References of "Quertemont, Etienne"
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See detailLa dépendance au cannabis : propriétés addictives, tolérance et sevrage
Quertemont, Etienne ULg; Tirelli, Ezio ULg

in Seutin, Vincent; Scuvée, Jacqueline; Quertemont, Etienne (Eds.) Regards croisés sur le cannabis (2010)

En dépit de controverses récurrentes, les données expérimentales récoltées dans de nombreuses études animales et humaines indiquent que le cannabis présente toutes les caractéristiques associées aux ... [more ▼]

En dépit de controverses récurrentes, les données expérimentales récoltées dans de nombreuses études animales et humaines indiquent que le cannabis présente toutes les caractéristiques associées aux autres drogues toxicomanogènes. Le cannabis induit manifestement une dépendance psychologique primaire chez l’homme et les modèles animaux ont démontré qu’il possède des propriétés renforçantes, quoique de moindre intensité que celles d’autres drogues comme la cocaïne ou les opiacés. La consommation chronique de cannabis produit une tolérance envers certains de ses effets, ce qui est susceptible d’entraîner un accroissement des doses utilisées par un utilisateur régulier. On reconnaît aussi au cannabis la capacité d’induire une véritable dépendance physiologique chez les plus gros consommateurs. Cette dépendance physiologique se manifeste par un syndrome de sevrage typique lors de l’arrêt de la consommation. Toutefois, il est clair que la dépendance au cannabis (aussi bien psychologique que physiologique) est moins sévère que celle induite par d’autres drogues majeures comme l’alcool, la cocaïne ou les opiacés. De plus, elle ne concerne qu’une petite fraction des consommateurs de cannabis. Depuis de nombreuses années, on s’interroge sur le risque d’escalade vers la consommation de drogues « plus dures » que produirait la consommation de cannabis. Les études scientifiques ont clairement démontré qu’il existe un lien statistique significatif entre usage de cannabis et consommation d’autres drogues illicites. Toutefois, la nature de cette relation statistique reste controversée. Selon les tenants de « la théorie de la porte d’entrée », le cannabis conduit directement, par des mécanismes biologiques, psychologiques ou sociaux, à une augmentation du risque de consommer des drogues telles que la cocaïne ou l’héroïne. Au contraire, les adeptes de « la théorie du facteur commun » soutiennent que les consommations de cannabis, d’héroïne ou de cocaïne sont expliqués par des facteurs généraux identiques, conduisant ainsi à une relation statistique qui ne serait qu’apparente et en aucun cas de nature causale. A l’heure actuelle, les données expérimentales disponibles ne permettent pas de trancher définitivement entre ces deux théories explicatives. [less ▲]

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See detailEffets du cannabis sur la santé psychologique
Quertemont, Etienne ULg; Blairy, Sylvie ULg; Ansseau, Marc ULg

in Seutin, Vincent; Scuvée, Jacqueline; Quertemont, Etienne (Eds.) Regards croisés sur le cannabis (2010)

Les individus intoxiqués au cannabis rapportent généralement des effets subjectifs plaisants, même si des symptômes désagréables ne sont pas à exclure chez certaines personnes ou à certaines occasions ... [more ▼]

Les individus intoxiqués au cannabis rapportent généralement des effets subjectifs plaisants, même si des symptômes désagréables ne sont pas à exclure chez certaines personnes ou à certaines occasions. L’intoxication cannabique aiguë perturbe différents processus cognitifs plus ou moins intensément. Les effets les plus nets sont probablement les altérations de la mémoire qui surviennent lors de l’intoxication cannabique, et en particulier la perturbation de la consolidation de nouveaux souvenirs. Toutefois, on observe également lors de l’intoxication cannabique une altération de la flexibilité mentale et comportementale rendant les comportements plus rigides et plus impulsifs. Enfin, le cannabis perturbe clairement l’estimation subjective de l’écoulement du temps, donnant ainsi l’impression d’un ralentissement du temps. Ces derniers effets expliquent d’ailleurs en partie l’accroissement lors d’une intoxication cannabique des risques d’accidents de conduite automobile. En conclusion, et compte tenu des difficultés méthodologiques mentionnées précédemment, on peut affirmer que les gros consommateurs de cannabis, surtout ceux qui ont fumé du cannabis quotidiennement pendant de longues périodes couvrant parfois des années, présentent un fonctionnement cognitif légèrement altéré. Les déficits cognitifs identifiés sont plutôt de faible magnitude, touchent généralement la mémoire et disparaissent le plus souvent après quelques semaines d’abstinence. Il semble donc que le cannabis produit des altérations cognitives essentiellement durant les périodes de consommation. Les effets observés dans les semaines qui suivent l’arrêt de la consommation chez les gros consommateurs sont vraisemblablement liés au syndrome de sevrage cannabique ou à la présence résiduelle de cannabis dans l’organisme. Le fait que les déficits cognitifs identifiés chez les consommateurs chroniques de cannabis abstinents ressemblent fortement aux effets de l’intoxication cannabique (légers troubles de la mémoire, réduction de la flexibilité mentale et impulsivité), renforce l’idée qu’il pourrait s’agir d’effets résiduels du cannabis qui mettent plus longtemps à se résorber chez les très gros consommateurs. A ce jour, les études scientifiques n’ont donc pas encore démontré de manière incontestable l’existence de troubles cognitifs persistants, voire permanents, chez les consommateurs réguliers de cannabis devenus abstinents depuis plusieurs mois, mais ils ne les ont pas exclus non plus. Une conclusion prudente serait dès lors que les déficits cognitifs persistants induits par la consommation régulière de grosses quantités de cannabis sont relativement limités et transitoires. Ceci n’exclut pas la survenue d’autres problèmes à long terme, comme par exemple le développement d’une addiction au cannabis, des difficultés sociales ou relationnelles ou d’autres effets sur la santé. D’autres études, méthodologiquement mieux contrôlées, seront cependant nécessaires pour conclure définitivement sur la question de l’existence d’altérations cognitives persistantes suite à la consommation chronique de cannabis. Compte tenu des résultats parfois contradictoires de la littérature scientifique, il n’est pas aisé de tirer des conclusions fermes à propos des effets du cannabis sur la santé psychologique et particulièrement sur les effets persistants susceptibles de se perpétuer au-delà des périodes d’intoxication. Alors que le tableau de l’intoxication/ivresse cannabique est relativement clair, les effets persistants d’une consommation abusive de cannabis sont l’objet d’âpres débats. On peut néanmoins tirer les conclusions suivantes. Les études les plus récentes concordent pour affirmer que l’abus de cannabis, surtout durant l’adolescence, est susceptible de provoquer des troubles psychotiques ou, de manière encore plus évidente, de les précipiter chez des individus fragiles. L’abus chronique de cannabis semble aussi favoriser les troubles de l’humeur, tels que dépression et trouble bipolaire. L’existence d’un syndrome amotivationnel qui serait induit par l’abus chronique de cannabis est plus controversée, même s’il est observé dans certaines études. Ce syndrome amotivationnel supposé est en partie lié à différents troubles cognitifs induits par le cannabis. S’il est avéré que la consommation chronique de cannabis provoque effectivement des altérations du fonctionnement cognitif et tout particulièrement de la mémoire, il reste à déterminer si ces déficits cognitifs persistent au-delà des périodes d’intoxications ou s’ils s’estompent progressivement après l’arrêt de l’abus de cannabis. [less ▲]

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See detailRegards croisés sur le cannabis
Seutin, Vincent ULg; Scuvée-Moreau, Jacqueline ULg; Quertemont, Etienne ULg

Book published by Mardaga (2010)

Multidisciplinary book which presents an up to date review of scientific data available on cannabis (neurobiology, toxicology, epidemiology, public health and treatment options

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See detailPsychostatistique descriptive et inférentielle Partim 1 - Exercices
Quertemont, Etienne ULg

Learning material (2009)

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See detailPsychostatistique descriptive et inférentielle Partim 1 - Théorie
Quertemont, Etienne ULg

Learning material (2009)

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See detailPsychostatistique descriptive et inférentielle Partim 2 - Théorie
Quertemont, Etienne ULg

Learning material (2009)

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See detailPsychostatistique descriptive et inférentielle Partim 2 - Exercices
Quertemont, Etienne ULg

Learning material (2009)

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See detailAcetaldehyde and the hypothermic effects of ethanol in mice.
Closon, Catherine ULg; Didone, Vincent ULg; Tirelli, Ezio ULg et al

in Alcoholism, Clinical & Experimental Research (2009), 33(11), 2005-14

BACKGROUND: Acetaldehyde, the first metabolite of ethanol, has been suggested to be involved in many behavioral effects of ethanol. However, few studies have investigated the hypothermic effects of ... [more ▼]

BACKGROUND: Acetaldehyde, the first metabolite of ethanol, has been suggested to be involved in many behavioral effects of ethanol. However, few studies have investigated the hypothermic effects of acetaldehyde or the contribution of acetaldehyde to ethanol-induced hypothermia. The aim of the present study is to better understand the hypothermic effects of acetaldehyde and the possible contribution of acetaldehyde in ethanol-induced hypothermia, especially under conditions leading to acetaldehyde accumulation. METHODS: Female Swiss mice were injected intraperitoneally with ethanol and acetaldehyde and their rectal temperatures were measured with a digital thermometer at various time points after the injections. Experiment 1 compared the hypothermic effects of various acetaldehyde doses (0 to 300 mg/kg) with a reference dose of ethanol (3 g/kg). Experiment 2 tested the effects of a pretreatment with the aldehyde dehydrogenase (ALDH) inhibitor cyanamide (25 mg/kg) on ethanol- and acetaldehyde-induced hypothermia. In experiments 3 and 4, mice received a combined pretreatment with cyanamide and the alcohol dehydrogenase (ADH) inhibitor 4-Methylpyrazole (10 mg/kg) before the injection of ethanol or acetaldehyde. RESULTS: Acetaldehyde at doses between 100 and 300 mg/kg induced significant hypothermic effects, but of shorter duration than ethanol-induced hypothermia. The inhibition of ALDH enzymes by cyanamide induced a strong potentiation of both ethanol- and acetaldehyde-induced hypothermia. The pretreatment with 4-MP prevented the potentiation of ethanol-induced hypothermia by cyanamide, but slightly increased the potentiation of acetaldehyde-induced hypothermia by cyanamide. CONCLUSIONS: The results of the present study clearly show that acetaldehyde has hypothermic properties in mice at least at relatively high concentrations. Furthermore, the accumulation of acetaldehyde following ALDH inhibition strongly enhanced the hypothermic effects of ethanol. These latter results confirm the hypothermic properties of acetaldehyde and show that acetate, the next step in ethanol metabolism, is not involved in these hypothermic effects. Finally, the experiment with 4-MP indicates that the potentiating effects of cyanamide are mediated by the peripheral accumulation of acetaldehyde, which then reaches the brain to induce a severe hypothermia. [less ▲]

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See detailEffects of the H(3) receptor inverse agonist thioperamide on cocaine-induced locomotion in mice: role of the histaminergic system and potential pharmacokinetic interactions.
Brabant, Christian ULg; Alleva, Livia ULg; Grisar, Thierry ULg et al

in Psychopharmacology (2009), 202(4), 673-87

RATIONALE: Previous studies have shown that intraperitoneal injections of thioperamide, an imidazole-based H(3) receptor inverse agonist that enhances histamine release in the brain, potentiate cocaine ... [more ▼]

RATIONALE: Previous studies have shown that intraperitoneal injections of thioperamide, an imidazole-based H(3) receptor inverse agonist that enhances histamine release in the brain, potentiate cocaine-induced hyperlocomotion. The present study examined the involvement of the histaminergic system in these effects of thioperamide in mice. MATERIALS AND METHODS: We investigated whether immepip, a selective H(3) agonist, could reverse the potentiating effects of thioperamide. Moreover, the non-imidazole H(3) inverse agonist A-331440 was tested on the locomotor effects of cocaine. Using high-performance liquid chromatography with ultraviolet detection, cocaine plasma concentrations were measured to study potential drug-drug interactions between thioperamide and cocaine. Finally, thioperamide was tested on the locomotor effects of cocaine in histamine-deficient knockout mice in order to determine the contribution of histamine to the modulating effects of thioperamide. RESULTS: Thioperamide potentiated cocaine-induced hyperlocomotion in normal mice, and to a higher extent, in histamine-deficient knockout mice. A-331440 only slightly affected the locomotor effects of cocaine. Immepip did not alter cocaine-induced hyperactivity but significantly reduced the potentiating actions of thioperamide on cocaine's effects. Finally, plasma cocaine concentrations were more elevated in mice treated with thioperamide than in mice that received cocaine alone. CONCLUSIONS: The present results indicate that histamine released by thioperamide through the blockade of H(3) autoreceptors is not involved in the ability of this compound to potentiate cocaine induced-hyperactivity. Our data suggest that thioperamide, at least at 10 mg/kg, increases cocaine-induced locomotion through the combination of pharmacokinetic effects and the blockade of H(3) receptors located on non-histaminergic neurons. [less ▲]

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See detailParametric analysis of the development and expression of ethanol-induced behavioral sensitization in female Swiss mice: effects of dose, injection schedule, and test context.
Didone, Vincent ULg; Quoilin, Caroline ULg; Tirelli, Ezio ULg et al

in Psychopharmacology (2008), 201(2), 249-60

RATIONALE: Repeated administrations of ethanol induce a progressive and enduring increase in its locomotor stimulant effects, a phenomenon termed behavioral sensitization that has not been systematically ... [more ▼]

RATIONALE: Repeated administrations of ethanol induce a progressive and enduring increase in its locomotor stimulant effects, a phenomenon termed behavioral sensitization that has not been systematically characterized. OBJECTIVE: The aim of the present studies was to characterize the development and expression of ethanol sensitization in female Swiss mice by examining (1) the doses of ethanol that induce behavioral sensitization, (2) the doses of acute ethanol challenges that are necessary to express behavioral sensitization, (3) the effects of the intervals between administrations, and (4) the context dependency of ethanol sensitization. MATERIALS AND METHODS: Mice were i.p. injected for 8 days with various ethanol doses, and locomotion was recorded for 5 min. Two days after the last sensitization session, ethanol sensitization was tested in 30-min test sessions. RESULTS: Mice repeatedly injected with 2.5 g/kg ethanol showed a progressive (200-300%) increase in locomotor activity. In response to a 2.5 g/kg ethanol challenge, the mice repeatedly treated with doses above 1.5 g/kg showed a significant sensitization. Following the induction of sensitization with the maximally effective sensitizing dose (2.5 g/kg), mice showed greater activation after challenges with 1.5, 2.0, 2.5, and 3.0 g/kg ethanol. The intervals (24, 48, or 96 h) between ethanol injections did not affect the induction or expression of sensitization. Finally, sensitization to 2.5 g/kg ethanol was expressed regardless of the context in which it was induced. CONCLUSIONS: Female Swiss mice develop a robust context-independent sensitization after repeated ethanol injections at all doses above 1.5 g/kg, including highly sedative doses such as 4 g/kg. [less ▲]

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See detailBehavioral effects of acetaldehyde in mice and rats: From reinforcement to amnesia
Quertemont, Etienne ULg; Didone, Vincent ULg; Closon, Catherine ULg

in Alcoholism, Clinical & Experimental Research (2008), 32(6), 289-289

Whereas human studies keep reporting evidence that acetaldehyde accumulation prevents alcohol drinking and alcoholism, animal studies support a rewarding rather than aversive role for acetaldehyde. In ... [more ▼]

Whereas human studies keep reporting evidence that acetaldehyde accumulation prevents alcohol drinking and alcoholism, animal studies support a rewarding rather than aversive role for acetaldehyde. In recent years, the reinforcing properties of acetaldehyde were demonstrated in various rodent strains and using different experimental methods. These results led to the hypothesis that acetaldehyde might be involved in the addictive properties of alcohol. In addition to its possible role in the reinforcing properties of alcohol, there is also evidence that acetaldehyde is involved in many other behavioral effects of ethanol. Using various behavioral procedures with both mice and rats, we have studied the behavioral effects of direct acetaldehyde injections. Additionally, in independent experiments we have compared the effects of ethanol in mice with or without a pre-treatment with the aldehyde dehydrogenase inhibitor cyanamide, which produces acetaldehyde accumulation. The results of these studies show that acetaldehyde produces a wide spectrum of behavioral effects, including reinforcement, aversion, sedation, ataxia and amnesia. These effects were mainly dependent upon acetaldehyde doses, with some of them showing an inverted U shape dose-response curve. These results also suggest that acetaldehyde might mediate or contribute to many of the behavioral effects of ethanol and especially to alcohol abuse and alcoholism. [less ▲]

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See detailCharacterization of the development of a behavioural sensitization in female Swiss mice
Didone, Vincent ULg; Quertemont, Etienne ULg

in Behavioural Pharmacology (2008), 19(5-6), 30-30

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See detailAcetaldehyde-related pathology: bridging the trans-disciplinary divide
Quertemont, Etienne ULg

in Novartis Foundation (Ed.) Acetaldehyde-related pathology: bridging the trans-disciplinary divide (2007)

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See detailThe psychostimulant and rewarding effects of cocaine in histidine decarboxylase knockout mice do not support the hypothesis of an inhibitory function of histamine on reward
Brabant, Christian ULg; Quertemont, Etienne ULg; Anaclet, Christelle et al

in Psychopharmacology (2007), 190(2), 251-263

RATIONALE AND OBJECTIVES: Lesion studies have shown that the tuberomammillary nucleus (TM) exerts inhibitory effects on the brain reward system. To determine whether histamine from the TM is involved in ... [more ▼]

RATIONALE AND OBJECTIVES: Lesion studies have shown that the tuberomammillary nucleus (TM) exerts inhibitory effects on the brain reward system. To determine whether histamine from the TM is involved in that reward inhibitory function, we assessed the stimulant and rewarding effects of cocaine in knockout mice lacking histidine decarboxylase (HDC KO mice), the histamine-synthesizing enzyme. If histamine actually plays an inhibitory role in reward, then it would be expected that mice lacking histamine would be more sensitive to the behavioral effects of cocaine. MATERIALS AND METHODS: The first experiment characterized spontaneous locomotion and cocaine-induced hyperactivity (0, 8, and 16 mg/kg, i.p.) in wild-type and HDC KO mice. The rewarding effects of cocaine were investigated in a second experiment with the place-conditioning technique. RESULTS: The first experiment demonstrated that histidine decarboxylase mice showed reduced exploratory behaviors but normal habituation to the test chambers. After habituation to the test chambers, HDC KO mice were slightly, but significantly, less stimulated by cocaine than control mice. This finding was replicated in the second experiment, when cocaine-induced activity was monitored with the place-conditioning apparatus. Furthermore, a significant place preference was present in both genotypes for 8 and 16 mg/kg cocaine, but not for 2 and 4 mg/kg. CONCLUSIONS: Our data confirm previous results demonstrating that HDC KO mice show reduced exploratory behaviors. However, contrary to the hypothesis that histamine plays an inhibitory role in reward, histamine-deficient mice were not more responsive to the psychostimulant effects of cocaine. [less ▲]

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See detailPreclinical and clinical pharmacology of alcohol dependence
Tambour, Sophie ULg; Quertemont, Etienne ULg

in Fundamental & Clinical Pharmacology (2007), 21(1), 9-28

In recent years, advances in neuroscience led to the development of new medications to treat alcohol dependence and especially to prevent alcohol relapse after detoxification. Whereas the earliest ... [more ▼]

In recent years, advances in neuroscience led to the development of new medications to treat alcohol dependence and especially to prevent alcohol relapse after detoxification. Whereas the earliest medications against alcohol dependence were fortuitously discovered, recently developed drugs are increasingly based on alcohol's neurobiological mechanisms of action. This review discusses the most recent developments in alcohol pharmacotherapy and emphasizes the neurobiological basis of anti-alcohol medications. There are currently three approved drugs for the treatment of alcohol dependence with quite different mechanisms of action. Disulfiram is an inhibitor of the enzyme aldehyde dehydrogenase and acts as an alcohol-deterrent drug. Naltrexone, an opiate antagonist, reduces alcohol craving and relapse in heavy drinking, probably via a modulation of the mesolimbic dopamine activity. Finally, acamprosate helps maintaining alcohol abstinence, probably through a normalization of the chronic alcohol-induced hyperglutamatergic state. In addition to these approved medications, many other drugs have been suggested for preventing alcohol consumption on the basis of preclinical studies. Some of these drugs remain promising, whereas others have produced disappointing results in preliminary clinical studies. These new drugs in the field of alcohol pharmacotherapy are also discussed, together with their mechanisms of action. [less ▲]

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See detailEffects of cyanamide and acetaldehyde accumulation on the locomotor stimulant and sedative effects of ethanol in mice
Tambour, Sophie ULg; Closon, Catherine; Tirelli, Ezio ULg et al

in Behavioural Pharmacology (2007), 18(8), 777-784

Ethanol administration induces both locomotor stimulant and sedative effects depending upon blood ethanol concentrations. Recent studies in rats and mice suggest that acetaldehyde, the first product of ... [more ▼]

Ethanol administration induces both locomotor stimulant and sedative effects depending upon blood ethanol concentrations. Recent studies in rats and mice suggest that acetaldehyde, the first product of ethanol metabolism, might be involved in the expression of both the stimulant and the sedative effects of ethanol. A number of studies have used the drug cyanamide in an attempt to clarify the role of acetaldehyde in the behavioral effects of ethanol. The results of such studies are, however, difficult to interpret because cyanamide is an inhibitor of the enzymes catalase and aldehyde dehydrogenase, two enzymes with opposite effects on brain acetaldehyde concentrations. This study was aimed at clarifying the effects of cyanamide on ethanol-induced locomotor stimulant and sedative effects in Swiss mice. The locomotor stimulant effects of ethanol were measured in standard activity boxes, whereas the sedative effects of ethanol were quantified using the loss of righting reflex procedure. Cyanamide prevented the locomotor stimulant effects of 2 g/kg ethanol, although this was mainly due to a potentiation of the inhibitory effects of ethanol as evidenced by a prolongation of ethanol-induced loss of righting reflex. Additionally, 4-methylpyrazole, an inhibitor of the enzyme alcohol dehydrogenase, prevented these effects of cyanamide. It is concluded that in vivo the effects of cyanamide are predominantly due to the inhibition of the enzyme aldehyde dehydrogenase, rather than to its effects on catalase. [less ▲]

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See detailAcute and chronic effects of acetaldehyde on learning and memory in mice
Quertemont, Etienne ULg; Tambour, Sophie ULg; Didone, Vincent ULg

in Alcohol & Alcoholism (2007), 42 Suppl. 1

Acetaldehyde has been postulated to mediate several of the behavioral effects of ethanol, including its reinforcing properties. At the highest doses, alcohol disrupts the acquisition and performance of ... [more ▼]

Acetaldehyde has been postulated to mediate several of the behavioral effects of ethanol, including its reinforcing properties. At the highest doses, alcohol disrupts the acquisition and performance of memory tasks, culminating with the blackout experience at high blood alcohol concentrations. However, it remains unknown whether acetaldehyde is involved in such memory impairments induced by acute ethanol. Additionally, chronic alcohol consumption in humans sometimes leads to persistent memory impairments partly due to serious brain damages. The Wernicke-Korsakoff syndrome, characterized by severe anterograde amnesia, is the most serious memory disorder induced by chronic alcohol. The aim of the present study was to show whether acute and chronic treatments with acetaldehyde, the first metabolite of ethanol, lead to similar memory impairments as ethanol in mice. Memory performances of Swiss and C57BL/6J mice were tested in both the passive avoidance task and the fear conditioning procedure. In the first part of the experiments mice were injected with acute acetaldehyde (50 to 300 mg/kg) immediately after the training phase. In the second part of the experiment, mice were tested for memory performance after 10 daily acetaldehyde injections. The first part of the experiments shows that acute acetaldehyde administrations produce a strong amnesic effect in both experimental paradigms. Additionally, the amnesic effects of acetaldehyde were more consistent than those observed after ethanol administration. In the second part of the studies, we show that 10 daily acetaldehyde injections to mice led to a severe and persistent anterograde amnesia in both the pavlovian and the operant learning tasks. In conclusion, acute acetaldehyde produces strong amnesic effects trough yet unknown pharmacological mechanisms. In addition, chronic acetaldehyde administration leads to persistent memory impairments. These results suggest that acetaldehyde might be involved in both the acute amnesic effects of high ethanol doses and the neurotoxic effects of chronic alcohol consumption. [less ▲]

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See detailNeurobiological and genetic aspects of alcohol addiction: a special focus on acetaldehyde, the first metabolite of ethanol
Quertemont, Etienne ULg

Scientific conference (2007)

Although alcoholism is one of the most common forms of addiction, its neurobiological mechanisms still remain unclear. The reinforcing properties of ethanol are mediated by the interaction of multiple ... [more ▼]

Although alcoholism is one of the most common forms of addiction, its neurobiological mechanisms still remain unclear. The reinforcing properties of ethanol are mediated by the interaction of multiple neurotransmitter systems, including dopamine, serotonin, glutamate, GABA, endogenous opioids and endocannabinoids. Additionally, long term changes in these neurotransmitter systems are believed to promote the development of alcoholism, probably through specific alterations of brain regions involved in motivation. In humans, it has been clearly demonstrated that alcohol dependence is a genetically heritable disease, at least to some extent. Twin and adoptions studies indicate that 50-60% of the phenotypic variations in alcohol dependence are accounted for by a genetic component. Among the multiple genes that are possibly involved in the development of alcohol dependence and addiction, there is very strong evidence that genes related to the metabolism of ethanol play a major role. For example, genetic polymorphisms in alcohol and aldehyde dehydrogenase enzymes strongly affect alcoholism susceptibility in humans. In recent years, several studies have also provided evidence that acetaldehyde, the first metabolite of ethanol, contributes to alcohol abuse and alcoholism. In rodents such as rats and mice, low doses of brain acetaldehyde induce reinforcing and stimulant effects, although high concentrations of peripheral blood acetaldehyde produce adverse reactions. These results led to the controversial theory that acetaldehyde mediates or at least contributes to the reinforcing and addictive properties of ethanol. [less ▲]

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See detailEffects of the H-3-receptor inverse agonist thioperamide on the psychornotor effects induced by acutely and repeatedly given cocaine in C57BL/6J mice
Brabant, Christian ULg; Quertemont, Etienne ULg; Tirelli, Ezio ULg

in Pharmacology, Biochemistry & Behavior (2006), 83(4), 561-569

Previous studies have shown that histamine H(3) blockers potentiate the psychomotor and rewarding effects of cocaine. The present study examined the influence of thioperamide, an inverse H(3) receptor ... [more ▼]

Previous studies have shown that histamine H(3) blockers potentiate the psychomotor and rewarding effects of cocaine. The present study examined the influence of thioperamide, an inverse H(3) receptor agonist, on the development of psychomotor sensitization and stereotyped activity induced by acute or intermittent cocaine in C57BL/6J mice. In the first experiment, mice were injected i.p. with saline, 10 or 20mg/kg thioperamide and saline or 8mg/kg cocaine, 10min apart, before being tested for their locomotor activity (providing data on the acute effects of thioperamide on cocaine-induced activity). Subsequently, mice were treated in the same manner every other day over six additional sessions. Sensitization was assessed by the responsiveness to a cocaine challenge (8mg/kg, i.p.) given 2 and 14days following the intermittent treatment. In experiments 2 and 3, we tested the effects of thioperamide (10 or 20mg/kg, i.p.) on gnawing and sniffing induced or affected by relatively high doses of cocaine (24 or 32mg/kg, s.c.), the drugs being given 10min apart. In the first experiment, both doses of thioperamide amplified cocaine-induced psychomotor hyperactivity almost on all experimental sessions. However, the histamine inverse agonist did not affect the induction of a psychomotor sensitization. All cocaine-treated mice showed similar levels of sensitized activity 2 and 14days after the intermittent treatments, whether they received thioperamide or not. The second and the third experiments showed that thioperamide did not affect gnawing and sniffing induced by cocaine. Taken together, these results indicate that H(3) receptors clearly contribute to the neurobiological mechanisms of the locomotor component of cocaine-induced psychomotor activation, but less likely to those underlying the development of cocaine behavioral sensitization or the expression of cocaine-induced oro-facial stereotypies. [less ▲]

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See detailLocomotor effects of ethanol and acetaldehyde after peripheral and intraventricular injections in Swiss and C57BL/6J mice
Tambour, Sophie ULg; Didone, Vincent ULg; Tirelli, Ezio ULg et al

in Behavioural Brain Research (2006), 172(1), 145-154

Several studies have suggested that acetaldehyde, the first product of ethanol metabolism, is involved in the locomotor stimulant effects of ethanol in mice, although it has never been formally tested ... [more ▼]

Several studies have suggested that acetaldehyde, the first product of ethanol metabolism, is involved in the locomotor stimulant effects of ethanol in mice, although it has never been formally tested whether acetaldehyde injected directly into the brain of mice has stimulant properties. Recently, it was also shown in rats that both ethanol and acetaldehyde can induce opposite locomotor effects according to the route of administration. Whereas peripheral administrations of ethanol and acetaldehyde induced locomotor depressant effects, their infusions directly into the brain produced locomotor stimulation. The aim of the present study was to characterize in mice the locomotor effects of ethanol and acetaldehyde injected either peripherally by the intraperitoneal route or centrally into the brain ventricles. Additionally, the effects of ethanol and acetaldehyde were compared in two strains of mice known for their differential sensitivity to the locomotor effects of ethanol, namely Swiss and C57BL/6J mice. Ethanol induced a biphasic effect on locomotor activity in Swiss mice, with stimulant effects at low to moderate doses and depressant effects at higher doses. Such a profile of effects was observed whatever the route of administration, peripheral or central. In C57BL/6J mice, ethanol only induced monophasic depressant effects. In this mouse strain, no evidence of the stimulant effects of ethanol was found after either an i.p. or an i.c.v. administration of ethanol. In contrast to ethanol, acetaldehyde yielded only depressant effects in both strains of mice after both peripheral and central administrations. These results indicate that the route of administration does not alter the locomotor effects of ethanol and acetaldehyde in mice. Additionally, the present study shows that the stimulant properties of acetaldehyde, even after direct infusion into the brain, are not as obvious as previously speculated. [less ▲]

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