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  • 1
    Electronic Resource
    Electronic Resource
    γ-Hydroxybutyrate modulation of glutamate levels in the hippocampus: an in vivo and in vitro study (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of γ-hydroxybutyric acid on extracellular glutamate levels in the hippocampus was studied by microdialysis in freely moving rats and in isolated hippocampal synaptosomes. Intra-hippocampal (CA1) perfusion with γ-hydroxybutyric acid (10 nm–1 mm) concentration-dependently influenced glutamate levels: γ-hydroxybutyric acid (100 and 500 nm) increased glutamate levels; 100 and 300 µm concentrations were ineffective; whereas the highest 1 mm concentration reduced local glutamate levels. The stimulant effect of γ-hydroxybutyric acid (100 nm) was suppressed by the locally co-perfused γ-hydroxybutyric acid receptor antagonist NCS-382 (10 µm) but not by the GABAB receptor antagonist CGP-35348 (500 µm). Furthermore, the γ-hydroxybutyric acid (1 mm)-induced reduction in CA1 glutamate levels was counteracted by NCS-382 (10 µm), and it was also reversed into an increase by CGP-35348. Given alone, neither NCS-382 nor CGP-35348 modified glutamate levels. In hippocampal synaptosomes, γ-hydroxybutyric acid (50 and 100 nm) enhanced both the spontaneous and K+-evoked glutamate efflux, respectively, both effects being counteracted by NCS-382 (100 nm), but not by CGP-35348 (100 µm). These findings indicate that γ-hydroxybutyric acid exerts a concentration-dependent regulation of hippocampal glutamate transmission via two opposing mechanisms, whereby a direct γ-hydroxybutyric acid receptor mediated facilitation is observed at nanomolar γ-hydroxybutyric acid concentrations, and an indirect GABAB receptor mediated inhibition predominates at millimolar concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00530.x
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  • 2
    Electronic Resource
    Electronic Resource
    Selective γ-hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of γ-hydroxybutyric acid (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 87 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Two γ-hydroxybutyric acid (GHB) analogues, trans-γ-hydroxycrotonic acid (t-HCA) and γ-(p-methoxybenzyl)-γ-hydroxybutyric acid (NCS-435) displaced [3H]GHB from GHB receptors with the same affinity as GHB but, unlike GHB, failed to displace [3H]baclofen from GABAB receptors. The effect of the GHB analogues, GHB and baclofen, on G protein activity and hippocampal extracellular glutamate levels was compared. While GHB and baclofen stimulated 5′-O-(3-[35S]thiotriphospate) [35S]GTPγS binding both in cortex homogenate and cortical slices, t-HCA and NCS-435 were ineffective up to 1 mm concentration. GHB and baclofen effect was suppressed by the GABAB antagonist CGP 35348 but not by the GHB receptor antagonist NCS-382. Perfused into rat hippocampus, 500 nm and 1 mm GHB increased and decreased extracellular glutamate levels, respectively. GHB stimulation was suppressed by NCS-382, while GHB inhibition by CGP 35348. t-HCA and NCS-435 (0.1–1000 µm) locally perfused into hippocampus increased extracellular glutamate; this effect was inhibited by NCS-382 (10 µm) but not by CGP 35348 (500 µm). The results indicate that GHB-induced G protein activation and reduction of glutamate levels are GABAB-mediated effects, while the increase of glutamate levels is a GHB-mediated effect. Neither t-HCA nor NCS-435 reproduced GHB sedative/hypnotic effect in mice, confirming that this effect is GABAB-mediated. The GHB analogues constitute important tools for understanding the physiological role of endogenous GHB and its receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.02037.x
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  • 3
    Electronic Resource
    Electronic Resource
    Differential Effects of lntrastriatal Neurotensin(1–13) and Neurotensin(8–13) on Striatal Dopamine and Pallidal GABA Release. A Dual-probe Microdialysis Study in the Awake Rat (1997)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 9 (1997), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the present dual-probe microdialysis study the effects of intrastriatal perfusion with the tridecapeptide neurotensin(1–13) [NT(1–13)] and its active fragment NT(8–13) on striatopallidal GABA and striatal dopamine release were investigated. The modulatory action of NT(1–13) on D2 receptor-mediated inhibition of striatal and pallidal GABA release was also studied. Both intrastriatal NT(1–13) (100 nM) and NT(8–13) (100 nM) increased striatal (139 and 149% respectively) and pallidal (130 and 164%) GABA release, and this effect was antagonized by intrastriatal perfusion with the neurotensin receptor antagonist SR48692 (100 nM). A similar increase (155%) in striatal dopamine release was observed following intrastriatal NT(1–13) (100 nM), but not NT(8–13) (100 and 500 nM). However, at the highest concentration studied (1 μM) NT(8–13) was associated with a rapid increase (130%) in striatal dopamine release. In a second study intrastriatal NT(1–13) (10 nM) counteracted the inhibition of striatal and pallidal GABA release induced by pergolide (500 and 1500 nM). The inhibitory action of the D2 agonist was restored when SR48692 (100 nM) was added to the perfusion medium. These results suggest that in the neostriatum the neurotensin receptor located postsynaptically on the striatopallidal GABA neurons seems to differ from the neurotensin receptor located on dopaminergic terminals, as indicated by the relative lack of effect of NT(8–13) on striatal dopamine release. Furthermore, the ability of NT(1–13) to counteract the pergolide-induced inhibition of both striatal and pallidal GABA release strengthens the evidence for antagonistic receptor-receptor interaction between postsynaptic striatal neurotensin and D2 receptors located on striatopallidal GABA neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1997.tb00750.x
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    Paper (German National Licenses)
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