Opioid antagonists block acetaldehyde-induced increments in dopamine neurons activity

Fois, Giulia R.; Diana, Marco

doi:10.1016/j.drugalcdep.2015.11.013

Cited by 5 publications

(4 citation statements)

References 22 publications

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“…Several evidences support the notion that the activation of MOP receptors expressed onto VTA GABA neurons and other GABA afferents (Johnson and North, 1992; Jalabert et al, 2011; Sánchez-Catalán et al, 2014), is critically involved in the stimulation of VTA DA neurons after ethanol or acetaldehyde (Mereu and Gessa, 1985; Xiao et al, 2007; Fois and Diana, 2016). Consistent with this idea, behavioral studies have shown that the microinjection of naltrexone or β-funaltrexamine (an irreversible MOP receptor antagonist) can prevent the motor activation induced by the intra-pVTA administration of ethanol or acetaldehyde (Sánchez-Catalán et al, 2009).…”

Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 86%

“…Consistent with this idea, behavioral studies have shown that the microinjection of naltrexone or β-funaltrexamine (an irreversible MOP receptor antagonist) can prevent the motor activation induced by the intra-pVTA administration of ethanol or acetaldehyde (Sánchez-Catalán et al, 2009). Moreover, such preventive effect has been also observed by using electrophysiological approaches (Xiao and Ye, 2008; Guan and Ye, 2010; Fois and Diana, 2016). …”

Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 87%

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Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Peana

Sánchez-Catalán

Hipólito

et al. 2017

Front. Behav. Neurosci.

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After decades of uncertainties and drawbacks, the study on the role and significance of acetaldehyde in the effects of ethanol seemed to have found its main paths. Accordingly, the effects of acetaldehyde, after its systemic or central administration and as obtained following ethanol metabolism, looked as they were extensively characterized. However, almost 5 years after this research appeared at its highest momentum, the investigations on this topic have been revitalized on at least three main directions: (1) the role and the behavioral significance of acetaldehyde in different phases of ethanol self-administration and in voluntary ethanol consumption; (2) the distinction, in the central effects of ethanol, between those arising from its non-metabolized fraction and those attributable to ethanol-derived acetaldehyde; and (3) the role of the acetaldehyde-dopamine condensation product, salsolinol. The present review article aims at presenting and discussing prospectively the most recent data accumulated following these three research pathways on this never-ending story in order to offer the most up-to-date synoptic critical view on such still unresolved and exciting topic.

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Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 86%

Section: Role Of Brain Ethanol-derived Acetaldehyde In the Effects Ofmentioning

confidence: 87%

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Peana

Sánchez-Catalán

Hipólito

et al. 2017

Front. Behav. Neurosci.

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“…In adult rats the opioid system has been demonstrated to mediate the reinforcing effects of acetaldehyde attributed to ethanol (Peana et al, 2010 ; Correa et al, 2012 ). In addition it has recently been demonstrated that the stimulation of the mesolimbic dopaminergic system induced by acetaldehyde is mediated by the endogenous opioid system (Fois and Diana, 2016 ). Based on these findings in adults, and with the knowledge that the fetal dopamine and opioid systems are functional, it could be inferred that similar mechanisms were acting for the reinforcing aspects of ethanol and acetaldehyde in the near-term fetus.…”

Section: Discussionmentioning

confidence: 99%

The Role of Acetaldehyde in the Increased Acceptance of Ethanol after Prenatal Ethanol Exposure

Gaztañaga

Angulo-Alcalde

Spear

et al. 2017

Front. Behav. Neurosci.

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Recent studies show that acetaldehyde, the first metabolite in the oxidation of ethanol, can be responsible for both, the appetitive and the aversive effects produced by ethanol intoxication. More specifically, it has been hypothesized that acetaldehyde produced in the periphery by the liver is responsible for the aversive effects of ethanol, while the appetitive effects relate to the acetaldehyde produced centrally through the catalase system. On the other hand, from studies in our and other laboratories, it is known that ethanol exposure during the last gestational days (GD) consistently enhances the postnatal acceptance of ethanol when measured during early ontogeny in the rat. This increased liking of ethanol is a conditioned appetitive response acquired by the fetus by the association of ethanol’s flavor and an appetitive reinforcer. Although this reinforcer has not yet been fully identified, one possibility points to acetaldehyde produced centrally in the fetus as a likely candidate. This hypothesis is supported by data showing that very early in the rat’s ontogeny brain catalases are functional, while the liver’s enzymatic system is still immature. In this study, rat dams were administered on GD 17–20 with water or ethanol, together with an acetaldehyde-sequestering agent (D-penicillamine). The offspring’s responses to ethanol was then assessed at different postnatal stages with procedures adequate for each developmental stage: on day 1, using the “odor crawling locomotion test” to measure ethanol’s odor attractiveness; on day 5, in an operant conditioning procedure with ethanol as the reinforcer; and on day 14 in an ethanol intake test. Results show that the absence of acetaldehyde during prenatal ethanol exposure impeded the observation of the increased acceptance of ethanol at any age. This seems to confirm the crucial role of acetaldehyde as a reinforcer in the appetitive learning occurring during prenatal ethanol exposure.

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“…ACD represents the possible candidate by which EtOH increases the release of β-endorphin which, in turn, can modulate the activity of other neurotransmitter systems such as mesolimbic dopamine (Font et al, 2013). In fact, it has been demonstrated that the opioid system participates in ACD-induced increments in dopaminergic neuronal activity (Fois and Diana, 2016). Specifically, opioid antagonists (naloxone and naltrexone) were found to abolish ACD-induced increase in the firing rate and bursting activity of the dopaminergic neurons of the ventral tegmental area.…”

Section: Role Of the Opioid System In The Modulation Of Prenatal Etohmentioning

confidence: 99%

Fetal Alcohol Programming of Subsequent Alcohol Affinity: A Review Based on Preclinical, Clinical and Epidemiological Studies

Miranda-Morales

D'aloisio

Anunziata

et al. 2020

Front. Behav. Neurosci.

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Opioid antagonists block acetaldehyde-induced increments in dopamine neurons activity

Cited by 5 publications

References 22 publications

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

The Role of Acetaldehyde in the Increased Acceptance of Ethanol after Prenatal Ethanol Exposure

Fetal Alcohol Programming of Subsequent Alcohol Affinity: A Review Based on Preclinical, Clinical and Epidemiological Studies

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