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  • 1
    Electronic Resource
    Electronic Resource
    Spatiotemporal Interaction of α2 Autoreceptors and Noradrenaline Transporters in the Rat Locus Coeruleus (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We investigated the roles of α2 autoreceptors and noradrenaline (NA) transporters on NA efflux and uptake in the rat locus coeruleus after electrical stimulation. NA efflux was evoked by various trains (50 pulses, 10-500 Hz) and measured by fast cyclic voltammetry. NA efflux and uptake half-time (t1/2) were stimulus-dependent, ranging from 43 ± 3 nM and 2.45 ± 0.21 s, respectively, with 500-Hz stimuli to 127 ± 11 nM and 4.41 ± 0.34 s, respectively, with 100-Hz trains. Based on these data, we calculate that each transporter removes 0.19 NA molecules from the extracellular space every second, a velocity compatible more with transporter-than channel-mode conduction. Dexmedetomidine (10 nM) decreased NA efflux by ∼30% on stimulations of ≤1 s in duration. BRL 44408 (1 μM) increased NA efflux on stimuli of ≥2 s (by up to 92 ± 16%). Desipramine (50 nM) increased NA efflux on stimuli of ≥1 s (by 113 ± 24%) but slowed NA uptake on all stimuli. When given together, the effects of desipramine and BRL 44408 were additive at stimuli of ≥1 s but showed potentiation on shorter trains. There was a significant time delay for the elevation of NA efflux by blockade of uptake (0.79 s) or autoreceptors (1.14 s), suggesting that both are located extrasynaptically and that NA must diffuse through the extracellular space to these structures. We suggest that released NA may interact with α2 autoreceptors and NA transporters as far as 10 μm from the release sites, an action compatible with a volume transmission role of NA in the locus coeruleus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0742350.x
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  • 2
    Electronic Resource
    Electronic Resource
    Selective Increase of α2A-Adrenoceptor Agonist Binding Sites in Brains of Depressed Suicide Victims (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The α2A- and α2C-adrenoceptor subtypes were evaluated in postmortem brains from suicides with depression (n = 22), suicides with other diagnoses (n = 12), and controls (n = 26). Membrane assays with the antagonist [3H]RX821002 (2-[3H]methoxyidazoxan) suggested the presence of α2A-adrenoceptors in the frontal cortex and both α2C-adrenoceptors and α2A-adrenoceptors in the caudate. The proportions in caudate were similar in controls (α2A, 86%; α2C, 14%), depressed suicides (α2A, 91%; α2C, 9%), and suicides with other diagnoses (α2A, 88%; α2C, 12%). Autoradiography of [3H]RX821002 binding under α2B/C-adrenoceptor-masking conditions confirmed the similar densities of α2A-adrenoceptors in the cortex, hippocampus, and striatum from controls and suicides. In the frontal cortex of depressed suicides, competition of [3H]RX821002 binding by (−)-adrenaline revealed a greater proportion (61 ± 9%) of α2A-adrenoceptors in the high-affinity conformation for agonists than in controls (39 ± 5%). Simultaneous analysis with the agonists [3H]clonidine and [3H]UK14304 and the antagonist [3H]RX821002 in the same depressed suicides confirmed the enhanced α2A-adrenoceptor density when evaluated by agonist, but not by antagonist, radioligands. The results indicate that depression is associated with a selective increase in the high-affinity conformation of the brain α2A-adrenoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70031114.x
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  • 3
    Electronic Resource
    Electronic Resource
    Altered presynaptic function in monoaminergic neurons of monoamine oxidase-A knockout mice (2002)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 15 (2002), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Monoamine oxidase-A knockout (MAO-A KO) mice have elevated brain serotonin (5-HT) and noradrenaline (NA) levels, and one would therefore anticipate increased monoamine release and compensatory changes in other aspects of presynaptic monoamine function. In this study we used voltammetry in brain slices from the locus coeruleus (LC), dorsal raphe (DRN) and striatum (CPu) in 7-week-old MAO-A KO and C3H control mice to measure stimulated monoamine efflux and its control by amine transporters and autoreceptors. In LC, peak NA efflux on stimulation (99 pulses, 100 Hz) was higher in MAO-A KO than C3H mice (938 ± 58 nm cf. 511 ± 42 nm; P 〈 0.001). The NA uptake half time (t½) was longer in MAO-A KO than in C3H mice (6.0 ± 0.9 s cf. 1.9 ± 0.3 s; P 〈 0.001) and the selective NA reuptake inhibitor desipramine (50 nm) had a smaller effect in MAO-A KO mice. NA transporter binding was significantly lower in the LC of MAO-A KO mice compared to C3H controls (P 〈 0.01) but not in the DRN. The α2 agonist dexmedetomidine (10 nm) decreased stimulated NA efflux more in C3H than in MAO-A KO mice (73.3% cf. 29.6% inhibition, P 〈 0.001). In DRN, peak 5-HT efflux on stimulation (99 pulses, 100 Hz) was greater (P 〈 0.01) in MAO-A KO (262 ± 44 nm) than C3H mice (157 ± 16 nm). Moreover, 5-HT uptake t½ was longer (P 〈 0.05) in MAO-A KO than in C3H mice (8.8 ± 1.1 s cf. 4.9 ± 0.6 s, P 〈 0.05) and the effect of citalopram (75 nm) was attenuated in MAO-A KOs. Serotonin transporter binding was also lower in both the DRN and LC of MAO-A KO mice. The 5-HT1A agonist 8-OH-DPAT (1 µm) decreased 5-HT efflux more in C3H than in MAO-A KO mice (38.3% inhibition cf. 21.6%, P 〈 0.001). In contrast, there were no significant differences between MAO-A KO and C3H mice in CPu dopamine efflux and uptake and the effect of the D2/3 agonist quinpirole was similar in the two strains. In summary, MAO-A KO mice show major dysregulation of monoaminergic presynaptic mechanisms such as autoreceptor control and transporter kinetics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2002.01986.x
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