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  • 1
    Electronic Resource
    Electronic Resource
    LSD and DOB: interaction with 5-HT2A receptors to inhibit NMDA receptor-mediated transmission in the rat prefrontal cortex (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Both the phenethylamine hallucinogen (–)-1-2,5-dimethoxy-4-bromophenyl-2-aminopropane (DOB), a selective serotonin 5-HT2A,2C receptor agonist, and the indoleamine hallucinogen d-lysergic acid diethylamide (LSD, which binds to 5-HT1A, 1B, 1D, 1E, 1F, 2A, 2C, 5, 6, 7, dopamine D1 and D2, and α1 and α2 adrenergic receptors), but not their non-hallucinogenic congeners, inhibited N-methyl-d-aspartate (NMDA)-induced inward current and NMDA receptor-mediated synaptic responses evoked by electrical stimulation of the forceps minor in pyramidal cells of the prefrontal cortical slices. The inhibitory effect of hallucinogens was mimicked by 5-HT in the presence of selective 5-HT1A and 5-HT3 receptor antagonists. The inhibitory action of DOB, LSD and 5-HT on the NMDA transmission was blocked by the 5-HT2A receptor antagonists r-(+)-α-(2,3-dimethoxyphenil)-1-[4-fluorophenylethyl]-4-piperidinemethanol (M100907) and ketanserin. However, at low concentrations, when both LSD and DOB by themselves only partially depressed the NMDA response, they blocked the inhibitory effect of 5-HT, suggesting a partial agonist action. Whereas N-(4-aminobutyl)-5-chloro-2-naphthalenesulphonamide (W-7, a calmodulin antagonist) and N-[2-[[[3-(4′-chlorophenyl)- 2-propenyl]methylamino]methyl]phenyl]-N-(2-hydroxyethyl)-4′-methoxy-benzenesulphonamide phosphate (KN-93, a Ca2+/CaM-KII inhibitor), but not the negative control 2-[N-4′methoxybenzenesulphonyl]amino-N-(4′-chlorophenyl)-2-propenyl-N-methylbenzylamine phosphate (KN-92), blocked the inhibitory action of LSD and DOB, the selective protein kinase C inhibitor chelerythrine was without any effect. We conclude that phenethylamine and indoleamine hallucinogens may exert their hallucinogenic effect by interacting with 5-HT2A receptors via a Ca2+/CaM-KII-dependent signal transduction pathway as partial agonists and modulating the NMDA receptors-mediated sensory, perceptual, affective and cognitive processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00726.x
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  • 2
    Electronic Resource
    Electronic Resource
    A pre- and postsynaptic modulatory action of 5-HT and the 5-HT2A, 2C receptor agonist DOB on NMDA-evoked responses in the rat medial prefrontal cortex (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Intracellular recordings were made from pyramidal neurons in layers V and VI of the rat medial prefrontal cortex in slice preparations to investigate the effect of the serotonin 5-HT2A,2C receptor agonist (–)-1-2,5-dimethoxy-4-bromophenol-2-aminopropane (DOB) and 5-hydroxytryptamine (5-HT) on N-methyl- d-aspartate (NMDA)-induced responses. Bath application of either DOB or 5-HT [in the presence of antagonists to 5-HT1A, 5-HT3 and γ-aminobutytric acid (GABA) receptors] produced a concentration-dependent biphasic modulation of the NMDA responses. They facilitated and inhibited NMDA responses at low (≤ 1 μm DOB and ≤ 50 μm 5-HT) and higher concentrations, respectively. Both the facilitating and inhibitory action were blocked by the highly selective 5-HT2A receptor antagonist r-(+)-α-(2,3-dimethoxyphenil)-1-[4-fluorophenylethyl]-4-piperidinemethanol (M100907) and the 5-HT2 receptor antagonist ketanserin, thus indicating that both facilitation and inhibition were mediated by the activation of the 5-HT2A receptor subtype. However, the facilitating, but not inhibitory, action of DOB showed a marked desensitization, suggesting that the facilitation and inhibition of NMDA responses resulted from activation of different 5-HT2A receptor subtypes and/or signal-transduction pathways. Indeed, the selective PKC inhibitor chelerythrine and the Ca2+/CaM-KII inhibitor KN-93 prevented the facilitating and inhibitory action of DOB, respectively. We have generated several lines of evidence to indicate the following scenario. Low concentrations of DOB, at presynaptic nerve terminals, markedly enhance NMDA-induced release of excitatory amino acids (EAAs), which then act upon both NMDA and non-NMDA receptors to elicit inward current. The massive inward current masks the postsynaptic inhibitory action of DOB. At higher concentrations, DOB inhibits the release of EAAs and discloses the postsynaptic inhibitory action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00708.x
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  • 3
    Electronic Resource
    Electronic Resource
    The effects of short-chain fatty acids on the neuronal membrane functions ofHelix pomatia. II. cholinoreceptive properties (1986)
    Springer
    Cellular and molecular neurobiology 6 (1986), S. 165-175 
    Details
    ISSN: 1573-6830
    Keywords: membrane receptor ; fluidity ; acetylcholine ; decenoic acid ; valeric acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. We have examined the effects of short-chain fatty acids on acetylcholine (ACh)-induced transmembrane currents using internally dialized neurons ofHelix. 2. Decenoic acid, which increased the fluidity of excitable membranes, caused dramatic changes in the voltage sensitivity of ACh currents consisting of an ACh-induced increase in membrane permeability for K+ and Na+ ions and a shift of theE rev of these ACh responses to more positive potentials. Valeric acid, which did not change the membrane fluidity, had no effect on this type of ACh response. 3. Changes of theE Na andE Cl had no effect on the size of the decenoic acid-induced shift of theE rev. But the influence of decenoic acid on the voltage sensitivity of ACh-induced currents almost disappeared after the change of theE K by the reduction of the internal K concentration. 4. Decenoic acid had no effect on ACh responses in which K+ ions were not involved in the generation of ACh-induced currents. 5. The results suggest that decenoic acid-induced changes in membrane fluidity modulate cholinoreceptive properties of the neuronal membrane by the inhibition of the K+ carrier involved in the generation of ACh responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711068
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    Paper (German National Licenses)
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