Recent Advances in Pharmacological Research on Alcohol

Wozniak, Krystyna M.; Linnoila, Markku

doi:10.1007/978-1-4899-1648-8_12

Cited by 15 publications

(8 citation statements)

References 280 publications

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“…For example, one theoretical paper which failed to present any human data regarding alcohol/cocaine interactions discussed none the less the role of ‘kindling of a limbic dyscontrol system’ and concluded that ‘despite uncertainty about the mechanisms of alcohol‐related enhancement of aggression, it is arguable that drinking may increase the probability of a cocaine‐associated episode of violence via the disinhibitory action of alcohol’ (Davis 1996, p. 1290). However, alcohol and cocaine each elevate extraneuronal dopamine and serotonin levels, and this may lead to deficits in impulse control and, thus, violent behaviour (Ritz, Kuhar & George 1992; Wozniak & Linnoila 1992).…”

Section: Resultsmentioning

confidence: 99%

Effects of concurrent use of alcohol and cocaine

2002

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The combination of alcohol and cocaine is popular among drug users, perhaps because of more intense feelings of 'high' beyond that perceived with either drug alone, less intense feelings of alcohol-induced inebriation and tempering of discomfort when coming down from a cocaine 'high'. A review is presented of the medical literature on psychological and somatic effects and consequences of combined use of alcohol and cocaine in man. The search was carried out with Medline, the Science Citation Index/Web of Science and Toxline. Exclusion and inclusion criteria for this search are identified. There is generally no evidence that the combination of the two drugs does more than enhance additively the already strong tendency of each drug to induce a variety of physical and psychological disorders. A few exceptions must be noted. Cocaine consistently antagonizes the learning deficits, psychomotor performance deficits and driving deficits induced by alcohol. The combination of alcohol and cocaine tends to have greater-than-additive effects on heart rate, concomitant with up to 30% increased blood cocaine levels. Both prospective and retrospective data further reveal that co-use leads to the formation of cocaethylene, which may potentiate the cardiotoxic effects of cocaine or alcohol alone. More importantly, retrospective data suggest that the combination can potentiate the tendency towards violent thoughts and threats, which may lead to an increase of violent behaviours.

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Section: Resultsmentioning

confidence: 99%

Effects of concurrent use of alcohol and cocaine

2002

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“…Ethanol does not have any specific receptors, and it exerts numerous pharmacological effects through various neurotransmitters and neuromodulators (Faingold et al, 1998). The ethanol-induced enhancement of the meso-limbic 'reward circuit' could underlie, at least in part, stimulation and euphoria (Ahlenius et al, 1973;Wozniak and Linnoila, 1992). Microdialysis studies in rats demonstrated that acute doses of ethanol increased the concentration of dopamine in the nucleus accumbens (Di Chiara and Imperato, 1985;Imperato and Di Chiara, 1986;Wozniak et al, 1991;Yoshimoto et al, 1992;Di Chiara et al, 1996) which is a part of the mesolimbic dopaminergic system.…”

Section: Discussionmentioning

confidence: 97%

“…Alcohol may affect the mood and cognitive processes relevant to social behaviour. Ethanol does not have specific binding receptors, yet it may influence the mental process through its interaction with several different neurotransmitter systems (Engel et al, 1992;Faingold et al, 1998); the aminergic systems (noradrenaline, dopamine and serotonin) on mood and attention (Wozniak and Linnoila, 1992), the opioid systems modifying craving for alcohol (Wozniak and Linnoila, 1992;Nylander et al, 1994), and the GABA A receptor on the sedation, anxiolytic and muscle relaxant (Cott et al, 1976;Engel and Liljequest, 1983). Although alcohol has been generally regarded as a CNS depressant, a previous study reported its stimulant-like properties (Pohorecky, 1978).…”

Section: Introductionmentioning

confidence: 97%

“…Higher levels (100 mg/dl), on the other hand, significantly impair mental and cognitive ability and cause sedation. These sedative effects are related either to generally impaired membrane functions or to depressive effects on arousal systems projecting from the brain stem (Wozniak and Linnoila, 1992). Alcohol might have biphasic effects on mood and cognitive process.…”

Section: Introductionmentioning

confidence: 99%

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Low doses of alcohol have a selective effect on the recognition of happy facial expressions

Kano

Gyoba

Kamachi³

et al. 2002

Human Psychopharmacology

113

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Alcohol is one of the most widely used recreational drugs, yet it is associated with undesirable social behaviour. It is used primarily for its psychoactive properties, increasing sociability and talkativeness. We hypothesize that low doses of alcohol can improve the performance related to positive emotional cognition. In this experiment, we examined the effect of low doses of alcohol on the processing of emotional facial expressions. Fifteen young male volunteers drank alcohol at volumes of 30, 60, 120 ml (0.14, 0.28, 0.56 g/kg) and performed discrimination tasks on morphed facial emotion expressions of anger, happiness, sadness and surprise-neutral. One-way ANOVA co-varying pretreatment performances revealed significant differences between alcohol levels in happy face discrimination ( p<0.01). Bonferroni correction demonstrated that low doses of alcohol caused a significantly better discrimination of happy faces, and that the performances were worse with higher doses ( p<0.001). No significance was observed with the other three emotional faces. These results indicate that low doses of alcohol affect positive emotional cognition of happy facial expressions.

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“…With regards to the NAc, rodent studies confirm that intra-NAc alcohol perfusions increase the release of dopamine in the same brain region (e.g. [59,38,[60][61][62]). An effect that is suggested to be regulated via a neuronal circuitry involving glycine receptors in the NAc as well as anterior ventral tegmental nAChR [59,63,64].…”

Section: Preclinical Evidence: Acute Alcohol Exposure and Dopaminementioning

confidence: 99%

Dopamine and Alcohol Dependence: From Bench to Clinic

Jayaram‐Lindström¹,

Ericson²,

Steensland³

et al. 2016

Recent Advances in Drug Addiction Research and Clinical Applications

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Alcohol dependence, a chronic relapsing psychiatric disorder, is a major cause of mortality and morbidity. The role of dopamine in alcohol-induced reward as well in the development of alcohol dependence is reviewed herein. Both preclinical and clinical studies have suggested that alcohol activates the mesolimbic dopamine system (defined as a dopamine projection from the ventral tegmental area (VTA) to the nucleus accumbens (NAc, i.e. ventral striatum)) leading to a euphoric sensation. Alcohol dependence is characterized by a disruption in the reward-related brain areas including fewer dopamine D2 receptors in ventral striatum. Investigations of the underlying dopaminergic mechanisms involved during the development and maintenance of alcohol dependence could identify novel targets. Human and rodent experimental studies show that dopamine receptor antagonists, agonists and partial agonists as well as dopamine stabilizers influencing dopamine transmission, alter alcohol-mediated behaviours and thus may be potential treatment targets for alcohol dependence. Although there exists promising preclinical results, the majority of placebo-controlled randomized clinical trials with traditional dopamine antagonists and agonists have so far have been discouraging. Furthermore, the severe side-effect profiles of many of these compounds may limit their clinical use. Newer dopamine agents, such as partial agonists and dopamine stabilizers, attenuate alcohol-mediated behaviours in rodents as well as humans. Preclinical as well as clinical studies have shown that substances indirectly targeting the mesolimbic dopamine system may be potential targets for attenuation of alcohol reward. Collectively, the data reviewed herein may contribute to further understanding the complex mechanisms involved in development of alcohol dependence and we suggest that the newer dopamine agents as well as indirect modulators of dopamine signalling deserve to be further evaluated for treatment of alcohol dependence.

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Recent Advances in Pharmacological Research on Alcohol

Cited by 15 publications

References 280 publications

Effects of concurrent use of alcohol and cocaine

Effects of concurrent use of alcohol and cocaine

Low doses of alcohol have a selective effect on the recognition of happy facial expressions

Dopamine and Alcohol Dependence: From Bench to Clinic

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