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Glutamatergic dysregulation

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https://www.readbyqxmd.com/read/27911305/nitrosylation-of-vesicular-transporters-in-brain-of-amyloid-precursor-protein-presenilin-1-double-transgenic-mice
#1
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...
November 26, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27890743/considering-future-pharmacotherapy-for-ptsd
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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)...
September 28, 2016: Psychoneuroendocrinology
https://www.readbyqxmd.com/read/27720198/the-role-of-genes-stress-and-dopamine-in-the-development-of-schizophrenia
#8
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...
August 6, 2016: Biological Psychiatry
https://www.readbyqxmd.com/read/27638036/mglu5-receptor-antagonist-blocks-bromocriptine-induced-conditioned-place-preference-in-bilateral-mesolimbic-lesioned-rat
#9
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
#10
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
#11
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...
September 10, 2016: Proteomics. Clinical Applications
https://www.readbyqxmd.com/read/27612187/maternal-protein-restriction-induced-hypertension-is-associated-to-oxidative-disruption-at-transcriptional-and-functional-levels-in-the-medulla-oblongata
#12
José L de Brito Alves, Jéssica M D de Oliveira, Diorginis J S Ferreira, Monique A de V Barros, Viviane O Nogueira, Débora S Alves, Hubert Vidal, Carol G Leandro, Cláudia J Lagranha, Luciano Pirola, João H da Costa-Silva
Maternal protein restriction during pregnancy and lactation predisposes the adult offspring to sympathetic overactivity and arterial hypertension. Although the underlying mechanisms are poorly understood, dysregulation of the oxidative balance has been proposed as a putative trigger of neural-induced hypertension. The aim of the study was to evaluate the association between the oxidative status at transcriptional and functional levels in the medulla oblongata and maternal protein restriction induced-hypertension...
December 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27582038/comprehensive-behavioral-study-and-proteomic-analyses-of-crmp2-deficient-mice
#13
Haruko Nakamura, Naoya Yamashita, Ayuko Kimura, Yayoi Kimura, Hisashi Hirano, Hiroko Makihara, Yuko Kawamoto, Aoi Jitsuki-Takahashi, Kumiko Yonezaki, Kenkichi Takase, Tomoyuki Miyazaki, Fumio Nakamura, Fumiaki Tanaka, Yoshio Goshima
Collapsin response mediator protein 2 (CRMP2) plays a key role in axon guidance, dendritic morphogenesis and cell polarization. CRMP2 is implicated in various neurological and psychiatric disorders. However, in vivo functions of CRMP2 remain unknown. We generated CRMP2 gene-deficient (crmp2(-/-) ) mice and examined their behavioral phenotypes. During 24-h home cage monitoring, the activity level during the dark phase of crmp2(-/-) mice was significantly higher than that of wild-type (WT) mice. Moreover, the time during the open arm of an elevated plus maze was longer for crmp2(-/-) mice than for WT mice...
October 2016: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/27565411/metabotropic-glutamate-receptor-2-3-density-and-its-relation-to-the-hippocampal-neuropathology-in-a-model-of-temporal-lobe-epilepsy-in-rats
#14
Idrish Ali, Stephanie Boets, Pieter Janssens, Annemie Van Eetveldt, Halima Amhaoul, Xavier Langlois, Stefanie Dedeurwaerdere
Dysregulation in the glutamatergic function is considered a major contributor to hyperexcitatory neuronal networks in mesial temporal lobe epilepsy (MTLE). Studies in animal models of MTLE have shown positive outcomes of augmenting group 2-metabotropic receptor functions that can regulate neuronal excitability from extrasynaptic locations. To assist in efficient translation of these findings to the clinical settings, we aimed to characterise the expression of mGluR2/3 receptors in the brain areas relevant to MTLE...
August 13, 2016: Epilepsy Research
https://www.readbyqxmd.com/read/27561972/role-of-glutamatergic-neurotransmission-in-the-enteric-nervous-system-and-brain-gut-axis-in-health-and-disease
#15
Viviana Filpa, Elisabetta Moro, Marina Protasoni, Francesca Crema, Gianmario Frigo, Cristina Giaroni
Several studies have been carried out in the last 30 years in the attempt to clarify the possible role of glutamate as a neurotransmitter/neuromodulator in the gastrointestinal tract. Such effort has provided immunohistochemical, biomolecular and functional data suggesting that the entire glutamatergic neurotransmitter machinery is present in the complex circuitries of the enteric nervous system (ENS), which participates to the local coordination of gastrointestinal functions. Glutamate is also involved in the regulation of the brain-gut axis, a bi-directional connection pathway between the central nervous system (CNS) and the gut...
December 2016: Neuropharmacology
https://www.readbyqxmd.com/read/27550843/dysregulation-of-the-glutamatergic-receptors-after-antidepressant-treatment-in-human-neural-progenitor-cells
#16
C Cruceanu, J P Lopez, W-T Tsai, G Turecki
No abstract text is available yet for this article.
August 23, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27530255/posterior-cerebellar-purkinje-cells-in-an-sca5-sparca1-mouse-model-are-especially-vulnerable-to-the-synergistic-effect-of-loss-of-%C3%AE-iii-spectrin-and-glast
#17
Emma M Perkins, Daumante Suminaite, Yvonne L Clarkson, Sin Kwan Lee, Alastair R Lyndon, Jeffrey D Rothstein, David Ja Wyllie, Kohichi Tanaka, Mandy Jackson
Clinical phenotypes of spinocerebellar ataxia type-5 (SCA5) and spectrin-associated autosomal recessive cerebellar ataxia type-1 (SPARCA1) are mirrored in mice lacking β-III spectrin (β-III(-/-)). One function of β-III spectrin is the stabilisation of the Purkinje cell-specific glutamate transporter EAAT4 at the plasma membrane. In β-III(-/-) mice EAAT4 levels are reduced from an early age. In contrast levels of the predominant cerebellar glutamate transporter GLAST, expressed in Bergmann glia, only fall progressively from 3 months onwards...
August 15, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27518770/mtor-inhibitors-rescue-premature-lethality-and-attenuate-dysregulation-of-gabaergic-glutamatergic-transcription-in-murine-succinate-semialdehyde-dehydrogenase-deficiency-ssadhd-a-disorder-of-gaba-metabolism
#18
Kara R Vogel, Garrett R Ainslie, K Michael Gibson
Recent studies have identified a role for supraphysiological gamma-aminobutyric acid (GABA) in the regulation of mechanistic target of rapamycin (mTOR), a protein kinase with pleiotropic roles in cellular development and homeostasis, including integration of growth factors and nutrient sensing and synaptic input in neurons (Lakhani et al. 2014; Vogel et al. 2015). Aldehyde dehydrogenase 5a1-deficient (aldh5a1 (-/-) ) mice, the murine orthologue of human succinic semialdehyde dehydrogenase deficiency (SSADHD), manifest increased GABA that disrupts mitophagy and increases mitochondria number with enhanced oxidant stress...
November 2016: Journal of Inherited Metabolic Disease
https://www.readbyqxmd.com/read/27507301/microrna-101b-is-downregulated-in-the-prefrontal-cortex-of-a-genetic-model-of-depression-and-targets-the-glutamate-transporter-slc1a1-eaat3-in-vitro
#19
Ya Bin Wei, Philippe A Melas, J Carlos Villaescusa, Jia Jia Liu, Ning Xu, Søren Hofman Christiansen, Heidi Elbrønd-Bek, David Paul Drucker Woldbye, Gregers Wegener, Aleksander A Mathé, Catharina Lavebratt
BACKGROUND: MicroRNAs (miRNAs) are small regulatory molecules that cause translational repression by base pairing with target mRNAs. Cumulative evidence suggests that changes in miRNA expression may in part underlie the pathophysiology and treatment of neuropsychiatric disorders, including major depressive disorder (MDD). METHODS: A miRNA expression assay that can simultaneously detect 423 rat miRNAs (miRBase v.17) was used to profile the prefrontal cortex (PFC) of a genetic rat model of MDD (the Flinders Sensitive Line [FSL]) and the controls, the Flinders Resistant Line (FRL)...
September 30, 2016: International Journal of Neuropsychopharmacology
https://www.readbyqxmd.com/read/27385796/glutamatergic-drive-facilitates-synaptic-inhibition-of-dorsal-vagal-motor-neurons-after-experimentally-induced-diabetes-in-mice
#20
Carie R Boychuk, Bret N Smith
The role of central regulatory circuits in modulating diabetes-associated glucose dysregulation has only recently been under rigorous investigation. One brain region of interest is the dorsal motor nucleus of the vagus (DMV), which contains preganglionic parasympathetic motor neurons that regulate subdiaphragmatic visceral function. Previous research has demonstrated that glutamatergic and GABAergic neurotransmission are independently remodeled after chronic hyperglycemia/hypoinsulinemia. However, glutamatergic circuitry within the dorsal brain stem impinges on GABAergic regulation of the DMV...
September 1, 2016: Journal of Neurophysiology
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