Short communicationEffects of methylenedioxymethamphetamine on the release of monoamines from rat brain slices
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Cited by (63)
Effects of a combination of 3,4-methylenedioxymeth amphetamine and caffeine on real time stimulated dopamine release in the rat striatum: Studies using fast cyclic voltammetry
2018, Journal of Neuroscience MethodsCitation Excerpt :In contrast to prior publications the present data were derived from experiments where dopamine D2 autoreceptors are not activated by endogenous dopamine (Bull & Sheehan, 1991). Limberger et al. (1991) has previously shown that dopamine D2 auoreceptors are only activated by stimulated endogenous dopamine following electrical stimulation lasting a minimum of 200 ms. As has previously been shown using the methodology of FCV (John and Jones, 2007; Iravani et al., 2000) and other techniques (Gudelsky et al., 1994; Fitzgerald and Reid, 1990; Johnson et al., 1986), we have also shown that MDMA applied alone enhances the amount of dopamine released and decreased the rate of its reuptake in striatal slices (increased reuptake time). We have also demonstrated, albeit at high concentrations, a stimulatory effect of caffeine on dopamine release as has also previously been demonstrated (Okada et al., 1997).
MeCP2-deficient mice have reduced α4 and α6 nicotinic receptor mRNA and altered behavioral response to nicotinic agonists
2017, Behavioural Brain ResearchProtracted treatment with MDMA induces heteromeric nicotinic receptor up-regulation in the rat brain: An autoradiography study
2014, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :We have cited above that nAChR up-regulation by nicotine and MDMA is a mechanistically-complex process that implies the interaction of the ligand with intracellular immature forms of the receptor. Nicotine is known to penetrate the cell membrane (Whiteaker et al., 1998), which allows such an interaction to occur, while MDMA is known to use the monoamine transporters, mainly the SERT (Fitzgerald and Reid, 1990), to access the intracellular compartments. Thus the different abilities of each brain area to take up MDMA could explain the main differences found in comparison to nicotine.
Schizophrenia-like disruptions of sensory gating by serotonin receptor stimulation in rats: Effect of MDMA, DOI and 8-OH-DPAT
2013, Pharmacology Biochemistry and BehaviorCitation Excerpt :It should be noted, that despite MDMA being a potent releaser of 5-HT, it cannot be ruled out that a part of its action on sensory gating is by secondary effects on dopaminergic and noradrenergic neurons. MDMA induces the release of both of these catecholamines, although to a lesser degree than it does 5-HT (de la Torre et al., 2004; Fitzgerald and Reid, 1990; Gold et al., 1989). Therefore, the MDMA-induced disruption of sensory gating might be partly due to the release of dopamine and/or noradrenaline, which have been shown to potently modulate sensory gating on their own at high doses, particularly dopamine.
A role for adenosine A<inf>1</inf> receptor blockade in the ability of caffeine to promote MDMA "ecstasy"-induced striatal dopamine release
2011, European Journal of Pharmacology