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  • 1
    Electronic Resource
    Electronic Resource
    Agonist-Dependent Internalization of γ-Aminobutyric AcidA/Benzodiazepine Receptors in Chick Cortical Neurons (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 57 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: An impermeant benzodiazepine receptor ligand was prepared by derivatization of the aminobenzodiazepine 1012-S with 4-sulfophenylisothiocyanate. The resulting N-sulfophenyl)-thiocarbamoyl derivative of 1012-S (SPTC-1012S) was purified by reverse-phase HPLC, and the predicted structure was verified by mass spectrometry. The apparent affinity of SPTC-1012S (IC50= 9.8 ± 2.9 nM) for displacement of [3H] flunitrazepam from intact chick cortical neurons was similar to that of 1012-S (IC50= 4.0 ±0.3 nM). However, at concentrations from 0.1 to 10 μM, 1012-S was consistently more efficacious than SPTC-1012S, a finding indicating that 6-8% of the benzodiazepine receptor pool was not accessible to the impermeant compound. This inaccessible pool was eliminated by permeabilization of the cells with saponin or Triton ±-100, a result suggesting that ∼7% of neuronal benzodiazepine receptors are intracellular. Acute treatment (1–4 h at 37°C) of neurons with 100μMγ-aminobutyric acid (GABA) or 100 nM clonazepam had little effect on the level of [3H] flunitrazepam binding but increased the proportion of intracellular receptors by 61 and 74%, respectively, compared with untreated controls. Similar treatment with 1 mM GABA increased the level of intracellular sites by 154–176%. The effect of GABA on receptor internalization was blocked by cotreatment with the GABAA receptor antagonist R 5135. The results suggest that SPTC-1012S can be used as a probe to study the internalization of the GABAA/benzodiazepine receptor complex under normal conditions or following acute or chronic treatment with agonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb08295.x
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  • 2
    Electronic Resource
    Electronic Resource
    Identification of GABAA/Benzodiazepine Receptors on Clathrin-Coated Vesicles from Rat Brain (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: To investigate the subcellular compartments that are involved in the endocytosis and intracellular trafficking of GABAA/benzodiazepine receptors, we have studied the distribution and properties of clonazepam-displaceable binding of [3H]flunitrazepam to membrane fractions from rat brain. The microsomal fraction was subjected to density centrifugation and gel filtration to isolate clathrin-coated vesicles. Homogeneity of the coated-vesicle fraction was demonstrated by using electron microscopy and by analysis of clathrin subunits and clathrin light-chain kinase. Vesicles exhibiting specific binding of [3H]flunitrazepam eluted from the sieving gel as a separate peak, which was coincident with that for coated vesicles. Scatchard analysis of equilibrium binding of [3H]flunitrazepam to coated vesicles yielded a KD value of 21 ± 4.7 nM and a Bmax value of 184 ± 28 fmol/mg. The KD value for coated vesicles was 12-19-fold that found with microsomal or crude synaptic membranes. This low-affinity benzodiazepine receptor was not identified on any other subcellular fraction and thus appears to be a novel characteristic of coated vesicles. The Bmaxvalue for coated vesicles, expressed per milligram of protein, corresponded to 16 and 115% of that found for crude synaptic and microsomal membrane fractions, respectively. Because the trafficking of neurotransmitter receptors via clathrin-coated vesicles is most likely to occur through endocytosis, the data suggest that an endocytotic pathway may be involved in the removal of GABAA/benzodiazepine receptors from the neuronal surfaces of the rat brain. This mechanism could play a role in receptor sequestration and down-regulation that is produced by exposure to GABA and benzodiazepine agonists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb13400.x
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  • 3
    Electronic Resource
    Electronic Resource
    Interferon Suppresses Sympathetic Neuronal Cell Death Caused by Nerve Growth Factor Deprivation (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: Cultured rat sympathetic neurons die within 48 h after being deprived of nerve growth factor. Addition of interferons (IFN-α/β or IFN-γ) prevented the cell death in a dose-dependent manner. Upon longer periods of nerve growth factor deprivation, IFNs failed to maintain survival. Thus, IFNs retarded neuronal death, but did not prevent it. Ligand binding, autoradiography, and cross-linking experiments demonstrated the presence of specific IFN-γ receptors on sympathetic neurons similar to those seen on other cell types. The possible relationships of the death-suppressing actions of IFNs are compared to the mechanisms of the antiviral or antiproliferative actions of IFNs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb04155.x
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  • 4
    Electronic Resource
    Electronic Resource
    Interaction of t-Butylbicyclophosphorothionate with γ-Aminobutyric Acid-Gated Chloride Channels in Cultured Cerebral Neurons (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The role of t-butylbicyclophosphorothionate (TBPS) as an antagonist of γ-aminobutyric acid (GABA) was studied with primary cultures of neurons from the chick embryo cerebrum. The addition of GABA stimulated the uptake of 36Cl− by neurons and the dose dependence of this effect followed hyperbolic kinetics with a K0.5= 1.3 μM for GABA. TBPS proved to be a potent inhibitor of GABA-dependent Cl− uptake (IC50= 0.30 μM). Analysis of the kinetics of this process revealed that TBPS is a noncompetitive inhibitor (Ki= 0.15 μM) with respect to GABA. Scatchard analysis of direct binding of [35S]TBPS to membranes isolated from neuronal cultures gave curvilinear plots. These could be resolved by nonlinear regression methods into two components with KD values of 3.1 nM and 270 nM. The TBPS binding constant for this lower affinity site agreed well with the IC50 and Ki values for inhibition of Cl− flux, suggesting that this site is physiologically relevant to GABA antagonism. GABA was a noncompetitive displacer of [35S]TBPS binding to the lower affinity site. The Ki value for this displacement by GABA (1.7 μM) was comparable to the value for GABA enhancement of Cl− flux. The binding of [35S]TBPS to its low-affinity site on neuronal membranes was ninefold higher in the presence of Cl− than with gluconate, an impermeant anion. The rank order for anion stimulation of [35S]TBPS binding was Br−≧ SCN− 〉 Cl−≧ NO−3 〉 I− 〉 F− 〉 gluconate. The EC50 value for Cl− enhancement of [35S]TBPS binding (160 mM) agreed well with the Km for Cl− influx via GABA-gated channels (140 mM). These results indicate that TBPS acts as a GABA antagonist via direct blockade of neuronal Cl− channels. A minimum density of 6.5 × 104 chloride channels per neuron was obtained from TBPS binding at saturation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb01774.x
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  • 5
    Electronic Resource
    Electronic Resource
    Multiple [35S]t-Butylbicyclophosphorothionate Binding Sites in Rat and Chicken Cerebral Hemispheres (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 45 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Specific binding of [35S]t-butylbicyclophosphorothionate (TBPS) to membranes from cerebral hemispheres of adult rat and chicken was determined over a range of radioligand concentrations from 0.25 to 500 nM. Scatchard plots of these data were curvilinear and non-linear regression analysis indicated binding to two sites that differ in affinity. For rat cerebrum, KD(1)= 1.15 nM, Bmax(1) 0.085 pmol/mg; KD(2)= 232 nM, Bmax(2)= 16.9 pmol/mg. For chicken cerebrum, KD(1)= 1.39 nM, Bmax(1)= 0.111 pmol/mg; KD(2)= 166 nM, Bmax(2)= 17.6 pmol/mg. This multiplicity of [35S]TBPS binding was further confirmed when unlabeled TBPS or picrotoxinin displaced radioligand. The displacement curves were biphasic and yielded Hill coefficients from 0.65 to 0.70. These displacement curves were also resolved into two components with distinct IC50 values for unlabeled TBPS (rat, 1.55 and 271 nM; chicken, 2.40 and 224 nM). The IC50 values were similar to the dissociation constants obtained from equilibrium binding measurements.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb05560.x
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  • 6
    Electronic Resource
    Electronic Resource
    Benzimidazole-5(6)-alanine and related compounds. I. Synthesis of amino acids as inhibitors of norepinephrine biosynthesis (1970)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 13 (1970), S. 741-742 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00298a038
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  • 7
    Electronic Resource
    Electronic Resource
    3-Alkyltyrosines. Potential antihypertensive agents (1971)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 14 (1971), S. 405-408 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00287a007
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  • 8
    Electronic Resource
    Electronic Resource
    MIXED-LINEAGE KINASES: A Target for the Prevention of Neurodegeneration (2004)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 44 (2004), S. 451-474 
    Details
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Notes: The activation of the c-Jun N-terminal kinase (JNK) pathway is critical for naturally occurring neuronal cell death during development and may be important for the pathological neuronal cell death of neurodegenerative diseases. The small molecule inhibitor of the mixed-lineage kinase (MLK) family of kinases, CEP-1347, inhibits the activation of the JNK pathway and, consequently, the cell death in many cell culture and animal models of neuronal death. CEP-1347 has the ability not only to inhibit cell death but also to maintain the trophic status of neurons in culture. The possible importance of the JNK pathway in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases provides a rationale for the use of CEP-1347 for the treatment of these diseases. CEP-1347 has the potential of not only retarding disease progression but also reversing the severity of symptoms by improving the function of surviving neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.pharmtox.44.101802.121840
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  • 9
    Electronic Resource
    Electronic Resource
    Isolation of Tunichrome B-1, a Reducing Blood Pigment of the Sea Squirt, Ascidia nigra (1986)
    s.l. : American Chemical Society
    Journal of natural products 49 (1986), S. 193-204 
    Details
    ISSN: 1520-6025
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/np50044a001
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  • 10
    Electronic Resource
    Electronic Resource
    The overall unit compressibility lines for real and simulated fluids (1990)
    s.l. : American Chemical Society
    Industrial & engineering chemistry research 29 (1990), S. 632-636 
    Details
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ie00100a021
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