normal infant PL is enriched in a subset of neural maturation (NM) genes compared to a nearby amygdala subregion; and 2) maternal deprivation would downregulate expression of NM transcripts (mRNA)...
December 4, 2016: Developmental Psychobiology
https://www.readbyqxmd.com/read/27916636/glutamate-dysregulation-and-glutamatergic-therapeutics-for-ptsd-evidence-from-human-studies
#9
REVIEW
Lynnette A Averill, Prerana Purohit, Christopher L Averill, Markus A Boesl, John H Krystal, Chadi G Abdallah
Posttraumatic stress disorder (PTSD) is a chronic and debilitating psychiatric disorder afflicting millions of individuals across the world. While the availability of robust pharmacologic interventions is quite lacking, our understanding of the putative neurobiological underpinnings of PTSD has significantly increased over the past two decades. Accumulating evidence demonstrates aberrant glutamatergic function in mood, anxiety, and trauma-related disorders and dysfunction in glutamate neurotransmission is increasingly considered a cardinal feature of stress-related psychiatric disorders including PTSD...
December 1, 2016: Neuroscience Letters
https://www.readbyqxmd.com/read/27911305/nitrosylation-of-vesicular-transporters-in-brain-of-amyloid-precursor-protein-presenilin-1-double-transgenic-mice
#10
Ying Wang, Zhu Zhou, Hua Tan, Shenghua Zhu, Yiran Wang, Yingxia Sun, Xin-Min Li, Jun-Feng Wang
Nitric oxide can attack thiol groups of cysteine residues in proteins and induce protein cysteine S-nitrosylation. Cholinergic and glutamatergic systems are dysregulated in Alzheimer's disease. Vesicular acetylcholine transporter (VAChT) and vesicular glutamate transporter 1 (VGLUT1) are important in packaging acetylcholine and glutamate into vesicles, which is an important step for neurotransmission. Previously we found that VAChT and VGLUT1 can be nitrosylated and that S-nitrosylation of these transporters inhibits vesicular uptake of acetylcholine and glutamate...
2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27890743/considering-future-pharmacotherapy-for-ptsd
#11
REVIEW
Matthew J Friedman, Nancy C Bernardy
Posttraumatic stress disorder (PTSD) is a prevalent, disabling, and often chronic condition that may develop following exposure to a traumatic event. Despite the immense social and economic ramifications of PTSD, there has been relatively little recent development of new pharmacotherapies. The majority of pharmacological randomized clinical trials (RCTs) that has been conducted are now dated. Existing treatments for PTSD primarily have come out of research that tested medications developed for other disorders such as antidepressants, anti-hypertensives, antipsychotics, anticonvulsants, and anxiolytics...
November 24, 2016: Neuroscience Letters
https://www.readbyqxmd.com/read/27863698/striatal-h3k27-acetylation-linked-to-glutamatergic-gene-dysregulation-in-human-heroin-abusers-holds-promise-as-therapeutic-target
#12
Gabor Egervari, Joseph Landry, James Callens, John F Fullard, Panos Roussos, Eva Keller, Yasmin L Hurd
BACKGROUND: Opiate abuse and overdose reached epidemic levels in the United States. However, despite significant advances in animal and in vitro models, little knowledge has been directly accrued regarding the neurobiology of the opiate-addicted human brain. METHODS: We used postmortem human brain specimens from a homogeneous European Caucasian population of heroin users for transcriptional and epigenetic profiling, as well as direct assessment of chromatin accessibility in the striatum, a brain region central to reward and emotion...
September 28, 2016: Biological Psychiatry
https://www.readbyqxmd.com/read/27817030/gene-expression-of-proteins-of-the-vesicle-cycle-in-the-striatum-and-motor-cortex-under-functional-failure-of-nigrostriatal-system
#13
E R Mingazov, M V Ugrumov
Degeneration of dopaminergic neurons in the substantia nigra and the decrease in the dopamine level in the striatum lead to dysfunctions of motor behavior. This is accompanied by dysregulation of neuro-transmission in glutamatergic neurons of the motor cortex and GABA-ergic neurons of the striatum. It is shown that dysregulation of the gene expression of vesicle cycle proteins in neurons of the motor cortex occurs at an early (presymptomatic) stage of degeneration of the nigrostriatal system, and in more severe degeneration (symptomatic stage) the level of gene expression of vesicle cycle proteins in the striatum decreases...
September 2016: Doklady. Biochemistry and Biophysics
https://www.readbyqxmd.com/read/27814639/dopamine-homeostasis-brain-functional-connectivity-in-reward-deficiency-syndrome
#14
Marcelo Febo, Kenneth Blum, Rajendra D Badgaiyan, David Baron, Panayotis K Thanos, Luis M Colon-Perez, Zsolt Demortrovics, Mark S Gold
Reward deficiency syndrome (RDS) was first proposed by Kenneth Blum in 1995 to provide a clinically relevant and predictive term for conditions involving deficits in mesocorticolimbic dopamine function. Genetic, molecular, and neuronal alterations in key components of this circuitry contribute to a reward deficit state that can drive drug-seeking, consumption, and relapse. Among the dysfunctions observed in RDS are dysregulated resting state networks, which recently have been assessed in detail in chronic drug users by, positron emission tomography, functional magnetic resonance imaging, and functional connectivity analysis...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/27773429/loss-of-glycine-transporter-1-causes-a-subtype-of-glycine-encephalopathy-with-arthrogryposis-and-mildly-elevated-cerebrospinal-fluid-glycine
#15
Alina Kurolap, Anja Armbruster, Tova Hershkovitz, Katharina Hauf, Adi Mory, Tamar Paperna, Ewald Hannappel, Galit Tal, Yusif Nijem, Ella Sella, Muhammad Mahajnah, Anat Ilivitzki, Dov Hershkovitz, Nina Ekhilevitch, Hanna Mandel, Volker Eulenburg, Hagit N Baris
Glycine is a major neurotransmitter that activates inhibitory glycine receptors and is a co-agonist for excitatory glutamatergic N-methyl-D-aspartate (NMDA) receptors. Two transporters, GLYT1 and GLYT2, regulate extracellular glycine concentrations within the CNS. Dysregulation of the extracellular glycine has been associated with hyperekplexia and nonketotic hyperglycinemia. Here, we report four individuals from two families who presented at birth with facial dysmorphism, encephalopathy, arthrogryposis, hypotonia progressing to hypertonicity with startle-like clonus, and respiratory failure...
November 3, 2016: American Journal of Human Genetics
https://www.readbyqxmd.com/read/27728875/different-contribution-of-glucocorticoids-in-the-basolateral-amygdala-to-the-formation-and-expression-of-opiate-withdrawal-associated-memories
#16
Daniel García-Pérez, Szilamer Ferenczi, Krisztina J Kovács, M Luisa Laorden, M Victoria Milanés, Cristina Núñez
Drug-withdrawal aversive memories generate a motivational state leading to compulsive drug taking, with plasticity changes in the basolateral amygdala (BLA) being essential in aversive motivational learning. The conditioned-place aversion (CPA) paradigm allows for measuring the negative affective component of drug withdrawal. First, CPA triggers association between negative affective consequences of withdrawal with context (memory consolidation). Afterwards, when the animals are re-exposed to the paired environment, they avoid it due to the association between the context and aversive memories (memory retrieval)...
December 2016: Psychoneuroendocrinology
https://www.readbyqxmd.com/read/27720198/the-role-of-genes-stress-and-dopamine-in-the-development-of-schizophrenia
#17
REVIEW
Oliver D Howes, Robert McCutcheon, Michael J Owen, Robin M Murray
The dopamine hypothesis is the longest standing pathoetiologic theory of schizophrenia. Because it was initially based on indirect evidence and findings in patients with established schizophrenia, it was unclear what role dopamine played in the onset of the disorder. However, recent studies in people at risk of schizophrenia have found elevated striatal dopamine synthesis capacity and increased dopamine release to stress. Furthermore, striatal dopamine changes have been linked to altered cortical function during cognitive tasks, in line with preclinical evidence that a circuit involving cortical projections to the striatum and midbrain may underlie the striatal dopamine changes...
January 1, 2017: Biological Psychiatry
https://www.readbyqxmd.com/read/27638036/mglu5-receptor-antagonist-blocks-bromocriptine-induced-conditioned-place-preference-in-bilateral-mesolimbic-lesioned-rat
#18
Omar Ouachikh, Carine Chassain, Guilhem Pagès, Franck Durif, Aziz Hafidi
Dopamine dysregulation syndrome (DDS) has been attributed to both dopamine replacement therapies (DRT) and the mesencephalic dopaminergic lesion. The DRT reinforcement effect is due to its action on the reward system, particularly on the nucleus accumbens (NAc). This nucleus receives two major projections, a glutamatergic from the prefrontal cortex and a dopaminergic from the posterior ventral tegmental area (pVTA). The latter modulate the former within the NAc. pVTA has been demonstrated to be implicated in the motivational effect of bromocriptine (dopamine 2 receptor (D2R) agonist) in bilateral pVTA-lesioned animals...
September 13, 2016: Behavioural Brain Research
https://www.readbyqxmd.com/read/27614205/transcriptome-assessment-of-the-pompe-gaa-mouse-spinal-cord-indicates-widespread-neuropathology
#19
Sara M F Turner, Darin J Falk, Barry J Byrne, David D Fuller
Pompe disease, caused by deficiency of acid alpha-glucosidase (GAA), leads to widespread glycogen accumulation and profound neuromuscular impairments. There has been controversy, however, regarding the role of central nervous system pathology in Pompe motor dysfunction. We hypothesized that absence of GAA protein causes progressive activation of neuropathological signaling, including pathways associated with cell death. To test this hypothesis, genomic data (Affymetrix Mouse Gene Array 2.0ST) from the mid-cervical spinal cord in 6- and 16-mo old Pompe (Gaa(-/-)) were evaluated (Broad Institute Molecular Signature Database), along with spinal cord histology...
September 9, 2016: Physiological Genomics
https://www.readbyqxmd.com/read/27612656/systems-biology-integration-of-proteomic-data-in-rodent-models-of-depression-reveals-involvement-of-the-immune-response-and-glutamatergic-signaling
#20
Lucia Carboni, Thanh-Phuong Nguyen, Laura Caberlotto
PURPOSE: The pathophysiological basis of major depression is incompletely understood. Recently, numerous proteomic studies have been performed in rodent models of depression to investigate the molecular underpinnings of depressive-like behaviours with an unbiased approach. The objective of the study is to integrate the results of these proteomic studies in depression models to shed light on the most relevant molecular pathways involved in the disease. EXPERIMENTAL DESIGN: Network analysis is performed integrating preexisting proteomic data from rodent models of depression...
December 2016: Proteomics. Clinical Applications
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