Alcohol intake, ethanol-induced narcosis and intoxication in rats following neonatal 6-hydroxydopamine or 5,7-dihydroxytryptamine treatment

Kiianmaa, Kalervo; Attila, L. M. J.

doi:10.1007/bf00499060

Cited by 25 publications

(3 citation statements)

References 21 publications

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“…However disruptions of DA signaling through lesioning of accumbens DA inputs do not impact voluntary ethanol intake (Rassnick et al 1993). Lesions of ascending NE tracts can generate increases (Kiianmaa and Attila 1979;Kiianmaa et al 1975) or decreases in ethanol intake Corcoran et al 1983).…”

Section: Effects Of Noradrenergic Receptor Modulation On Alcohol-related Behaviors and Neural Systemsmentioning

confidence: 99%

Central Noradrenergic Interactions with Alcohol and Regulation of Alcohol-Related Behaviors

Vazey

Hartog

Moorman

2018

Handbook of Experimental Pharmacology

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Alcohol use disorder (AUD) results from disruption of a number of neural systems underlying motivation, emotion, and cognition. Patients with AUD exhibit not only elevated motivation for alcohol but heightened stress and anxiety, and disruptions in cognitive domains such as decision-making. One system at the intersection of these functions is the central norepinephrine (NE) system. This catecholaminergic neuromodulator, produced by several brainstem nuclei, plays profound roles in a wide range of behaviors and functions, including arousal, attention, and other aspects of cognition, motivation, emotional regulation, and control over basic physiological processes. It has been known for some time that NE has an impact on alcohol seeking and use, but the mechanisms of its influence are still being revealed. This chapter will discuss the influence of NE neuron activation and NE release at alcohol-relevant targets on behaviors and disruptions underlying alcohol motivation and AUD. Potential NE-based pharmacotherapies for AUD treatment will also be discussed. Given the basic properties of NE function, the strong relationship between NE and alcohol use, and the effectiveness of current NE-related treatments, the studies presented here indicate an encouraging direction for the development of precise and efficacious future therapies for AUD.

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Section: Effects Of Noradrenergic Receptor Modulation On Alcohol-related Behaviors and Neural Systemsmentioning

confidence: 99%

Central Noradrenergic Interactions with Alcohol and Regulation of Alcohol-Related Behaviors

Vazey

Hartog

Moorman

2018

Handbook of Experimental Pharmacology

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“…Studies have also shown that the anticipation of a reward increases the firing of accumbal dopamine neurons [41]. It should, however, be mentioned that results from studies with lesion of the mesocorticolimbic dopamine pathways have shown contradicting results with both decreased [48][49][50] and unaltered alcohol intake [51][52][53][54][55][56]. These inconsistent results indicate that the role of accumbal dopamine in reinforcement is complex and highlights that the rewarding properties of alcohol may extend beyond direct or indirect effects on dopamine, involving interactions with several other neurotransmitters including acetylcholine, glutamate, GABA, serotonin (5HT), noradrenaline, taurine and opioids, as well as hormones and peptides [24,57,58].…”

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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“…Previous studies witl, rats tad skown that neonatal treatment witl tl,e neurotoxin 6-! ydroxydopamine I01 (6-OHDA), which causes lesions of catecholaminergic neurons, produces severe, long-lasting impairments in avoidance learning (Shaywitz et al, 1976 and without affecting early sleep-wake behavior (Adrien, 1981) or adult voluntary alcohol consumption (Kiianmaa and Attila, 1979). Early clomipramine exposure, however, has not been found to affect avoidance learning in rats (Mirmiran et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Effect of neonatal nomifensine exposure on adult behavior and brain monoamines in rats

Hilakivi

Ahtee

et al. 1987

J. Neural Transmission

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The aim of the study was to examine the effects of early postnatal exposure to nomifensine, an inhibitor of catecholamine uptake, on concurrent active (REM) sleep, on later alcohol related behavior and on monoamine concentrations in various brain regions of rats. For these purposes rats were given daily injections of 10 mg/kg nomifensine s.c. between the 7th and the 18th postnatal days. During the nomifensine exposure active sleep, expressed as a percentage of total sleeping time, was reduced. At one month of age, the nomifensine rats showed increased ambulation and had lower defecation scores in the open-field than the controls. Neonatal exposure to nomifensine increased voluntary intake of 10% (v/v) alcohol when the rats were 2-3 months of age. The rats, however, did not exhibit preservation in the T-maze, and similarly to control rats suppressed drinking 0.1 M lithium chloride even when thirsty. Measurement of cerebral monoamine concentrations at the age of 3 months suggested that neonatal nomifensine treatment interferes with the noradrenergic and serotonergic systems in several regions of the brain. Concentrations of noradrenaline and 5-hydroxyindoleacetic acid (5-HIAA) were decreased in the cerebral cortex and frontal cortex, concentration of 5-HIAA was decreased in the neostriatum, and concentrations of noradrenaline, 5-hydroxytryptamine (5-HT) and 5-HIAA were elevated in the lower brain stem. Taken together, these findings show that exposure to nomifensine during the 2nd and 3rd postnatal weeks suppresses neonatal active sleep, causes changes in the adult open-field behavior, and increases voluntary alcohol intake, perhaps due to a long-lasting alteration in brain monoamines.

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Alcohol intake, ethanol-induced narcosis and intoxication in rats following neonatal 6-hydroxydopamine or 5,7-dihydroxytryptamine treatment

Cited by 25 publications

References 21 publications

Central Noradrenergic Interactions with Alcohol and Regulation of Alcohol-Related Behaviors

Central Noradrenergic Interactions with Alcohol and Regulation of Alcohol-Related Behaviors

Dopamine and Alcohol Dependence: From Bench to Clinic

Effect of neonatal nomifensine exposure on adult behavior and brain monoamines in rats

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