Research reportRelease of serotonin induced by 3,4-methylenedioxymethamphetamine (MDMA) and other substituted amphetamines in cultured fetal raphe neurons: further evidence for calcium-independent mechanisms of release
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Melanin-concentrating hormone does not modulate serotonin release in primary cultures of fetal raphe nucleus neurons
2019, NeuropeptidesCitation Excerpt :In particular, primary cell cultures from the raphe nuclei at E14 have been reported to contain serotonergic neurons with specific in vivo features: 5-HT synthesis from its precursor tryptophan, reuptake process mediated by SERT, vesicle storage and calcium-dependent release, as well as functional auto-receptors (5-HT1A) (Becquet et al., 1991, 1993a, 1993b; Héry et al., 1999; Lautenschlager et al., 2000). Published reports on the serotonergic metabolism in such neurons have measured [3H]-5-HT extracellular levels under different conditions (Yamamoto et al., 1981; Becquet et al., 1991; Becquet et al., 1993a; Becquet et al., 1993b; Wichems et al., 1995; Héry et al., 1999; Lautenschlager et al., 2000; Birthelmer et al., 2007). Although this approach is highly sensitive, it involves the risks and challenges inherent to working with radioactive reagents.
The neurotoxicity of amphetamines during the adolescent period
2015, International Journal of Developmental NeuroscienceCitation Excerpt :METH also prolongs monoaminergic transmission by inhibiting MAO activity, which results in an additional increase of cytosolic DA (Larsen et al., 2002). MDMA interaction with the monoaminergic system is similar to that of AMPH and METH, but it has more significant effects on the 5-HT system, namely, inducing the reverse transport of 5-HT via 5-HTT and VMAT (Baumann et al., 2005; Berger et al., 1992; Crespi et al., 1997; Green et al., 2003; Partilla et al., 2006; Wichems et al., 1995). The cytoplasmatic non-vesicular stored 5-HT should, in normal conditions, be degraded by MAO, however as MDMA is a competitive inhibitor of MAO-A activity, it will contribute to the accumulation of extracellular 5-HT after MDMA exposure (Leonardi and Azmitia, 1994).
The modulatory action of harmane on serotonergic neurotransmission in rat brain
2015, Brain ResearchCitation Excerpt :However, a Ca2+-independent release component has been reported in various systems much owing to the involvement of carrier-mediated processes (Piccolino and Pignatelli, 1996; Seiden et al., 1993). This method of release was noted to occur with amphetamines and its derivatives by the reversal of the direction of neurotransmitter flow as a result in change of Na+ gradient across the lipid bilayer (Seiden et al., 1993; Wichems et al., 1995). This method of release is reported to be Ca2+-independent, Na+-dependent and blocked by uptake inhibitors (Seiden et al., 1993).
Differences in the locomotor-activating effects of indirect serotonin agonists in habituated and non-habituated rats
2012, Pharmacology Biochemistry and BehaviorCitation Excerpt :It is not clear why there is circadian variability in the response to MDMA, but one possible explanation is that the ability of MDMA to provoke 5-HT release varies over the light/dark cycle. MDMA preferentially releases 5-HT from the newly synthesized cytoplasmic pool (Wichems et al., 1995), and the neurochemical and electrophysiological effects of MDMA are potentiated by administration of the 5-HT precursor l-tryptophan, which increases 5-HT synthesis (Bradberry et al., 1990; Sprouse et al., 1990; Evans et al., 2008). As the rate of 5-HT synthesis increases during the light phase (Héry et al., 1972), it is likely that the ability of MDMA to induce 5-HT release peaks during the light phase of the diurnal cycle.
Sustained exposure to 3,4-Methylenedioxymethamphetamine induces the augmentation of exocytotic serotonin release in rat organotypic raphe slice cultures
2010, Journal of Pharmacological Sciences5,7-Dihydroxitryptamine toxicity to serotonergic neurons in serum free raphe cultures
2008, European Journal of Pharmacology