Hippocampal nicotinic receptors have a modulatory role for ethanol and MDMA interaction in memory retrieval.
Maryam Rostami, Ameneh Rezayof, Sakineh Alijanpour, Khadijeh Alsadat Sharifi
Brain Research May 23, 2017 DOI: 10.1016/j.brainres.2017.05.026 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Adult male NMRI mice |
| Interventions | Ethanol MDMA Nicotine |
| Dose | Ethanol 1 g/kg i.p. (post-training or pre-test) and 0.25 g/kg i.p. (pre-test, with MDMA); MDMA 0.25-1 µg/mouse intra-CA1; Nicotine 0.1-1 µg/mouse intra-CA1 (and 0.3-0.9 µg/mouse in one experiment) |
| Topics | MDMA |
| Keywords | Animals Mice Ethanol N-methyl-3,4-methylenedioxyamphetamine Nicotine Receptors, nicotinic Adrenergic uptake inhibitors Nicotinic agonists Microinjections Analysis of variance Random allocation Motor activity Avoidance learning Dose-response relationship, drug Male Ca1 region, hippocampal Memory retrieval Dorsal hippocampus |
| Key findings | Ethanol produced state-dependent learning in mice, and intra-CA1 MDMA both induced amnesia with an ineffective ethanol dose and potentiated ethanol state-dependent learning. Nicotine microinjection into the dorsal hippocampus improved amnesia from combined MDMA and ethanol and enhanced MDMA's effect on ethanol state-dependent learning, suggesting functional interactions among ethanol, MDMA, and nicotine via dorsal hippocampal nicotinic acetylcholine receptors. |
Abstract
The aim of the current study was to examine the effect of dorsal hippocampal nicotinic acetylcholine receptors (nAChRs) activation on the functional interaction between ethanol and 3,4-methylenedioxy-N-methylamphetamine (MDMA or ecstasy) in memory retrieval. The dorsal hippocampal CA1 regions of adult male NMRI mice were bilaterally cannulated and memory retrieval was measured in a step-down type passive avoidance apparatus. Post-training or pre-test systemic administration of ethanol (1g/kg, i.p.) induced amnesia. Pre-test administration of ethanol reversed pre-training ethanol-induced amnesia, suggesting ethanol state-dependent learning. Pre-test intra-CA1 microinjection of different doses of MDMA (0.25-1µg/mouse) with an ineffective dose of ethanol (0.25g/kg, i.p.) also induced amnesia. Interestingly, pre-test intra-CA1 microinjection of MDMA (0.25-1µg/mouse) potentiated ethanol state-dependent learning. On the other hand, the activation of the dorsal hippocampal nAChRs by pre-test microinjection of nicotine (0.1-1µg/mouse, intra-CA1) improved amnesia induced by the co-administration of MDMD and ethanol. It is important to note that intra-CA1 microinjection of the same doses of MDMA or nicotine could not affect memory formation by itself. Pre-test intra-CA1 microinjection of nicotine (0.3-0.9µg/mouse) could not reverse amnesia induced by pre-training administration of ethanol while this treatment enhanced MDMA response on ethanol state-dependent learning. Thus, it can be concluded that there may be functional interactions among ethanol, MDMA and nicotine via the dorsal hippocampal nicotinic acetylcholine receptor mechanism in memory retrieval and drug state-dependent learning.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
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- Role of 5-HT1A receptors in the basolateral amygdala on 3,4-methylenedioxymethamphetamine-induced prosocial effects in mice. European Journal of Pharmacology March 10, 2023
- Nicotine and modafinil combination protects against the neurotoxicity induced by 3,4-Methylenedioxymethamphetamine in hippocampal neurons of male rats. Journal of chemical neuroanatomy October 2021
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