Richard W OlsenShow email address
University of California Los Angels, USA. | Department of Molecular & Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic ...
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Richard W Olsen:Expert Impact
Concepts for whichRichard W Olsenhas direct influence:Gabaa receptors,Gabaa receptor,Aminobutyric acid,Receptors gaba,Angelman syndrome,Mammalian brain,Spraguedawley receptors,Protein kinase.
Richard W Olsen:KOL impact
Concepts related to the work of other authors for whichfor which Richard W Olsen has influence:Gabaa receptors,Aminobutyric acid,Rat brain,Ion channels,Angelman syndrome,Central nervous,Benzodiazepine receptor.
KOL Resume for Richard W Olsen
University of California Los Angels, USA.
Department of Molecular & Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA. Electronic address:
University of California Los Angels
Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, California, Los Angeles 90095 USA
Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California, USA
Department of Molecular and Medical Pharmacology (A.K.L., Y.S., F.Y., R.W.O., J.L.), and Department of Neurobiology (X.M.S.), David Geffen School of Medicine at University of California at Los Angeles, and Division of Oral Biology and Medicine, School of Dentistry (I.S.), University of California and Titus Family Department of Clinical Pharmacy, University of Southern California School of Pharmacy (D.L.D., J.L.), Los Angeles, California.
Brain Research Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
Department of Molecular & Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Drug Discovery Biology and Department of Pharmacology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia (A.C., P.M.S., C.J.L.); Collège de France and CNRS URA 2182, Institut Pasteur, Paris, France (J.-P.C.); Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington (W.A.C.); PIQUR Therapeutics AG, Basel, Switzerland (D.F.); Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, Louisiana (T.P.B.); Signal Transduction Laboratory, Molecular Endocrinology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (J.A.C.); Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California (R.W.O.); Division of Neuroscience, School of Medicine, University of Dundee, Scotland, United Kingdom (J.A.P.); Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan (R.R.N.); Institut de Genomique Fonctionelle, CNRS, Montpellier, France (J.-P.P.); Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina (T.P.K.); Department of Pharmacology, University of California, Irvine, California (F.J.E.); and Research Solutions SARL, Paris, France (M.S.)
Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California;
David Geffen School of Medicine at UCLA Department of Molecular & Medical Pharmacology Los Angeles California
the Departments of Molecular and Medical Pharmacology and.
Departments of Molecular and Medical Pharmacology and
University of California David Geffen School of Medicine Los Angeles California
From the Department of Psychology and Brain Research Institute (JDC, NSJ, MSF), University of California, Los Angeles, California; and Department of Molecular and Medical Pharmacology (MDM, RWO), Geffen School of Medicine, University of California, Los Angeles, California
Departments of Molecular and Medical Pharmacology,
Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, Los Angeles, California 90095
University of California, Los Angeles, California, U.S.A
Department of Molecular and Medical Pharmacology, UCLA, Los Angeles, CA, USA
Department of Molecular and Medical Pharmacology, Geffen School of Medicine, University of California, Los Angeles, CA 90095-1735, USA
From the Division of Oral Biology & Medicine, UCLA School of Dentistry, Los Angeles, California (JL, IS); Department of Molecular & Medical Pharmacology, Geffen School of Medicine at the University of California, Los Angeles, California (AS, JL, RWO); and Departments of Anesthesiology and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania (DC, GEH)
Department of Molecular and Medical Pharmacology, Geffen School of Medicine, University of California, Los Angeles, Room 23-120 CHS, 650 Charles E. Young Drive South, Los Angeles, CA 90095-1735, USA
Department of Molecular and Medical Pharmacology, Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California 90095,
Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095
University of California,; Los Angeles, CA
Department of Molecular and Medical Pharmacology, UCLA School of Medicine, 650 Young Drive S., Los Angeles, CA 90095-1735, USA
Department of Molecular and Medical Pharmacology, School of Medicine (E.C., J.L., R.W.O.), and 2Division of Oral Biology and Medicine, School of Dentistry (J.L., I.S.), University of California Los Angeles, Los Angeles, California
Department of Molecular and Medical Pharmacology, CHS 23-120, UCLA School of Medicine, Los Angeles, CA 90095-1735, USA
Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095
Department of Pharmacology, UCLA School of Medicine, Los Angeles, California, 90095
Brain Research Institute, and
Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
Mental Retardation Research Center,
Brain Research Institute, University of California, Los Angeles, California, 90095-1761
Department of Molecular & Medical Pharmacology, UCLA School of Medicine, 90095-1735, Los Angeles, California, USA
|behavioral sensitivity gaboxadol||#1|
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|rat cerebellum thalamus||#1|
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|propofol neurosteroid thdoc||#1|
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|select gabaar subunits||#1|
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|cie rats gabaa||#1|
|mipscs cie treatment||#1|
|list native subtypes||#1|
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Prominent publications by Richard W Olsen
A Single Glycine Residue at the Entrance to the First Membrane-Spanning Domain of the γ-Aminobutyric Acid Type A Receptor β2 Subunit Affects Allosteric Sensitivity to GABA and Anesthetics
[ PUBLICATION ]
Site-directed mutagenesis of the gamma-aminobutyric acid type A (GABA(A)) receptor beta(2) subunit has demonstrated that conversion of a conserved glycine residue located at the entrance to the first transmembrane domain into the homologous rho(1) residue phenylalanine alters the modulating effects of four different i.v. anesthetics: pentobarbital, alphaxalone, etomidate, and propofol. Using the baculovirus expression system in Spodoptera frugiperda 9 cells, anesthetic-induced ...
|Known for Gaba Receptors | Aminobutyric Acid | Point Mutation | Ligand Binding | Sequence Homology|
Binding of the GABAA Receptor‐Associated Protein (GABARAP) to Microtubules and Microfilaments Suggests Involvement of the Cytoskeleton in GABARAPGABAA Receptor Interaction
[ PUBLICATION ]
GABA(A) receptor-associated protein (GABARAP) was isolated on the basis of its interaction with the gamma2 subunit of GABA(A) receptors. It has sequence similarity to light chain 3 (LC3) of microtubule-associated proteins 1A and 1B. This suggests that GABARAP may link GABA(A) receptors to the cytoskeleton. GABARAP associates with tubulin in vitro. However, little is known about the mechanism for the interaction, and it is not clear whether the interaction occurs in vivo. Here, we report ...
|Known for Interaction Gabarap | Tubulin Microtubules | Gabaa Receptor | Proteins Binding | Gamma2 Subunit|
[ PUBLICATION ]
The effects of various convulsant and anticonvulsant drugs have been studied using in vitro assays for the postsynaptic action of the neurotransmitter γ-aminobutyric acid (GABA). GABA caused a receptor-ionophore mediated increase in chloride permeability in crayfish muscle. At 100 μM concentrations, benzyl penicillin, bicuculline, diethyl barbiturate, diazepam, imipramine, and haloperidol partially inhibited this response while picrotoxinin inhibited it 100% (I50 = 3 μM). Muscimol ...
|Known for Aminobutyric Acid | Diazepam Gaba | Effects Drugs | Muscimol Bicuculline | Crayfish Muscle|
Subunit specificity and interaction domain between GABAA receptor‐associated protein (GABARAP) and GABAA receptors
[ PUBLICATION ]
GABARAP (GABA(A) receptor-associated protein) interacts with both microtubules and GABA(A) receptors in vitro and in vivo and is capable of modulating receptor channel kinetics. In this study, we use the intracellular loop of 15 GABA(A) receptor subunits to show that the interaction between GABARAP and GABA(A) receptor is specific for the gamma subunits. Pharmacological characterization of proteins purified by GABARAP affinity column indicates that native GABA(A) receptors interact with ...
|Known for Gabaa Receptor | Gamma2 Subunit | Interaction Domain | Protein Gabarap | Intracellular Loop|
We have investigated the GABAA receptor mRNA composition in 13 cell lines, using 13 subunit-specific oligo-primers (alpha 1-6, beta 1-3, gamma 1-3, and delta) and reverse transcriptase PCR amplification. Cell lines (B35, B65, B103, B104, RINm5F, Rat1, PC12, C6, C17, C27, beta TC3, NB41A3, AtT-20), derived from diverse tissue origins, were investigated in order to identify homogeneous cellular sources with distinctive GABAA receptor subunits. Fifteen GABAA receptor subunits have been ...
|Known for Cell Lines | Gabaa Receptor | Subunit Mrna | Beta Tc3 | Alpha 1|
[ PUBLICATION ]
The trafficking of GABA(A) receptors is an important component of the pathway that regulates plasticity of inhibitory synapses. The 17 kDa GABA(A) receptor-associated protein (GABARAP) has been implicated in the trafficking of GABA(A) receptors because of its ability to interact not only with the gamma2 subunit of the receptor but also with microtubules and the N-ethylmaleimide-sensitive factor (NSF). To elucidate the role of GABARAP in the trafficking of GABA(A) receptors, we have ...
|Known for Gabaa Receptors | Plasma Membrane | Gabarap Trafficking | Gamma2 Subunit | Proteins Neurons|
Protein kinase C and cAMP-dependent protein kinase phosphorylate the beta subunit of the purified gamma-aminobutyric acid A receptor.
[ PUBLICATION ]
A number of recent studies have suggested that phosphorylation of the gamma-aminobutyric acid A (GABAA) receptor could modulate receptor function. Activators of protein kinase C and cAMP-dependent protein kinase have been shown to influence GABAA receptor function. In addition, Sweetnam et al. [Sweetnam, P. M., Lloyd, J., Gallombardo, P., Malison, R. T., Gallager, D. W., Tallman, J. F. & Nestler, E. J. (1988) J. Neurochem. 51, 1274-1284] have reported that a kinase associated with a ...
|Known for Protein Kinase | Beta Subunit | Phosphorylation Gabaa Receptor | Aminobutyric Acid | Affinity Electrophoresis|
Purification and Properties of the Cholinergic Receptor Protein from Electrophorus electricus Electric Tissue
[ PUBLICATION ]
The acetylcholine (nicotinic) receptor from the electric organ of Electrophorus electricus has been purified approx. 300-fold from Triton X-100 extracts of electroplax membrane fragments. The receptor protein was first adsorbed from crude extracts on an affinity column containing 1,3-bis(tri-ethylammonium ethoxy)-4-iodoacetamidobenzene diiodide, an analogue of flaxedil, linked to Sepharose 2B, then eluted with a solution of flaxedil and concentrated. The receptor protein was further ...
|Known for Receptor Protein | Electrophorus Electricus | Affinity Chromatography | Triton X100 | Electric Organ|
Altered GABAA Receptor Subunit and Splice Variant Expression in Rats Treated With Chronic Intermittent Ethanol
[ PUBLICATION ]
BACKGROUND: Intermittent chronic administration of ethanol to rats has been shown previously to produce a hyperexcitable, kindling-like state, accompanied by reduced inhibitory synaptic transmission in the hippocampus and changes in gamma-aminobutyric acid type A (GABAA) receptors. Further information is needed on the detailed changes in GABAA receptors and their time course and persistence, as is comparison to changes after chronic, continuous ethanol.
METHODS: GABAA receptors were ...
|Known for Gabaa Receptor | Chronic Intermittent Ethanol | Messenger Rats | Gamma2 Subunit | Expression Hippocampus|
The glutamate analog (RS)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA), displaced 11% of the binding of L-[3H]glutamate to rat brain membranes, amounting to 22% of the specific binding displaceable by excess non-radioactive glutamate. AMPA-sensitive L-[3H]glutamate binding was additive with that displaced by kainic acid (1 microM) plus N-methyl-D-aspartate (10 microM) when low concentrations of non-radioactive AMPA (1 microM) were employed to determine non-specific ...
|Known for Ampa Binding | Rat Brain | Glutamate Receptors | Kainic Acid | 10 Microm|
Subunit-Specific Association of Protein Kinase C and the Receptor for Activated C Kinase with GABA Type A Receptors
[ PUBLICATION ]
GABA receptors (GABA(A)) are the major sites of fast synaptic inhibition in the brain and can be assembled from five subunit classes: alpha, beta, gamma, delta, and epsilon. Receptor function can be regulated by direct phosphorylation of beta and gamma2 subunits, but how kinases are targeted to GABA(A) receptors is unknown. Here we show that protein kinase C-betaII (PKC-betaII) is capable of directly binding to the intracellular domain of the receptor beta1 and beta3 subunits, but not to ...
|Known for Protein Kinase | Receptors Pkc | Receptor Function | Beta Subunits | Major Sites|
Type-A receptors for the neurotransmitter GABA (γ-aminobutyric acid) are ligand-gated chloride channels that mediate inhibitory neurotransmission. Each subunit of the pentameric receptor protein has ligand-binding sites in the amino-terminal extracellular domain and four membrane-spanning regions, one of which forms a wall of the ion channel1. Each subunit also has a large intracellular loop that may be a target for protein kinases and be required for subcellular targeting and membrane ...
|Known for Gabaa Receptors | Cultured Cloning | Neurotransmitter Gaba | Receptor Protein | Γ2 Subunit|
Decreased surface expression of the δ subunit of the GABAA receptor contributes to reduced tonic inhibition in dentate granule cells in a mouse model of fragile X syndrome
[ PUBLICATION ]
While numerous changes in the GABA system have been identified in models of Fragile X Syndrome (FXS), alterations in subunits of the GABAA receptors (GABAARs) that mediate tonic inhibition are particularly intriguing. Considering the key role of tonic inhibition in controlling neuronal excitability, reduced tonic inhibition could contribute to FXS-associated disorders such as hyperactivity, hypersensitivity, and increased seizure susceptibility. The current study has focused on the ...
|Known for Tonic Inhibition | Δ Subunit | Granule Cells | Fmr1 Mice | Dentate Gyrus|
Altered Pharmacology of Synaptic and Extrasynaptic GABAA Receptors on CA1 Hippocampal Neurons Is Consistent with Subunit Changes in a Model of Alcohol Withdrawal and Dependence
[ PUBLICATION ]
Previously, we reported (Cagetti, Liang, Spigelman, and Olsen, 2003) that chronic intermittent ethanol (CIE) treatment leads to signs of alcohol dependence, including anxiety and hyperactivity, accompanied by reduced synaptic gamma-aminobutyric acid (A) receptor (GABAAR) function and altered sensitivity to its allosteric modulators consistent with a measured switch in subunit composition. In this study, we separated the synaptic and extrasynaptic components of GABAAR activation in ...
|Known for Altered Pharmacology | Extrasynaptic Gabaa Receptors | Cie Treatment | Alcohol Dependence | Hippocampal Neurons|