Stress Abolishes the Effect of Previous Chronic Ethanol Consumption on Drug Place Preference and on the Mesocorticolimbic Brain Pathway

Moreira-Silva, Daniel; Morais-Silva, Gessynger; Fernandes-Santos, Juliana; Planeta, Cleópatra da Silva; Marin, Marcelo Tadeu

doi:10.1111/acer.12388

Cited by 9 publications

(5 citation statements)

References 45 publications

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“…In an ethanol-induced CPP study 45 (dose: 2.0 g/kg), adult DBA/2 J mice spent around 60% of the test on the CS + , which is similar to our data in Swiss mice. DBA/2 J mice, however, exhibited a negative correlation between ethanol intake and ethanol-induced CPP 45 , whereas pre-exposure to ethanol potentiates ethanol conditioning in the Swiss mice 46 . Adolescent Swiss mice also show, when compared to adult counterparts, lower levels of sensitization to ethanol 6 yet after the sensitization ethanol intake escalates more pronounced in the adolescents than in the adults 47 , Studies with the outbred strain OF1 have shown that pre-exposure to ethanol or to stress during adolescence enhances subsequent cocaine-induced CPP 48 and ethanol self-administration 49 , respectively.…”

Section: Discussionmentioning

confidence: 83%

Effects of environmental enrichment upon ethanol-induced conditioned place preference and pre-frontal BDNF levels in adolescent and adult mice

Pautassi

Suarez

Hoffmann

et al. 2017

Sci Rep

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Environmental enrichment (EE) provides a non-pharmacological tool to alter drug-induced reward, yet its effects on ethanol-induced reward remain controversial. We analyzed adolescent vs. adult (mice) differences in the influence of EE on ethanol-induced conditioned place preference (CPP). The effects of these treatments on brain-derived neurotrophic factor (BDNF) levels in the prefrontal cortex were examined in a separate group of animals. Ethanol-induced CPP was found in adults, and it was similar in EE and in animals reared under standard housing conditions (SC). Adolescents kept under EE, but not those in SC, exhibited CPP. Among SC, but not among EE, adolescents, BDNF levels were significantly lower in those treated with ethanol than in those given vehicle. These results indicate that, compared to adults, adolescent exhibited reduced sensitivity to ethanol’s rewarding effects, yet the youth but not the adults exhibited sensitivity to the promoting effect of EE upon CPP by ethanol. Ethanol significantly reduced BDNF levels in adolescents reared under standard housing conditions, but not in adult mice nor in adolescents given EE housing conditions. The present results add to the plethora of adolescent-specific responses to ethanol or to environmental stimuli that may put the youth at risk for escalation of ethanol intake.

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Section: Discussionmentioning

confidence: 83%

Effects of environmental enrichment upon ethanol-induced conditioned place preference and pre-frontal BDNF levels in adolescent and adult mice

Pautassi

Suarez

Hoffmann

et al. 2017

Sci Rep

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“…Ethanol-withdrawal and stress change the activity of similar brain structures related to the encoding of motivational salience of a stimulus (i.e., mesocorticolimbic dopaminergic pathway) and emotional behavior (e.g., amygdala and other limbic structures) [4]. When experienced together, forcedswim stress and ethanol consumption increase dopaminergic content within the amygdala, abolishing drug conditioned place preference [47]. Stress induces the activation of dopamine release in medial prefrontal cortex neurons, which in turn inhibits dopamine release in the nucleus accumbens [48].…”

Section: Discussionmentioning

confidence: 99%

Interaction Between Social Defeat Stress and Chronic Ethanol Exposure on Behaviors During Ethanol Withdrawal and Pro-Inflammatory Cytokines in Mice

Morais-Silva¹,

Portilho²,

Fernandes-Santos³

et al. 2021

Psychoneuroimmunol J

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Stress and ethanol consumption are known to affect the immune system, interfering in individual health, and resistance to opportunistic diseases. When experienced together, stress and ethanol seem to interact uniquely, altering each other effects depending on the exposure schedule. However, the effects of social stress on chronic ethanol exposure effects on the immune system are not well elucidated.To study this interaction, we chronically treated male swiss mice with ethanol after repeated social defeat stress (SDS) exposure. Some animals were tested in the elevated plus-maze (EPM) and open field (OF) while another cohort had plasmatic TNF-α, TGF-β1, CXCL-1, CCL-2, and VEGF quantified. Mice exposed to SDS or ethanol withdrawal showed increased anxiety-like behaviors in the EPM, while ethanol withdrawal decreased locomotor activity. Both alterations were attenuated in the groups exposed to SDS and ethanol withdrawal. Ethanol and stress alone increased plasmatic CXCL-1, while only stress affected CCL-2 and VEGF. Our results suggest that SDS exposure and ethanol withdrawal attenuated the increase in anxietylike behaviors, but did not alter each other effects on cytokine content.

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“…CPP was evaluated as described by Ref. [15] with small modifications. During the even days of conditioning phase (days 2, 4, 6 and 8), animals were s.c. treated with conessine (1.0 or 10.0 mg/kg) or vehicle one hour before i.p.…”

Section: Conditioned Place Preferencementioning

confidence: 99%

“…Control animals received vehicle and saline every day. Preconditioning and postconditioning tests were conducted as already described by [15]. Time spent (in seconds) in each compartment during preconditioning and postconditioning tests was measured by the behavioral analysis software ANY-maze (Stoelting Co., Wood Dale, IL-USA) and the compartment preference in postconditioning test was compared to the initial preference in preconditioning test (N = 9-10 animals per group).…”

Section: Conditioned Place Preferencementioning

confidence: 99%

“…The technique for quantification of norepinephrine, dopamine, serotonin, homovanillic acid (HVA), 3,4 dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindolacetic acid (5HIAA) was based on assays described by Ref. [15] with modifications. The volumes of perchloric acid were as follows: 60 L for PFC, VTA and SN and 80 L for NAc and CPu.…”

Section: Neurotransmitters Quantification By Hpclmentioning

confidence: 99%

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Conessine, an H3 receptor antagonist, alters behavioral and neurochemical effects of ethanol in mice

Morais-Silva

Ferreira-Santos

Marin

2016

Behavioural Brain Research

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Ethanol abuse potential is mainly due to its reinforcing properties, crucial in the transition from the recreational to pathological use. These properties are mediated by mesocorticolimbic and nigrostriatal dopaminergic pathways and neuroadaptations in these pathways seem to be responsible for addiction. Both pathways are modulated by other neurotransmitters systems, including neuronal histaminergic system. Among the histamine receptors, H3 receptor stands out due to its role in modulation of histamine and other neurotransmitters release. Thus, histaminergic system, through H3 receptors, may have an important role in ethanol addiction development. Aiming to understand these interactions, conessine, an H3 receptor antagonist, was given to mice subjected to the evaluation of ethanol-induced psychostimulation, ethanol CPP and quantification of norepinephrine, dopamine, serotonin and their metabolites in mesocorticolimbic and nigrostriatal pathways following acute ethanol treatment. Systemic conessine administration exacerbated ethanol effects on locomotor activity. Despite of conessine reinforcing effect on CPP, this drug did not alter acquisition of ethanol CPP. Ethanol treatment affects the serotoninergic neurotransmission in the ventral tegmental area, the dopaminergic neurotransmission in the pre-frontal cortex (PFC) and caudate-putamen nucleus (CPu) and the noradrenergic neurotransmission in the CPu. In the PFC, conessine blocked ethanol effects on dopaminergic and noradrenergic neurotransmission. The blockade of H3 receptors and ethanol seem to interact in the modulation of dopaminergic neurotransmission of nigrostriatal pathway, decreasing dopamine metabolites in substantia nigra. In conclusion, conessine was able to change psychostimulant effect of ethanol, without altering its reinforcing properties. This exacerbation of ethanol-induced psychostimulation would be related to alterations in dopaminergic neurotransmission in the nigrostriatal pathway.

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Stress Abolishes the Effect of Previous Chronic Ethanol Consumption on Drug Place Preference and on the Mesocorticolimbic Brain Pathway

Cited by 9 publications

References 45 publications

Effects of environmental enrichment upon ethanol-induced conditioned place preference and pre-frontal BDNF levels in adolescent and adult mice

Effects of environmental enrichment upon ethanol-induced conditioned place preference and pre-frontal BDNF levels in adolescent and adult mice

Interaction Between Social Defeat Stress and Chronic Ethanol Exposure on Behaviors During Ethanol Withdrawal and Pro-Inflammatory Cytokines in Mice

Conessine, an H3 receptor antagonist, alters behavioral and neurochemical effects of ethanol in mice

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