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Mechanisms of [3H]glycine release from mouse spinal cord synaptosomes selectively labelled through GLYT2 transporters
No full textGlycinergic nerve endings in hippocampus and spinal cord release glycine by different mechanisms in response to identical depolarizing stimuli
No full textNeuropeptide S selectively inhibits the release of 5-HT and noradrenaline from mouse frontal cortex nerve endings
No full textBackground and purpose: Neuropeptide S (NPS) is a recently identified neurotransmitter/neuromodulator able to increase arousal and wakefulness while decreasing anxiety-like behaviour. As several classical transmitters play a role in arousal and anxiety, we here investigated the possible presynaptic regulation of transmitter release by NPS. Experimental approach: Synaptosomes purified from mouse frontal cortex were prelabelled with [(3)H]5-hydroxytryptamine (5-HT), noradrenaline, dopamine, choline, D-aspartate or GABA and depolarized in superfusion with 12-15 mmol.L(-1) KCl to evoke [(3)H]neurotransmitter exocytosis. NPS was added at different concentrations (0.001 to 100 nmol.L(-1)). Key results: NPS behaved as an extremely potent inhibitor of the evoked overflow of [(3)H]5-HT and [(3)H]noradrenaline exhibiting EC(50) values in the low picomolar range. The inhibitory action of NPS on [(3)H]5-HT release was mimicked by [Ala(2)]NPS that was, however, about 100-fold less potent than the natural peptide. NPS (up to 100 nmol.L(-1)) was unable to affect the depolarization-evoked overflow of [(3)H]D-aspartate and [(3)H]GABA. The neuropeptide only weakly reduced the overflow of [(3)H]dopamine and [(3)H]ACh when added at relatively high concentrations. Conclusions and implications: NPS, at low picomolar concentrations, can selectively inhibit the evoked release of 5-HT and noradrenaline in the frontal cortex by acting directly on 5-hydroxytryptaminergic and noradrenergic nerve terminals. These direct effects may explain only in part the unique behavioural activities of NPS, while an indirect involvement of other transmitters, especially of glutamate, must be considered
The GABA(B) receptor antagonists CGP35348 and CGP52432 inhibit glycine exocytosis: study with GABA(B1)- and GABA(B2)-deficient mice
No full textGABA(B) presynaptic receptors modulate glycine exocytosis from mouse spinal cord and hippocampus glycinergic nerve endings
No full textGlycine release and modulation of glycine exocytosis by presynaptic receptors have been rarely studied. We here investigate on the existence and the pharmacological profile of GABAB receptors regulating glycine release in mouse spinal cord and hippocampus. Synaptosomes were preincubated with [3H]glycine in presence of the glycine transporter 1 inhibitor NFPS, in order to study release from glycinergic terminals selectively labelled through the glycine transporter 2, and depolarized in superfusion with concentrations of KCl (12 and 15mM) previously found to elicit exocytosis of glycine. Exposure of synaptosomes to (−)-baclofen caused inhibition of [3H]glycine overflow: EC50 = 0.62±0.08 μM, Emax ~ 65% in the spinal cord and EC50 = 0.58±0.07 μM, Emax ~ 55% in the hippocampus. The effect of 3μM (−)-baclofen in the spinal cord was prevented by the GABAB receptor antagonists CGP 52432 (IC50 = 22.6±2.15 μM) and CGP 35348 (IC50 = 5.99±1.21 μM), whereas phaclofen was ineffective. In the hippocampus, the CGP antagonists were more potent than in the spinal cord, their IC50 values amounting to 0.81±0.08 μM and to 0.94±0.09 μM, respectively; phaclofen (100–300 μM) was a weak antagonist. It is concluded that: (i) glycinergic nerve terminals in spinal cord and hippocampus possess GABAB receptors mediating inhibition of the evoked glycine exocytosis; (ii) the pharmacological profiles of the receptors are qualitatively similar in the two regions; (iii) low concentrations of GABAB antagonists appear able to preferentially inhibit the receptors located on hippocampal glycinergic nerve endings
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Trafficking of presynaptic AMPA receptors mediating neurotransmitter release: neuronal selectivity and relationship with sensitviity to cyclothiazide
No full textIonic dysregulations typical of ischemia provoke release of glycine and GABA by multiple mechanisms
No full textFunctional interactions between presynaptic NMDA receptors and metabotropic glutamate receptors co-expressed on rat and human noradrenergic terminals
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