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  • 1
    Online Resource
    Online Resource
    Washington, D.C. :American Psychiatric Publishing,
    Keywords: Molecular neurobiology. ; Neurochemistry. ; Electronic books.
    Description / Table of Contents: Solomon Snyder has been instrumental in the establishment of modern psychopharmacology. Science and Psychiatry is a collection of some of his best scientific papers from the past forty years, representing important advances in psychopharmacology and molecular biology.
    Type of Medium: Online Resource
    Pages: 1 online resource (514 pages)
    Edition: 1st ed.
    ISBN: 9781585628827
    DDC: 573.8/4
    Language: English
    Note: Cover -- Contents -- About the Author -- Foreword: Sol Snyder: Audacious Scientist, Leader of the Scientifice Community, and Remarkable Human Being! -- Introduction -- Part I: DISCOVERY AND CHARACTERIZATION OF THE OPIATE RECEPTOR -- Commentary: Radioligand Binding Methodologies: New Inventions, New Directions -- 1 Opiate Receptor: Demonstration in Nervous Tissue -- 2 Opiate Agonists and Antagonists Discriminated by Receptor Binding in Brain -- 3 Historical Review: Opioid Receptors -- Part II: CHARACTERIZATION OF THE ENKEPHALINS -- Commentary: The Discovery of Endogenous Opiates and Their Receptors: A Snyderian Saga of Skill and Judgment -- 4 Opiate Receptor in Normal and Drug Altered Brain Function -- 5 Morphine-Like Peptides in Mammalian Brain: Isolation, Structure Elucidation, and Interactions With the Opiate Receptor -- 6 Opioid Peptide Enkephalin: Immunohistochemical Mapping in Rat Central Nervous System -- Part III: DOPAMINE RECEPTORS AND INFLUENCES OF NEUROLEPTICS -- Commentary: Dopamine Receptor Binding and Its Therapeutics -- 7 Dopamine Receptor Binding Predicts Clinical and Pharmacological Potencies of Antischizophrenic Drugs -- 8 Antischizophrenic Drugs: Chronic Treatment Elevates Dopamine Receptor Binding in Brain -- 9 Dopamine Receptors, Neuroleptics, and Schizophrenia -- Part IV: DRUG EFFECTS EXPLAINED AS ACTIONS ON NEUROTRANSMITTER RECEPTORS -- Commentary: Perspectives on Simplicity and Discovery -- 10 Antischizophrenic Drugs and Brain Cholinergic Receptors: Affinity for Muscarinic Sites Predicts Extrapyramidal Effects -- 11 Tricyclic Antidepressants: Therapeutic Properties and Affinity for α-Noradrenergic Receptor Binding Sites in the Brain -- Part V: DRUG ACTIONS AND SEROTONIN RECEPTOR SUBTYPES. , Commentary: Clinical Data Stimulation of Basic Research: The Far-Reaching Clinical Significance of Serotonin Receptor Subtype Identification -- 12 Long-Term Antidepressant Treatment Decreases Spiroperidol-Labeled Serotonin Receptor Binding -- 13 Two Distinct Central Serotonin Receptors With Different Physiological Functions -- Part VI: INOSITOL PHOSPHATES AND ACTIONS OF LITHIUM -- Commentary: Lithium, Second Messengers, and Downstream Effects -- 14 Lithium Blocks a Phosphoinositide-Mediated Cholinergic Response in Hippocampal Slices -- 15 Solubilization, Purification, and Characterization of an Inositol Trisphosphate Receptor -- 16 Second Messenger Systems and Psychoactive Drug Action: Focus on the Phosphoinositide System and Lithium -- 17 Purified Inositol 1,4,5-Trisphosphate Receptor Mediates Calcium Flux in Reconstituted Lipid Vesicles -- Part VII: NITRIC OXIDE AS A NEUROTRANSMITTER -- Commentary: Just Say "Yes": Snyder's Approach to the Difficult Problem of NO -- 18 Nitric Oxide Mediates Glutamate-Linked Enhancement of cGMP Levels in the Cerebellum -- 19 Cloned and Expressed Nitric Oxide Synthase Structurally Resembles Cytochrome P-450 Reductase -- 20 Behavioral Abnormalities in Male Mice Lacking Neuronal Nitric Oxide Synthase -- Part VIII: D-AMINO ACIDS AS NEUROTRANSMITTERS -- Commentary: Disruptive Science: Incongruent Findings Lead to Novel Insights Into How the Brain Works -- 21 D-Aspartate Localizations Imply Neuronal and Neuroendocrine Roles -- 22 Serine Racemase: A Glial Enzyme Synthesizing D-Serine to Regulate Glutamate-N-Methyl-D-Aspartate Neurotransmission -- 23 Serine Racemase: Activation by Glutamate Neurotransmission via Glutamate Receptor Interacting Protein and Mediation of Neuronal Migration -- Part IX: NEURAL MESSENGERS OF CELL LIFE AND DEATH -- Commentary: Beyond Neurotransmitters. , 24 Cytochrome c Binds to Inositol 1,4,5-Trisphosphate Receptors, Amplifying Calcium-Dependent Apoptosis -- 25 Bilirubin Benefits: Cellular Protection by a Biliverdin Reductase Antioxidant Cycle -- 26 S-Nitrosylated GAPDH Initiates Apoptotic Cell Death by Nuclear Translocation Following Siah1 Binding -- Part X: WHAT MAKES FOR CREATIVE DISCOVERY IN SCIENCE? -- Commentary: What Creates Creative Science and Scientists? -- 27 The Audacity Principle in Science -- Index -- A -- B -- C -- D -- E -- F -- G -- H -- I -- J -- K -- L -- M -- N -- O -- P -- Q -- R -- S -- T -- U -- V -- W -- Y -- Z.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    CNS drug reviews 5 (1999), S. 0 
    ISSN: 1527-3458
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: G protein-coupled receptor (GPCR) signaling cascades may be key substrates for the antidepressant effects of chronic electroconvulsive seizures (ECS). To better understand changes in these signaling pathways, alterations in levels of mRNA's encoding regulators of G protein signaling (RGS) protein subtypes-2, -4, -7, -8 and -10 were evaluated in rat brain using northern blotting and in situ hybridization. In prefrontal cortex, RGS2 mRNA levels were increased several-fold 2 h following an acute ECS. Increases in RGS8 mRNA were of lesser magnitude (30%), and no changes were evident for the other RGS subtypes. At 24 h following a chronic ECS regimen, RGS4, -7, and -10 mRNA levels were reduced by 20–30%; only RGS10 was significantly reduced 24 h after acute ECS. Levels of RGS2 mRNA were unchanged 24 h following either acute or chronic ECS. In hippocampus, RGS2 mRNA levels were markedly increased 2 h following acute ECS. More modest increases were seen for RGS4 mRNA expression, whereas levels of the other RGS subtypes were unaltered. At 24 h following chronic ECS, RGS7, -8 and -10 mRNA levels were decreased in the granule cell layer, and RGS7 and -8 mRNA levels were decreased in the pyramidal cell layers. Only RGS8 and -10 mRNA levels were significantly reduced in hippocampus 24 h following an acute ECS. Paralleling neocortex, RGS2 mRNA content was unchanged in hippocampus 24 h following either acute or chronic ECS. In ventromedial hypothalamus, RGS4 mRNA content was increased 24 h following chronic ECS, whereas RGS7 mRNA levels were only increased 24 h following an acute ECS. The increased RGS4 mRNA levels in hypothalamus were significant by 2 h following an acute ECS. These studies demonstrate subtype-, time-, and region-specific regulation of RGS proteins by ECS, adaptations that may contribute to the antidepressant effects of this treatment.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have recently demonstrated that mRNA expression of cyclic AMP (cAMP) response element-binding protein (CREB) is down-regulated in CATH.a cells (a neural-derived cell line) by activation of the cAMP pathway. We now demonstrate that this down-regulation can be accounted for by a decrease in the rate of CREB gene transcription. It was found that cycloheximide, a protein synthesis inhibitor, prevented the forskolin-induced decrease in CREB mRNA levels in CATH.a cells. Nuclear run-on assays demonstrated that forskolin decreased the rate of CREB transcription by close to 50%. Moreover, forskolin decreased chloramphenicol acetyltransferase (CAT) activity in CATH.a cells transiently transfected with a construct containing 1,240 bp of CREB promoter fused to a CAT reporter plasmid. Possible mechanisms by which activation of the cAMP pathway leads to a decrease in CREB gene transcription are discussed.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study examines the possible involvement of nitric oxide (NO)-stimulated endogenous ADP-ribosylation in long-term potentiation (LTP). LTP was induced in hippocampal slices by stimulation of Schaffer collateral inputs to the CA1 pyramidal neurons. Basal and sodium nitroprusside (SNP), which generates NO, stimulation of endogenous ADP-ribosylation was then studied in CA1 subfields isolated from the slices. Control slices received no treatment or were tetanized in the presence of aminophosphonovaleric acid, an NMDA receptor antagonist that blocks the development of LTP. SNP-stimulated ADP-ribosylation of endogenous proteins was reduced by 40–70% in LTP slices relative to control slices. LTP was also associated with a small but significant reduction in basal ADP-ribosylation activity. The results demonstrate that the induction of LTP is associated with regulation of endogenous ADP-ribosylation and suggest a role for this type of covalent modification in some aspect of LTP.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Previous studies have implicated adaptations in the cyclic AMP system in mechanisms of opiate tolerance, dependence, and withdrawal in the rat locus coeruleus. It has been speculated that such adaptations may occur at the level of gene expression. To understand better the mechanism by which opiates produce these in-tracellular adaptations, we studied morphine regulation of the state of phosphorylation of cyclic AMP response element-binding protein (CREB), a transcription factor that mediates some of the effects of the cyclic AMP system on gene expression. We show here, by use of a back phosphorylation and immunoprecipitation procedure, that acute morphine decreases the state of phosphorylation of CREB, an effect that becomes completely attenuated after chronic morphine administration. In contrast, acute precipitation of opiate withdrawal, via administration of an opiate receptor antagonist, increases the phosphorylation state of CREB. Such regulation of CREB phosphorylation could be part of the molecular pathway by which opiates produce changes in gene expression that lead to addiction.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 57 (1991), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cholera and pertussis toxin-mediated ADP-ribo-sylation has been used extensively to study regulation of guanine nucleotide binding proteins (G proteins) in the nervous system, but much less is known about possible endogenous ADP-ribosylation of G proteins in brain. The present study demonstrates endogenous ADP-ribosylation, in the absence of cholera and pertussis toxins, of four predominate proteins in homogenates of rat cerebral cortex. These proteins showed apparent molecular masses of 20, 42, 45, and SO kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The 42- and 45-kDa proteins comigrated precisely with the major cholera toxin-labeled bands. Furthermore, the endogenous ADP-ribosylated and cholera toxin-ADP-ribosylated bands yielded identical 32p-labeled peptide fragments by one-dimensional peptide mapping, indicating that they are probably the same proteins, presumably the α-subunits of Gs. In contrast, peptide maps of the 50-kDa protein, which migrated close to a 48-kDa cholera toxin-labeled band, demonstrated that this protein is distinct from the toxin-labeled band and from Gsα. Levels of endogenous ADP-ribosylation activity showed regional heterogeneity in brain, with a nearly threefold variation observed among the brain regions examined. Chronic administration (7 days) of corticosterone significantly increased overall levels of endogenous ADP-ribosylation, indicating that components of this system may be under hormonal control in vivo. Attempts to identify neurotransmitters or second messenger systems that regulate endogenous ADP-ribosylation activity in brain have so far been unsuccessful with one exception. Sodium nitroprusside, which increases the formation of nitric oxide, dramatically stimulated the endogenous ADP-ribosylation of a 36-kDa protein, as reported previously by others, and, under certain conditions, also stimulated ADP-ribosylation of the 42-, 45-, and 50-kDa proteins, although to a lesser extent than the 36-kDa protein. These findings demonstrate that GSα and additional, as yet unidentified, proteins are ADP-ribosylated in brain in the absence of bacterial toxins and suggest that such endogenous covalent modification may regulate the functional activity of these proteins in vivo.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The influence of chronic administration of antidepressants on cyclic AMP-dependent protein kinase activity was examined in rat frontal cortex. Chronic administration of imipramine, tranylcypromine, or electroconvulsive seizures decreased cyclic AMP-dependent protein kinase activity in soluble fractions by ∼25%, whereas enzyme activity was increased in the particulate fractions by ∼20%. In contrast, enzyme activity in crude homogenates was not altered. This effect appears to be specific to antidepressant jdrugs, because representatives of several other classes of psychotropic drugs—namely, haloperidol, morphine, and diazepam—failed to alter either soluble or particulate levels of cyclic AMP-dependent protein kinase activity in this brain region following chronic administration. When the total particulate fraction was subfractionated, it was found that chronic imipramine treatment significantly increased the activity of cyclic AMP-dependent protein kinase in crude nuclear fractions but not in crude synaptosomal or microsomal fractions. Taken together, the data raise the possibility that chronic antidepressant treatments may stimulate the translocation of cyclic AMP-dependent protein kinase from the cytosol to the nucleus. This effect would represent a novel action of antidepressants that could contribute to the long-term adaptive changes in brain thought to be essential for the blinical actions of these treatments.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 63 (1994), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Based on the established role of β-adrenergic receptor kinase (βARK) and β-arrestin in the desensitization of several G protein-coupled receptors, we investigated the effect of chronic morphine administration on βARK and β-arrestin levels in selected brain areas. Levels of βARK were measured by blot immunolabeling analysis using antibodies specific for two known forms of βARK, i.e., βARK1 and βARK2. It was found that chronic morphine treatment produced an ∼35% increase in levels of βARK1 immunoreactivity in the locus coeruleus, but not in several other brain regions studied. In contrast, chronic morphine treatment failed to alter levels of βARK2 immunoreactivity in any of the brain regions studied. Levels of β-arrestin immunoreactivity, measured using an antiserum that recognizes two major forms of this protein in brain, were also found to increase (by ∼20%) in the locus coeruleus. It is proposed that chronic morphine regulation of βARK1 and β-arrestin levels may contribute to opioid-receptor tolerance that is known to occur in this brain region.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We studied the chronic actions of lithium on rat brain by investigating its effects on cyclic AMP-dependent protein phos-phorylation by use of a back-phosphorylation procedure. We identified one heavily regulated phosphoprotein in frontal cortex as the 32-kDa dopamine- and cyclic AMP-regulated phosphoprotein (DARPP-32). Immunoblot experiments demonstrated that chronic lithium regulation of DARPP-32 back-phosphorylation is associated with equivalent increases in levels of DARPP-32 immunoreactivity. Lithium regulation of DARPP-32 immunoreactivity required chronic drug administration and was not observed in several other brain regions examined. Moreover, chronic administration of the antidepressant imipramine or tranylcypromine produced a similar increase in levels of DARPP-32 in frontal cortex, whereas other types of psychotropic drugs, including haloperidol. morphine, and cocaine, did not influence DARPP-32 levels. Increased levels of DARPP-32 could reflect a common functional effect on frontal cortex of long-term exposure to lithium and some other antidepressant medications, an effect possibly related to the clinical actions of these drugs.
    Type of Medium: Electronic Resource
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