Neuronal Activity Regulates Alternative Exon Usage
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(12) Patent Application Publication (10) Pub. No.: US 2017/0009296A1 Glessner Et Al
US 20170009296A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2017/0009296A1 Glessner et al. (43) Pub. Date: Jan. 12, 2017 (54) ASSOCIATION OF RARE RECURRENT (60) Provisional application No. 61/376.498, filed on Aug. GENETIC VARATIONS TO 24, 2010, provisional application No. 61/466,657, ATTENTION-DEFICIT, HYPERACTIVITY filed on Mar. 23, 2011. DISORDER (ADHD) AND METHODS OF USE THEREOF FOR THE DAGNOSS AND TREATMENT OF THE SAME Publication Classification (71) Applicant: The Children's Hospital of Philadelphia, Philadelphia, PA (US) (51) Int. Cl. CI2O I/68 (2006.01) (72) Inventors: Joseph Glessner, Mullica Hill, NJ A63L/454 (2006.01) (US); Josephine Elia, Penllyn, PA (52) U.S. Cl. (US); Hakon Hakonarson, Malvern, CPC ........... CI2O I/6883 (2013.01); A61 K3I/454 PA (US) (2013.01); C12O 2600/156 (2013.01); C12O (21) Appl. No.: 15/063,482 2600/16 (2013.01) (22) Filed: Mar. 7, 2016 Related U.S. Application Data (57) ABSTRACT (63) Continuation of application No. 13/776,662, filed on Feb. 25, 2013, now abandoned, which is a continu ation-in-part of application No. PCT/US 11/48993, Compositions and methods for the detection and treatment filed on Aug. 24, 2011. of ADHD are provided. Patent Application Publication Jan. 12, 2017. Sheet 1 of 18 US 2017/000929.6 A1 Figure 1A ADHD Cases and Parentsi Siblings O SO Samples8 O 1. 1. 250C 40 gE 520 - Samples 3. Figure 1B Patent Application Publication Jan. 12, 2017. Sheet 2 of 18 US 2017/000929.6 A1 S&s sess'. ; S&s' ' Ny erre 8 Y-8 W - - 8 - - - - 8 - W - 8-8- W - 8 w w W & . -
(Arc/Arg3.1) in the Nucleus Accumbens Is Critical for the Acqui
Behavioural Brain Research 223 (2011) 182–191 Contents lists available at ScienceDirect Behavioural Brain Research j ournal homepage: www.elsevier.com/locate/bbr Research report Expression of activity-regulated cytoskeleton-associated protein (Arc/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and reinstatement of morphine-induced conditioned place preference ∗ Xiu-Fang Lv, Ya Xu, Ji-Sheng Han, Cai-Lian Cui Neuroscience Research Institute and Department of Neurobiology, Peking University Health Science Center, Key Laboratory of Neuroscience, the Ministry of Education and Ministry of Public Health, 38 Xueyuan Road, Beijing 100191, PR China a r t i c l e i n f o a b s t r a c t Article history: Activity-regulated cytoskeleton-associated protein (Arc), also known as activity-regulated gene 3.1 Received 27 January 2011 (Arg3.1), is an immediate early gene whose mRNA is selectively targeted to recently activated synaptic Received in revised form 1 April 2011 sites, where it is translated and enriched. This unique feature suggests a role for Arc/Arg3.1 in coupling Accepted 18 April 2011 synaptic activity to protein synthesis, leading to synaptic plasticity. Although the Arc/Arg3.1 gene has been shown to be induced by a variety of abused drugs and its protein has been implicated in diverse Key words: forms of long-term memory, relatively little is known about its role in drug-induced reward memory. In Activity regulated cytoskeleton-associated this study, we investigated the potential role of Arc/Arg3.1 protein expression in reward-related associa- protein/activity-regulated gene (Arc/Arg3.1) tive learning and memory using morphine-induced conditioned place preference (CPP) in rats. -
The Effect of Rosmarinic Acid on Apoptosis and Nnos Immunoreactivity Following Intrahippocampal Kainic Acid Injections in Rats
Basic and Clinical January, February 2020, Volume 11, Number 1 Research Paper: The Effect of Rosmarinic Acid on Apoptosis and nNOS Immunoreactivity Following Intrahippocampal Kainic Acid Injections in Rats Safoura Khamse1* , Seyed Shahabeddin Sadr1,2 , Mehrdad Roghani3* , Mina Rashvand1 , Maryam Mohammadian4 , Narges Mare- fati1 , Elham Harati1 , Fatemeh Ebrahimi1 1. Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 2. Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. 3. Neurophysiology Research Center, Shahed University, Tehran, Iran. 4. Department of Physiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran. Use your device to scan and read the article online Citation: Khamse, S., Sadr, Sh., Roghani, M., Rashvand, M., Mohammadian, M., & Marefati, N., et al. The Effect of Ros- marinic Acid on Apoptosis and nNOS Immunoreactivity Following Intrahippocampal Kainic Acid Injections in Rats Basic and Clinical Neuroscience, 11(1), 41-48. http://dx.doi.org/10.32598/bcn.9.10.340 http://dx.doi.org/10.32598/bcn.9.10.340 A B S T R A C T Introduction: Kainic Acid (KA) is an ionotropic glutamate receptor agonist. KA can induce neuronal overactivity and excitotoxicity. Rosmarinic Acid (RA) is a natural polyphenolic Article info: compound with antioxidant, anti-apoptotic, anti-neurodegenerative, and anti-inflammatory Received: 12 Apr 2018 properties. This study aimed to assess the effect of RA on apoptosis, nNOS-positive neurons First Revision: 10 May 2018 number, as well as Mitogen-Activated Protein Kinase (MAPK) and Cyclooxygenase-2 (COX- Accepted: 27 Oct 2018 2) immunoreactivity, following intrahippocampal Kainic acid injection in rats. -
Kainic Acid-Induced Neurotoxicity: Targeting Glial Responses and Glia-Derived Cytokines
388 Current Neuropharmacology, 2011, 9, 388-398 Kainic Acid-Induced Neurotoxicity: Targeting Glial Responses and Glia-Derived Cytokines Xing-Mei Zhang1 and Jie Zhu1,2, 1Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden; 2Department of Neurology, The First Hospital of Jilin University, Changchun, China Abstract: Glutamate excitotoxicity contributes to a variety of disorders in the central nervous system, which is triggered primarily by excessive Ca2+ influx arising from overstimulation of glutamate receptors, followed by disintegration of the endoplasmic reticulum (ER) membrane and ER stress, the generation and detoxification of reactive oxygen species as well as mitochondrial dysfunction, leading to neuronal apoptosis and necrosis. Kainic acid (KA), a potent agonist to the -amino- 3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate class of glutamate receptors, is 30-fold more potent in neuro- toxicity than glutamate. In rodents, KA injection resulted in recurrent seizures, behavioral changes and subsequent degeneration of selective populations of neurons in the brain, which has been widely used as a model to study the mechanisms of neurode- generative pathways induced by excitatory neurotransmitter. Microglial activation and astrocytes proliferation are the other characteristics of KA-induced neurodegeneration. The cytokines and other inflammatory molecules secreted by activated glia cells can modify the outcome of disease progression. Thus, anti-oxidant and anti-inflammatory treatment could attenuate or prevent KA-induced neurodegeneration. In this review, we summarized updated experimental data with regard to the KA-induced neurotoxicity in the brain and emphasized glial responses and glia-oriented cytokines, tumor necrosis factor-, interleukin (IL)-1, IL-12 and IL-18. -
Synapse Development Organized by Neuronal Activity-Regulated Immediate- Early Genes Seungjoon Kim1, Hyeonho Kim1 and Ji Won Um1
Kim et al. Experimental & Molecular Medicine (2018) 50:11 DOI 10.1038/s12276-018-0025-1 Experimental & Molecular Medicine REVIEW ARTICLE Open Access Synapse development organized by neuronal activity-regulated immediate- early genes Seungjoon Kim1, Hyeonho Kim1 and Ji Won Um1 Abstract Classical studies have shown that neuronal immediate-early genes (IEGs) play important roles in synaptic processes critical for key brain functions. IEGs are transiently activated and rapidly upregulated in discrete neurons in response to a wide variety of cellular stimuli, and they are uniquely involved in various aspects of synapse development. In this review, we summarize recent studies of a subset of neuronal IEGs in regulating synapse formation, transmission, and plasticity. We also discuss how the dysregulation of neuronal IEGs is associated with the onset of various brain disorders and pinpoint key outstanding questions that should be addressed in this field. Introduction experience-dependent synaptic changes and maturation Numerous studies have shown that neural activity plays of neural circuits. an important role in regulating synaptic strength, neuro- More than dozens of neuronal IEGs were identified by fi 1– 12 1234567890():,; 1234567890():,; nal membrane properties, and neural circuit re nement Paul Worley, Elly Nedivi, and colleagues , owing to the 3. In particular, sensory experiences continually influence use of the subtractive hybridization method, in combi- brain development at synaptic, circuit, and organismal nation with various neural stimulation protocols, most levels, as Hubel4 and Wiesel5 elegantly demonstrated in notably seizure paradigms. Among them, cAMP- their work on visual cortex organization during the cri- responsive element-binding protein (CREB) has been tical period5. -
Electrophysiological Mechanisms of Kainic Acid- Induced Epileptiform Activity in the Rat Hippocampal Slice’
0270-6474/84/0405-1312$02,00/O The Journal of Neuroscience Copyright 0 Society for Neuroscience Vol. 4, No. 5, pp. 1312-1323 Printed in U.S.A. May 1984 ELECTROPHYSIOLOGICAL MECHANISMS OF KAINIC ACID- INDUCED EPILEPTIFORM ACTIVITY IN THE RAT HIPPOCAMPAL SLICE’ ROBERT S. FISHER’ AND BRADLEY E. ALGER Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 Received August 29, 1983; Revised December 28, 1983; Accepted January 4, 1984 Abstract Depression of GABA-mediated IPSPs has been proposed to be a crucial factor in the onset of epileptiform activity in most models of epilepsy. To test this idea, we studied epileptiform activity induced by bath application of the excitatory neurotoxin kainic acid (KA) in the rat hippocampal slice. Repetitive field potential firing, spontaneous or evoked, occurred during exposure to KA. Intracellular records from 52 CA1 pyramidal cells during changes from control saline to saline containing i PM KA indicated that KA depolarized cells an average of about 5 mV and caused a 15% decrease in input resistance. Action potentials and current-induced burst afterhyperpolariza- tions did not change significantly. In several cells the tonic effects of KA were preceded by a transient phase of sporadic, spontaneous depolarizations of 2 to 10 mV and 50 to 200 msec duration. These phasic depolarizations were blocked by hyperpolarization. The major effect of 1 PM KA was a depression of synaptic potentials. Initially, KA depressed fast GABA-mediated IPSPs and slow, non-GABA-mediated late hyperpolarizing potentials to 23% and 40% of control values, respectively. IPSP depression correlated closely with onset of burst potential firing in response to synaptic stimulation. -
Podocin Inactivation in Mature Kidneys Causes Focal Segmental Glomerulosclerosis and Nephrotic Syndrome
BASIC RESEARCH www.jasn.org Podocin Inactivation in Mature Kidneys Causes Focal Segmental Glomerulosclerosis and Nephrotic Syndrome Ge´raldine Mollet,*† Julien Ratelade,*† Olivia Boyer,*†‡ Andrea Onetti Muda,*§ ʈ Ludivine Morisset,*† Tiphaine Aguirre Lavin,*† David Kitzis,*† Margaret J. Dallman, ʈ Laurence Bugeon, Norbert Hubner,¶ Marie-Claire Gubler,*† Corinne Antignac,*†** and Ernie L. Esquivel*† *INSERM, U574, Hoˆpital Necker-Enfants Malades, Paris, France; †Faculte´deMe´ decine Rene´ Descartes, Universite´ Paris Descartes, Paris, France; ‡Pediatric Nephrology Department and **Department of Genetics, Hoˆpital Necker- Enfants Malades, Assistance Publique-Hoˆpitaux de Paris, Paris, France; §Department of Pathology, Campus ʈ Biomedico University, Rome, Italy; Department of Biological Sciences, Imperial College London, London, England; and ¶Max-Delbruck Center for Molecular Medicine, Berlin, Germany ABSTRACT Podocin is a critical component of the glomerular slit diaphragm, and genetic mutations lead to both familial and sporadic forms of steroid-resistant nephrotic syndrome. In mice, constitutive absence of podocin leads to rapidly progressive renal disease characterized by mesangiolysis and/or mesangial sclerosis and nephrotic syndrome. Using established Cre-loxP technology, we inactivated podocin in the adult mouse kidney in a podocyte-specific manner. Progressive loss of podocin in the glomerulus recapitu- lated albuminuria, hypercholesterolemia, hypertension, and renal failure seen in nephrotic syndrome in humans. Lesions of FSGS appeared -
NMDA Agonists Using ALZET Osmotic Pumps
ALZET® Bibliography References on the Administration of NMDA Agonists Using ALZET Osmotic Pumps Aspartic Acid P7453: M. Domercq, et al. Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition. Glia 2005;52(1):36-46 ALZET Comments: Oligonucleotide, antisense; oligonucleotide sense; kainate, dihydro-; aspartic acid, DL-threo-B-benzyloxy-; Saline, sterile; CSF/CNS (optic nerve); Rabbit; 1003D; 3 days; Controls received mp w/ vehicle, or contralateral nerves; antisense (glutamate transporters GLAST + GLT-1); animal info (adult, male, white New Zealand). P6888: J. Darman, et al. Viral-induced spinal motor neuron death is non-cell-autonomous and involves glutamate excitotoxicity. Journal of Neuroscience 2004;24(34):7566-7575 ALZET Comments: Aspartic acid, dl-threo-B-hydroxy; spermine, 1-naphthyl acetyl; CSF/CNS (intrathecal, subarachnoid space); Rat; 1007D; 7 days; Controls received mp w/ saline; enzyme inhibitors (GLT-1, GluR2). P3908: A. Hirata, et al. AMPA receptor-mediated slow neuronal death in the rat spinal cord induced by long-term blockade of glutamate transporters with THA. Brain Research 1997;771(37-44 ALZET Comments: Aspartic acid, dl-threo-B-hydroxy; Glutamate, l-; CSF, artificial;; CSF/CNS (subarachnoid space, intrathecal); Rat; 2ML1; no duration posted; dose-response; cannula position verified. P0289: R. M. Mangano, et al. Chronic infusion of endogenous excitatory amino acids into rat striatum and hippocampus. Brain Res. Bull 1983;10(47-51 ALZET Comments: Aminobutyric acid, Y-; Aspartic acid, dl-threo-B-hydroxy; Aspartic acid, l-; Cysteine sulfinic acid; Glutamic acid, l-; Radio-isotopes; 3H tracer; Acetate; Saline; CSF/CNS (corpus striatum); CSF/CNS (hippocampus); Rat; 2002; 2 weeks; comparison of injec. -
Homer1 Promotes Dendritic Spine Growth Through Ankyrin-G and Its Loss Reshapes the Synaptic Proteome
Molecular Psychiatry (2021) 26:1775–1789 https://doi.org/10.1038/s41380-020-00991-1 ARTICLE Homer1 promotes dendritic spine growth through ankyrin-G and its loss reshapes the synaptic proteome 1 1 2 1,5 2 Sehyoun Yoon ● Nicolas H. Piguel ● Natalia Khalatyan ● Leonardo E. Dionisio ● Jeffrey N. Savas ● Peter Penzes 1,3,4 Received: 22 February 2020 / Revised: 24 November 2020 / Accepted: 7 December 2020 / Published online: 4 January 2021 © The Author(s), under exclusive licence to Springer Nature Limited part of Springer Nature 2021. This article is published with open access Abstract Homer1 is a synaptic scaffold protein that regulates glutamatergic synapses and spine morphogenesis. HOMER1 knockout (KO) mice show behavioral abnormalities related to psychiatric disorders, and HOMER1 has been associated with psychiatric disorders such as addiction, autism disorder (ASD), schizophrenia (SZ), and depression. However, the mechanisms by which it promotes spine stability and its global function in maintaining the synaptic proteome has not yet been fully investigated. Here, we used computational approaches to identify global functions for proteins containing the Homer1-interacting PPXXF motif within the postsynaptic compartment. Ankyrin-G was one of the most topologically important nodes in the postsynaptic peripheral 1234567890();,: 1234567890();,: membrane subnetwork, and we show that one of the PPXXF motifs, present in the postsynaptically-enriched 190 kDa isoform of ankyrin-G (ankyrin-G 190), is recognized by the EVH1 domain of Homer1. We use proximity ligation combined with super- resolution microscopy to map the interaction of ankyrin-G and Homer1 to distinct nanodomains within the spine head and correlate them with spine head size. -
Subconvulsive Dose of Kainic Acid Transiently Increases the Locomotor Activity of Adult Wistar Rats
Physiol. Res. 64: 263-267, 2015 https://doi.org/10.33549/physiolres.932793 SHORT COMMUNICATION Subconvulsive Dose of Kainic Acid Transiently Increases the Locomotor Activity of Adult Wistar Rats V. RILJAK1, D. MAREŠOVÁ1, J. POKORNÝ1, K. JANDOVÁ1 1Institute of Physiology, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic Received March 28, 2014 Accepted September 1, 2014 On-line October 15, 2014 Summary Kainic acid (KA) is agonist for kainate subtype Kainic acid (KA) is a potent neurotoxic substance valuable in receptors of excitatory amino acids (Monaghan and research of temporal lobe epilepsy. We tested how subconvulsive Cotman 1982) and its administration was revealed as a dose of KA influences spontaneous behavior of adult Wistar rats. good strategy to model the clinical and neuropathological Animals were treated with 5 mg/kg of KA and tested in Laboras features of temporal lobe epilepsy (Olney et al. 1974). open field test for one hour in order to evaluate various Most commonly, a systemic administration of KA in behavioral parameters. Week after the KA treatment animals convulsive dose (10 mg/kg) is used to induce status were tested again in Laboras open field test. Finally, rat’s brains epilepticus leading to massive excitotoxic damage of were sliced and stained with Fluoro-Jade B to detect possible neuronal tissue (Doble 1999, Riljak et al. 2007). The KA neuronal degeneration. Treatment with KA increased the time induced status epilepticus is followed by latent period and spent by locomotion (p<0.01), exploratory rearing (p<0.05) and occurrence of spontaneous recurrent seizures (Albala et animals traveled longer distance (p<0.01). -
Neuroprotective Effect of Citicoline on Retinal Cell Damage Induced by Kainic Acid in Rats
Neuroprotective Effect of Citicoline on Retinal Cell Damage Induced by Kainic Acid in Rats Yong Seop Han, MD, In Young Chung, MD, Jong Moon Park, MD, PhD, Ji Myeong Yu, MD, PhD Department of Ophthalmology, College of Medicine, Gyeongsang National University, Jinju, Korea Purpose: To examine whether citicoline has a neuroprotective effect on kainic acid (KA)-induced retinal damage. Methods: KA (6 nmol) was injected into the vitreous of rat eyes. Citicoline (500mg/kg, i.p.) was administered to the rats once before and twice a day after KA-injection for 3- and 7-day intervals. The neuroprotective effects of citicoline were estimated by measuring the thickness of the various retinal layers using hematoxylin-eosin (H&E) staining. In addition, immunohistochemistry was conducted to elucidate the expression of endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS). Results: Morphometric analysis of retinal damage in KA-injected eyes showed significant cell loss in the inner nuclear layer (INL) and inner plexiform layer (IPL) of the retinas at 3 and 7 days after KA injection, but not in the outer nuclear layer (ONL). At 3 days after citicoline treatment, no significant changes were detected in the retinal thickness and immunoreactivities of eNOS and nNOS. The immunoreactivities of eNOS and nNOS increased in the retina at 7 days after the KA injection. However, prolonged treatment for 7 days significantly attenuated the immunoreactivities and the reduction of thickness. Conclusions: The results indicate that citicoline -
L-Theanine Research Page 1 Updated: April 2008
L-theanine Research Page 1 Updated: April 2008 Bryan, J. Psychological effects of dietary components of tea: caffeine and L-theanine. Nutr Rev, Vol 66, 2, pp 82-90. Feb 2008 Bukowski, J. L-theanine intervention enhances human gamma delta T lymphocyte function. Nutr Rev, Vol 66, 2, pp 96-102. Feb 2008. Haskell, C.F The effects of L-theanine, caffeine and their combination on cognition and mood. Biol Psychol, Vol 77, 2, pp 113-22, Feb 2008. Egashira, N. L-theanine prevents memory impairment induced by repeated cerebral ischemia in rats. Phytother Res, Vol 22, 1, pp 65-8, Jan 2008. Percival, S. Bioactive food components that enhance γδT Cell function may play a role in cancer prevention. Journal of Nutrition, Vol 138, 1, pp 1- 4, 2008 Rogers, P.J. Time for tea: mood, blood pressure and cognitive performance effects of caffeine and theanine administered alone and together. Psychopharmacology, Vol 195, 4, pp 569-577, Jan 2008. Yokogoshi, H. Effect of unique amino acid in green tea, L-theanine, on an enhancement of dopamine release and inhibitory neurotransmitters. Yakugaku Zashi, Vol 127, 4, pp 46-48, 2007 (Japanese). Kurihara, S. Enhancement of antigen-specific immunoglobulin G production in mice by co-administration of L-cystine and L-theanine. Journal of Veterinary Medical Science, Vol 69, 12, pp 1263. 2007. Yamada, T. L-theanine, r-glutamylethylamide, increases neurotransmission concentrations and neurotrophin mRNA levels in the brain during lactation. Life Sciences. Vol 81, 16, pp 1247-1255. 2007. Dimpfel, W. Theogallin and L-theanine as active ingredients in decaffeinated green tea extract, characterization in the freely moving rat by means of quantitative field potential analysis.