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  • 1
    Online Resource
    Online Resource
    Neuropharmacology : Studies of Narcotic Drugs. (1975)
    San Diego :Elsevier Science & Technology,
    Details
    Keywords: Narcotics. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (65 pages)
    Edition: 1st ed.
    ISBN: 9781483140001
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=1604022
    Language: English
    Note: Front Cover -- Neuropharmacology -- Copyright Page -- CHAPTER 1. CHOLINERGIC MECHANISMS IN NARCOTICANALGESICS -- REFERENCES -- CHAPTER 2. THE USE OF AMINE FLUORESCENCEHISTOCHEMISTRY IN THE STUDY OF DRUGS,ESPECIALLY MORPHINE, ON THE CNS -- REFERENCES -- CHAPTER 3. EFFECT OF METHADONE AND DEXTROMORAMIDEON DOPAMINE METABOLISM: COMPARISON WITHHALOPERIDOL AND AMPHETAMINE -- EFFECT ON ADENYLATE CYCLASE -- CONCLUSIONS -- REFERENCES -- CHAPTER 4. PREDICTIVE VALUES OF PHARMACOLOGICALMODELS TO STUDY OPIATE DEPENDENCE -- REFERENCES -- CHAPTER 5. ACTION OF OPIATES, ANTIPSYCHOTICS,AMPHETAMINE AND APOMORPHINE ON DOPAMINERECEPTORS IN RAT STRIATUM: IN VIVO CHANGES OF3,5-CYCLIC AMP CONTENT AND ACETYLCHOLINETURNOVER RATE -- INTRODUCTION -- EXPERIMENTAL STUDIES -- REFERENCES -- CHAPTER 6. STRUCTURAL FEATURES ASSOCIATED WITHNARCOTICS AND NARCOTIC ANTAGONISTS -- REFERENCES.
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  • 2
    Online Resource
    Online Resource
    Neuroplasticity : New Biochemical Mechanisms. (2012)
    Tarporley :Springer Healthcare,
    Details
    Keywords: Neuroplasticity. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (78 pages)
    Edition: 1st ed.
    ISBN: 9781908517180
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=884466
    DDC: 612.82
    Language: English
    Note: Title Page -- Copyright Page -- Table of Contents -- CONTRIBUTOR BIOGRAPHIES -- FOREWORD -- NEUROPLASTICITY - A NEW APPROACH TO THE PATHOPHYSIOLOGY OF DEPRESSION -- I Introduction -- II From neurotransmitter deficits to neuroplasticity - the evolution of a concept -- III Depression and reduced hippocampal volume -- IV Structural plasticity beyond the hippocampus -- V Structural plasticity of glutamatergic axons -- VI The impact of glia -- VII Conclusions -- References -- GLUTAMATE-MEDIATED NEUROPLASTICITY DEFICITS IN MOOD DISORDERS -- I Introduction -- II The glutamatergic system -- III Glutamatergic projections and anatomical substrates of mood-related disorders -- IV Glutamatergic alterations in psychiatric illness: clinical evidence -- Depressive illness -- Anxiety disorders -- V Understanding glutamate's involvement in neuroplasticity: functional implications in relation to psychiatric illness -- Long-term potentiation -- Morphological plasticity -- Treatment implications -- VI Conclusions -- References -- REGULATION OF CELLULAR PLASTICITY IN MOOD DISORDERS: THE ROLE OF THE AMPA RECEPTOR -- I Introduction -- II Neuroplasticity, glutamate, and glutamate receptors -- III Glutamate receptors -- IV NMDA receptors and their interaction with AMPA receptors -- V AMPA receptors -- VI Effects of stress on glutamate and glutamate receptors -- VII AMPA receptor phosphorylation and tianeptine -- VIII Relationships between AMPA receptor phosphorylation and antidepressant effect -- IX Conclusions -- References -- CELLULAR PLASTICITY AND THE PATHOPHYSIOLOGY OF DEPRESSION -- I Introduction -- II Depression-induced changes in brain morphology and function -- III Effects of stress and depression on the hippocampus -- IV Beyond the hippocampus: the prefrontal cortex -- V Animal models of depression. , VI Effects of stress on glutamatergic neurotransmission in the hippocampus -- VII Structural changes -- VIII Modulation of stress-induced changes in the glutamate system -- Effects of tianeptine on preventing stress-induced impairment in LTP -- Effects of tianeptine on inhibiting glutamate-dependent stress-induced changes in hippocampal morphology -- Effects of tianeptine on inhibiting stress-induced changes in glutamatergic neurotransmission -- IX Clinical implications -- X Conclusions -- References -- CLINICAL CONSEQUENCES OF THE ROLE OF GLUTAMATE AND NEUROPLASTICITY IN DEPRESSIVE DISORDER -- I Introduction -- II Relevency of stress in the model of depression regarding the role of europlasticity -- III The place of neuroplasticity in the delay before treatment efficacy can be observed -- IV The role of neuroplasticity and glutamate in non-pharmacological treatments -- V Are depressive episodes neurotoxic? -- VI Conclusions -- References -- Index.
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  • 3
    Online Resource
    Online Resource
    Licenciamento Ambiental Municipal de Natal/RN : Desafios e Barreiras Na Simplificação de Procedimentos. (2023)
    Belo Horizonte :Editora Dialética,
    Details
    Keywords: Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (129 pages)
    Edition: 1st ed.
    ISBN: 9786527003335
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=30828776
    Language: Portuguese
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  • 4
    Electronic Resource
    Electronic Resource
    Imidazenil: A Potent Benzodiazepine Partial Positive Modulator of GABAergic Transmission Virtually Devoid of Tolerance Liability (1995)
    Oxford, UK : Blackwell Publishing Ltd
    CNS drug reviews 1 (1995), S. 0 
    Details
    ISSN: 1527-3458
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3458.1995.tb00282.x
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  • 5
    Electronic Resource
    Electronic Resource
    Stimulation of Brain Pregnenolone Synthesis by Mitochondrial Diazepam Binding Inhibitor Receptor Ligands In Vivo (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Evidence that neurosteroids are potent modulators of the action of GABA at GABAA receptors has prompted the investigation of the mechanism that controls brain neurosteroid synthesis by glial cell mitochondria in vivo. In vitro studies suggest that the interaction of the diazepam binding inhibitor (DBI)—a polypeptide that is abundant in steroidogenic cells—with glial mitochondrial DBI receptors (MDRs) is a crucial step in the physiological regulation of neurosteroid biosynthesis. MDRs bind 4-chlorodiazepam (4′-CD), N,N-di-n-hexyl-2-(4-fluorophenyl)-indol-3-acetamide (FGIN-1–27), and the isoquinoline carboxamide PK 11195 with high affinity, and these ligands have been used to investigate whether the stimulation of glial MDRs increases brain pregnenolone production in vivo. Adrenalectomized and castrated (A-C) male rats (to eliminate peripheral sources of pregnenolone) were pretreated with trilostane (to prevent pregnenolone metabolism to progesterone), and the pregnenolone content in brain regions dissected after fixation with a 0.8-s exposure to microwave irradiation focused to the head was determined by HPLC followed by specific radioimmunoassay. The forebrain and cerebellum of A-C rats contained 4–7 ng of pregnenolone/g of tissue, and the olfactory bulb contained 10–14 ng/g. These concentrations of brain pregnenolone are only 30–40% lower than those of shamoperated rats. In contrast, the plasma pregnenolone content of sham-operated rats was 2–3 ng/ml, but it was only 0.15–0.20 ng/ml in the plasma of A-C rats. In A-C rats, treatment with the MDR ligands 4-CD and FGIN-1–27 increased the pregnenolone content in the brain but failed to change the plasma or peripheral tissue content of this steroid. The effect of 4′-CD on brain pregnenolone content was maximal (70–100% increase) at the dose of 18 μmol/kg, 5–10 min after intravenous injection. The effect of oral administration of FGIN-1–27 on brain pregnenolone content was maximal (80–150% increase) at doses of 400–800 μmollkg and peaked at ∼ 1 h. That this effect of FGIN-1–27 was mediated by the MDR was documented by pre-treatment with the MDR partial agonist PK 11195 (100 μmol/kg, i.p.). PK 11195 did not affect basal brain pregnenolone content but prevented the accumulation of brain pregnenolone induced by FGIN-1–27. FGIN-1–27 and 4-CD failed to increase the brain concentration of dehydre epiandrosterone in A-C rats. These data suggest that glial cell MDRs play a role in neurosteroid biosynthesis in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb13647.x
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  • 6
    Electronic Resource
    Electronic Resource
    Islet-Activating Protein Inhibits the β-Adrenergic Receptor Facilitation Elicited by γ-Aminobutyric AcidB Receptors (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: γ-Aminobutyric acidB (GABAB) receptor recognition sites that inhibit cyclic AMP formation, open potassium channels, and close calcium channels are coupled to these effector systems by guanine nucleotide binding proteins (G proteins). These G proteins are ADP-ribosylated by islet-activating protein (IAP), also known as pertussis tokin. This process prevents receptor coupling to these G proteins. In slices of cerebral cortex and hippocampus from rat, stimulation of GABAB receptors with baclofen, a receptor agonist, also potentiates the accumulation of cyclic AMP stimulated by β-adrenergic agonists. It was unknown whether those GA-BAB receptors that potentiate the β-adrenergic response were also sensitive to IAP. IAP was injected intracerebroventric-ularly into rats to ADP-ribosylate IAP-sensitive G proteins. Four days after the IAP injection, 38% and 52% of these G proteins from cerebral cortex and hippocampus, respectively, were ADP-ribosylated by the IAP injection. In slices of both structures prepared from IAP-treated rats, the GABAB receptor-mediated potentiation of the β-adrenergic receptor response was attenuated. Thus, many GABAB receptor-mediated responses are coupled to IAP-sensitive G proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11769.x
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  • 7
    Electronic Resource
    Electronic Resource
    Magnesium Ions Inhibit the Stimulation of Inositol Phospholipid Hydrolysis by Endogenous Excitatory Amino Acids in Primary Cultures of Cerebellar Granule Cells (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 48 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Omission of Mg2+ from the incubation buffer results in a six- to eightfold increase in [3H]inositol-1-phosphate ([3H]Ins-1-P) accumulation in primary cultures of cerebellar granule cells at 7–9 days in vitro. This increase is reversed by low concentrations of 2-amino-5-phosphonovalerate (APV), a result indicating that the absence of Mg2+ facilitates the activation of a specific receptor by the endogenous excitatory amino acids (presumably l-glutamate and l-aspartate) released from the granule cells. The absence of Mg2+ also potentiates the action of exogenously applied N-methyl-d-aspartate (NMDA), l-glutamate, l-aspartate, and kainate. In contrast, the action of quisqualate is virtually unaffected by Mg2+ and is resistant to APV inhibition. Addition of the depolarizing agent veratridine enhances the accumulation of [3H]Ins-1-P also in Mg2+-containing buffer. The action of veratridine is antagonized by APV, a result suggesting that, under depolarized conditions, the NMDA receptor can be activated by the endogenously released excitatory amino acids, despite the presence of Mg2+. Accordingly, in the presence of Mg2+, veratridine potentiates the action of exogenously applied NMDA but does not facilitate the action of quisqualate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb05611.x
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  • 8
    Electronic Resource
    Electronic Resource
    Regionaland Interspecies Differences in Brain Progesterone Metabolism (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Metabolites of [3H]progesterone were studied in slices prepared from different brain regions of male rat, mouse, and monkey. The major metabolites were 5α-dihydroprogesterone (5α-DHP) and 3α,5α-tetrahydroprogesterone (3α,5α-THP) in rat brain slices, 5α-DHP and 20α- dihydroprogesterone (20α-DHP) in mouse brain slices, and 20α-DHP in monkey brain slices. In rat olfactory bulb slices, 5α-DHP represented 25.2 ± 3.3% of total radioactivity and 3α,5α-THP 17.5 ± 2.8%, whereas in rat medulla oblongata slices, 5α-DHP was 31.3 ± 3.5% and 3α,5α- THP 5.4 ± 1.5% of total radioactivity. In slices from other rat brain regions, both metabolites represented 12–20% of total radioactivity.-The highest metabolite content in mouse brain was also detected in olfactory bulb slices, where 5α-DHP represented 16.6 ± 4.6% and 20α-DHP 9.5 ± 2.3% of total radioactivity. In cortical and corpus callosum slices of monkey brain, 26.8 ± 4.4% and 2.4 ± 0.5% of total radioactivity, respectively, were converted to 20α-DHP, and less than 3% of total radioactivity could be attributed to any of the other metabolites detected. The 3α,α-THP content in both rat and monkey brain was below 1 nM, but increased in rat brain to 6.7 ± 2.5 nM after electroshock. Endogenous 3α,5α-THP might play an important role in the regulation of rat behavior through the modulation of GABA action on the GABAA receptor. The significant interspecies differences in the brain progesterone metabolism should be considered in evaluating the functional role of neurosteroids in various species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb07440.x
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  • 9
    Electronic Resource
    Electronic Resource
    N-Methyl-d-Aspartate-Sensitive Glutamate Receptors Induce Calcium-Mediated Arachidonic Acid Release in Primary Cultures of Cerebellar Granule Cells (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In primary cultures of cerebellar granule cells, glutamate, aspartate, and N-methyl-d-aspartate (NMDA) induced a dose-dependent release of [3H]arachidonic acid ([3H]AA) which was selective for these agonists and was inhibited by NMDA receptor antagonists. The agonist-induced [3H]AA release was reduced by quinacrine at concentrations that inhibited phospholipase A2 (PLA2) but affected neither the activity of phospholipase C (PLC) nor the hydrolysis of phosphoinositides induced by glutamate or quisqualate. Thus, the increased formation of AA was due to the receptor-mediated activation of PLA2 rather than to the action of PLC followed by diacylglycerol lipase. The receptor-mediated [3H]AA release was dependent on the presence of extracellular Ca2+ and was mimicked by the Ca2+ ionophore ionomycin. Pretreatment of granule cells with either pertussis or cholera toxin failed to inhibit the receptor-mediated [3H]AA release. Hence, in cerebellar granule cells, the stimulation of NMDA-sensitive glutamate receptors leads to the activation of PLA2 that is mediated by Ca2+ ions entering through the cationic channels functioning as effectors of NMDA receptors. A coupling through a toxin-sensitive GTP-binding protein can be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb05771.x
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  • 10
    Electronic Resource
    Electronic Resource
    Isolation and Characterization of a Rat Brain Triakontatetraneuropeptide, a Posttranslational Product of Diazepam Binding Inhibitor: Specific Action at the Ro 5-4864 Recognition Site (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: This report describes the purification and characterization from rat brain of triakontatetraneuropeptide (TTN, DBI 17-50), a major biologically active processing product of diazepam binding inhibitor (DBI). Brain TTN was purified by immunoaffinity chromatography with polyclonal octa-decaneuropeptide, DBI 33-50) antibodies coupled to CNBr-Sepharose 4B followed by two reverse-phase HPLC steps. The amino acid sequence of the purified peptide is: Thr-Gln-Pro-Thr-Asp-Glu-Glu-Met-Leu-Phe-Ile-Tyr-Ser-His-Phe-Lys-Gln-Ala-Thr-Val-Gly-Asp-Val-Asn-Thr-Asp-Arg-Pro-Gly-Leu-Leu-Asp-Leu-Lys. Synthetic TTN injected intra-cerebroventricularly into rats induces a proconflict activity (IC50 0.8 nmol/rat) that is prevented by the specific “peripheral” benzodiazepine (BZ) receptor antagonist isoquinoline carboxamide, PK 11195, but not by the “central” BZ receptor antagonist imidazobenzodiazepine, flumazenil. TTN displaces [3H]Ro 5-4864 from synaptic membranes of olfactory bulb with a Ki of approximately 5 μM. TTN also enhances picrotoxinin inhibition of γ-aminobutyric acid (GABA)-stimulated [3H]flunitrazepam binding. These data suggest that TTN, a natural DBI processing product acting at “Ro 5-4864 preferring” BZ binding site subtypes, might function as a putative neuromodulator of specific GABAA receptor-mediated effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07425.x
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