Acute kinetic and dynamic interactions of zimelidine with ethanol

Naranjo, Claudio A.; Sellers, Edward M.; Kaplan, Howard L.; Hamilton, Carolyn; Khouw, V

doi:10.1038/clpt.1984.236

Cited by 27 publications

(11 citation statements)

References 3 publications

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“…Zimeli dine, however, was reported not to block the effects of ethanol on psychomotor performance [Scott et al, 1982], It is apparent from the data presented by Weingartner et al [1983a], however, that zimelidine had little effect on the impairment of recognition memory produced by eth anol and that acute administration of zimelidine alone had almost as great an effect in impairing recall as did ethanol. More recently another study involving human volunteers failed to obtain similar results [Naranjo et al, 1984]. In this study ethanol-induced impairments of psy chomotor performance and of memory were enhanced by zimelidine.…”

Section: Discussionmentioning

confidence: 48%

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Zimelidine Does Not Antagonise the Effects of Alcohol or Diazepam on the Acquisition of Conditioned Fear in Mice

Sanger¹,

Joly²

1986

Neuropsychobiology

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Recent work has suggested that, in man, the specific inhibitor of serotonin reuptake, zimelidine, can block the effects of ethanol on memory processes without affecting psychomotor performance decrements produced by ethanol. The present study was carried out to investigate whether a similar interaction between ethanol and zimelidine could be observed in mice. Using a 2-trial conditioned fear test known to be sensitive to the effects of benzodiazepines and similar drugs, it was found that ethanol, administered before the first trial, produced a dose-related disruption of fear conditioning as shown on the second trial. In a second experiment several doses of zimelidine were administered at the same time as a dose of either ethanol or diazepam. No evidence was obtained for a zimelidine-induced antagonism of the effects of either ethanol or diazepam.

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Section: Discussionmentioning

confidence: 48%

“…In these, and other, studies it was also observed that zimelidine did not affect the actions of ethanol on psychomotor performance in tasks not involving memory [Sco/i et al, 1982). Other researchers, however, have reported that zimelidine can potentiate the psychomotor impairment produced byethanol [Naranjo et al, 1984].…”

mentioning

confidence: 96%

Zimelidine Does Not Antagonise the Effects of Alcohol or Diazepam on the Acquisition of Conditioned Fear in Mice

Sanger¹,

Joly²

1986

Neuropsychobiology

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“…Therefore, serotonin uptake inhibitors may decrease appetite, or desire to eat, and also decrease desire to drink alcohol. In the outpatient studies, increases in abstinent days were frequently observed (Naranjo et al, 1984b;, indicating that these drugs may exert their main effect before the initiation of drinking. Consistent with these findings, decreases in desire to drink were also reported with zimeldine (Amit et al, 1985), fluoxetine (Gorelick and Paredes, 1992) and viqualine .…”

Section: Effects Of Serotonin Uptake Inhibitors On Alcohol Intake In mentioning

confidence: 98%

“…No consistent temporal relationship between the few side effects and decreases in drinking could be discerned. In addition, serotonin uptake inhibitors do not produce an alcohol-sensitizing reaction and have not been found to have any adverse pharmacokinetic interactions with alcohol (Naranjo et al, 1984b;Lemberger et al, 1985;Lader et al, 1986;Sullivan et al, 1989;Shaw et ai., 1989).…”

Section: Effects Of Serotonin Uptake Inhibitors On Alcohol Intake In mentioning

confidence: 98%

Serotonin-altering medications and desire, consumption and effects of alcohol-treatment implications

Naranjo

Bremner

1994

Toward a Molecular Basis of Alcohol Use and Abuse

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SummaryThe relationship between serotonin neurotransmission and alcohol consumption (AC) was first determined in preclinical studies. AC generally increases following treatments which decrease serotonin activity, and levels of 5-HT and metabolites are low in some brain regions of alcohol-preferring rats. Pharmacological treatments which enhance serotonergic neurotransmission (uptake inhibitors, releasers, agonists) consistently reduce AC in rats. Serotonin uptake inhibitors (SUI; e.g., citalopram, fluoxetine) have been studied extensively in humans. In several double-blind randomized, placebo-controlled trials, SUI consistently decreased short-term (2-4 weeks) AC by averages of 15% to 20% in nondepressed mildly/moderately dependent alcoholics who received no other treatment. Some subjects decreased AC by up to 60%. The effects of SUI on AC were dose-dependent and not related to side effects (few and mild) or changes in anxiety or depression (not observed). SUI decreased desire to drink and liking for alcohol, suggesting a mechanism of action, to be considered in the development of treatments to reduce AC and prevent relapse. However, while an adjunctive brief psychosocial intervention enhanced the short-term effect of a SUI, the long-term (l2-week) effects of SUI and placebo were similar. Other drugs acting on the 5-HT system have been tested in humans, but results are inconclusive. For example, buspirone, a 5-HT IA receptor partial agonist, reduced anxiety and alcohol craving, but not AC; a 5-HT partial agonist, m-CPP, increased craving in abstinent alcoholics; modest reductions in AC were observed with a 5-HT) antagonist, ondansetron (0.5 mg/day, but not 4 mg/day). Ritanserin, a 5-HT2 antagonist, reduced desire to drink and prevented relapse in a small (n=5) study, and there was some indication that it reduced desire to drink and enhanced alcohol effects without reducing AC, in another study. The therapeutic potential of these medications is being studied. SUI and other serotonin-altering medications are promising new neuropharmacological treatments for AC.

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“…The overall activity of other neurotransmitters is altered during alcoholic withdrawal, including that ofdopamine [16], serotonin [17], acetylcholine [18], gamma-amino-butyric acid [19] and leu-enkephalin [20]. However, studies of the effect of these alterations on hangover were not evident.…”

Section: Adaptation and Neurotransmittersmentioning

confidence: 99%

Alcoholic hangover and performance: a review

Lemon

1993

Drug and Alcohol Review

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The study of alcoholic hangover is reviewed, with particular concern given to its effects upon skills performance. Different models of hangover, and the evidence gathered in their support, are surveyed. Several factors appear to contribute to hangover, and individuals may be differentially susceptible to these influences. The severity of hangover is affected by dose, coproducts of manufacture, and a number of psychological variables. Hangover is differentiated from post-intoxication effects on performance, and the results of a variety of studies on these effects are considered. Post-intoxication effects have been found in a variety of tasks, but no tasks have been consistently affected in a number of studies. This may reflect the fact that few studies have used the same tasks to assess performance. Proposed mechanisms of post-intoxication effects are considered, and the most consistent symptom accompanying impaired performance is found to be fatigue. This notion finds some support in electroencephalographic data collected during the period following intoxication.

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Acute kinetic and dynamic interactions of zimelidine with ethanol

Cited by 27 publications

References 3 publications

Zimelidine Does Not Antagonise the Effects of Alcohol or Diazepam on the Acquisition of Conditioned Fear in Mice

Zimelidine Does Not Antagonise the Effects of Alcohol or Diazepam on the Acquisition of Conditioned Fear in Mice

Serotonin-altering medications and desire, consumption and effects of alcohol-treatment implications

Alcoholic hangover and performance: a review

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