Ethanol Modulates Corticotropin Releasing Hormone Release From the Rat Hypothalamus: Does Acetaldehyde Play a Role?

Cannizzaro, Carla; Barbera, Marco; Plescia, Fulvio; Cacace, Silvana; Tringali, Giuseppe

doi:10.1111/j.1530-0277.2009.01127.x

Cited by 33 publications

(21 citation statements)

References 47 publications

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“…Indeed, ACD appears to be a 1000-fold more potent reinforcement than ethanol in the posterior VTA (Rodd et al, 2005). Besides, ACD involvement in recruiting the neuroendocrine stress system (Cannizzaro et al, 2010; Escrig et al, 2012) may be crucial in the development of negative emotional states, thus leading to the progressive loss of control in drinking behavior and compulsive alcohol intake (Koob, 2013). A major finding of the present study was the pharmacological probing of ACD reinforcing and motivational properties, addressing the AM281 effect in the distinct addiction-related behaviors explored, namely drug-seeking, relapse and punishment resistance.…”

Section: Discussionmentioning

confidence: 99%

Acetaldehyde as a drug of abuse: insight into AM281 administration on operant-conflict paradigm in rats

Plescia¹,

Brancato²,

Marino³

et al. 2013

Front. Behav. Neurosci.

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Increasing evidence focuses on acetaldehyde (ACD) as the mediator of the rewarding and motivational properties of ethanol. Indeed, ACD stimulates dopamine release in the nucleus accumbens and it is self-administered under different conditions. Besides the dopaminergic transmission, the endocannabinoid system has been reported to play an important role in ethanol central effects, modulating primary alcohol rewarding effect, drug-seeking, and relapse behavior. Drug motivational properties are highlighted in operant paradigms which include response-contingent punishment, a behavioral equivalent of compulsive drug use despite adverse consequences. The aim of this study was thus to characterize ACD motivational and rewarding properties employing an operant-conflict paradigm in which rats, trained to lever press in order to get ACD solution (0.9%), undergo extinction, reinstatement and conflict sessions, according to a modified Geller–Seifter procedure. Furthermore, the role played by CB1 receptor system in modulating ACD-induced effects were investigated through the administration of CB1 receptor antagonist, AM281 (1 mg/kg, i.p.) during the extinction-, relapse-, and conflict-experiments. Our results indicate that ACD is able to induce and maintain an operant behavior, a high number of responses during extinction, an increase in the lever presses during the reinstatement phase, and a higher emission of punished responses during the conflict experiments, when compared to controls. The administration of AM281 is able to decrease ACD-seeking behavior during extinction, the number of lever presses during reinstatement and to strongly decrease the punished responses for ACD. Our data strengthen the idea that ACD may be responsible for the central effects of ethanol, and pinpoint at the CB1 system as one of the neural substrates underlying its addictive properties.

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Section: Discussionmentioning

confidence: 99%

Acetaldehyde as a drug of abuse: insight into AM281 administration on operant-conflict paradigm in rats

Plescia¹,

Brancato²,

Marino³

et al. 2013

Front. Behav. Neurosci.

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“…Interestingly, high doses of alcohol (at least twice as large as that administered in the present study) have been shown to stimulate the HPA axis causing ACTH and cortisol release (McCaul et al, 2001; Inder et al, 1995; Reddy and Sarkar, 1993; Rivier, 1996; Rivier and Vle, 1988; Silveri and Spear 2004). These increases are thought to result from actions of alcohol upon hypothalamic paraventricular CRH neurons or their afferents (Ogilvie et al, 1998; Rivier and Lee, 1996) and may be mediated by local metabolism of alcohol to acetaldehyde (Cannizzaro et al, 2010). In this study, we demonstrate that alcohol can inhibit HPA axis activity and glucocorticoid release after it has been activated by an external stimulus.…”

Section: Discussionmentioning

confidence: 99%

Bidirectional Interactions Between Acute Psychosocial Stress and Acute Intravenous Alcohol in Healthy Men

Childs

O’Connor

Wit

2011

Alcoholism: Clinical and Experimental Research

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Background The biological mechanisms by which acute stress increases alcohol consumption are unclear. One potential mechanism is that stress acts by altering the pharmacological and subjective effects of alcohol. Acute stress produces a cascade of physiological and psychological effects, each with a distinctive time course. In this study, we investigated whether different phases of response to an acute stress alter the subjective effects of intravenous alcohol, by administering the drug at two different times after the stress. Methods Healthy men (N=25) participated in two sessions; one with the Trier Social Stress Test, the other with a non-stressful control task, each followed by infusions of intravenous alcohol (targeting 40mg% in 5 min) and placebo. One group of participants received alcohol within 1 min of completing the tasks (Alc0, N=11), followed by placebo 30 min later. In the other group (Alc30, N=14), the order of alcohol and placebo infusions was reversed. Subjective effects (i.e., Anxiety, Stimulation, Want more) and physiological measures (heart rate, blood pressure, salivary cortisol) were measured before and at repeated intervals after the tasks and infusions. Results Stress did not change the subjective effects of alcohol in either group. However, when individual differences in alcohol responses were considered, stress differentially altered the stimulant-like and sedative effects of alcohol. Among individuals who exhibited predominantly stimulant responses to alcohol in the non-stressful condition, stress decreased the stimulant-like effects of alcohol and ‘wanting more’. By contrast, among participants who did not report stimulation after alcohol in the control session, stress decreased the sedative effects and increased ‘want more’. In addition, alcohol administered immediately after the TSST dampened cortisol responses yet prolonged negative subjective responses to the stress. Conclusions These findings demonstrate that there are bi-directional relationships between alcohol and stress. Alcohol influences responses to stress, and stress changes reactions to alcohol, depending on an individual's pattern of response to alcohol. This study highlights the fact that stress-alcohol interactions vary among individual drinkers, suggesting that the effects of stress on motivation to drink alcohol may also differ between individuals.

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“…21,[39][40][41] Moreover, ACD is able to induce and maintain an addictive behaviour in which seeking and relapse are modulated by the eCB 12,42 so that ACD is believed to play a primary role in the "first-hit" of alcohol reinforcement and in the induction of relapse. 21,22,39,[43][44][45][46] Indeed, the ECS 21 contributes to alcohol's rewarding effect, and to the occurrence of an addictive phenotype by fine tuning synaptic transmission: the eCB in fact, are key activitydependent messengers that, by short and long-term decreases in synaptic transmission, regulate glutamatergic and GABAergic synapses.…”

Section: Ecs-mediated Alcohol Reinforcing Effectsmentioning

confidence: 99%

The endocannabinoid‐alcohol crosstalk: Recent advances on a bi‐faceted target

Lavanco

Castelli

Brancato

et al. 2018

Clin Exp Pharma Physio

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Increasing evidence has focusesed on the endocannabinoid system as a relevant player in the induction of aberrant synaptic plasticity and related addictive phenotype following chronic excessive alcohol drinking. In addition, the endocannabinoid system is implicated in the pathogenesis of alcoholic liver disease. Interestingly, whereas the involvement of CB receptors in alcohol rewarding properties is established, the central and peripheral action of CB signalling is still to be elucidated. This review aims at giving the input to deepen knowledge on the role of the endocannabinoid system, highlighting the advancing evidence that suggests that CB and CB receptors may play opposite roles in the regulation of both the reinforcing properties of alcohol in the brain and the mechanisms responsible for cell injury and inflammation in the hepatic tissue. The manipulation of the endocannabinoid system could represent a bi-faceted strategy to counteract alcohol-related dysfunction in central transmission and liver structural and functional disarrangement.

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Ethanol Modulates Corticotropin Releasing Hormone Release From the Rat Hypothalamus: Does Acetaldehyde Play a Role?

Abstract: These data show that both EtOH and acetaldehyde are able to increase hypothalamic CRH release from the rat hypothalamus and that acetaldehyde itself appears to be the mediator of EtOH activity.

Cited by 33 publications

References 47 publications

Acetaldehyde as a drug of abuse: insight into AM281 administration on operant-conflict paradigm in rats

Acetaldehyde as a drug of abuse: insight into AM281 administration on operant-conflict paradigm in rats

Bidirectional Interactions Between Acute Psychosocial Stress and Acute Intravenous Alcohol in Healthy Men

The endocannabinoid‐alcohol crosstalk: Recent advances on a bi‐faceted target

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