Cyclooxygenase inhibitors antagonize the rate-depressant effects of ethanol on fixed-ratio responding

George, Frank R.; Meisch, Richard A.

doi:10.1016/0741-8329(90)90095-t

Cited by 7 publications

(4 citation statements)

References 37 publications

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“…Prostaglandin synthatase inhibitors, which inhibit actions of the enzyme complex cyclooxygenase, significantly antagonize the effects of alcohol. This suggests that certain effects of ethanol are mediated at least partly through a prostaglandinrelated pathway (George & Meisch, 1990). In the present study, COX-2 inhibitors rofecoxib or nimesulide attenuated the various behavioural alterations due to alcohol withdrawal, thus providing the first evidence regarding its beneficial effect in alcohol physical dependence, while the non-selective COXinhibitor naproxen, which displays a high potency towards the COX-1 isoform, was not effective in reversing the symptoms, showing that the COX-2 isoenzyme, but not COX-1 inhibitors, plays a large role in ethanol withdrawal symptoms.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of cyclooxygenase‐2 (COX‐2) inhibitors but not non‐selective cyclooxygenase (COX)‐inhibitors on ethanol withdrawal‐induced behavioural changes

2005

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Cyclooxygenase (COX) is reported to play a significant role in neurodegeneration. Recent studies have shown that chronic ethanol administration up-regulates cyclooxygenase expression. In the present study we examined the effect of nimesulide (a preferential COX-2 inhibitor), rofecoxib (a highly selective COX-2 inhibitor) or naproxen (a non-selective COX-inhibitor displaying high affinity towards the COX-1 isoenzyme) on alcohol-induced withdrawal symptoms. Mice were made physically dependent on alcohol by the chronic administration of ethanol (2 g/kg of 10% v/v), intragastrically, twice on day 1 and then once-daily on successive days for a total of 7 days. Nimesulide [2.5 mg/kg, intraperitoneally (i.p.)], rofecoxib (2 mg/kg, i.p.) or naproxen (7 mg/kg, i.p.) were administered daily for 7 days before administering alcohol intragastrically. After 24 hours of the last alcohol administration, the treatments were reversed and the mice were tested for withdrawal, so that the animals that had received COX-inhibitors followed 30 minutes later by ethanol on days 1-7 were challenged with saline. Similarly, the animals which received saline followed 30 minutes later by ethanol received only saline. Behavioural analysis revealed hyperlocomotor activity, increased anxious response and increased hyperalgesia in mice. Also, alcohol withdrawal decreased the threshold for Pentylenetetrazole-(PTZ)-induced convulsions. Pretreatment with COX-inhibitors rofecoxib (2 mg/kg, i.p.) or nimesulide (2.5 mg/kg, i.p.) displayed significant protection against ethanol-induced withdrawal symptoms, while naproxen (7 mg/kg, i.p.) was not effective in reversing alcohol-induced withdrawal symptoms. The results of the present study suggest strongly the possible role of cyclooxygenases, particularly COX-2 inhibitors, on ethanol-induced withdrawal symptoms and the potential use of COX-2 inhibitors in their prevention and treatment.

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Section: Discussionmentioning

confidence: 99%

Protective effect of cyclooxygenase‐2 (COX‐2) inhibitors but not non‐selective cyclooxygenase (COX)‐inhibitors on ethanol withdrawal‐induced behavioural changes

2005

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“…100 Blocking PG production attenuates the behavioral effects of alcohol, and it can be inferred that PGs have a role in the development of alcohol addiction. 101 Chronic alcohol consumption also is associated with paradoxical regulation of PGE 1 and PGE 2 . 102 In another study overproduction of PGE 1 has been associated with cocaine abuse.…”

Section: Addictionmentioning

confidence: 99%

<p>Prostaglandins as the Agents That Modulate the Course of Brain Disorders</p>

Famitafreshi

Karimian

2020

DNND

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Neurologic and neuropsychiatric diseases are associated with great morbidity and mortality. Prostaglandins (PGs) are formed by sequential oxygenation of arachidonic acid in physiologic and pathologic conditions. For the production of PGs cyclooxygenase is a necessary enzyme that has two isoforms, that are named COX-1 and COX-2. COX-1 produces type 1 prostaglandins and on the other hand, COX-2 produces type 2 prostaglandins. Recent studies suggest PGs abnormalities are present in a variety of neurologic and psychiatric disorders. In a disease state, type 2 prostaglandins are mostly responsible and type 1 PGs are not so important in the disease state. In this review, the importance of prostaglandins especially type 2 in brain diseases has been discussed and their possible role in the initiation and outcome of brain diseases has been assessed. Overall the studies suggest prostaglandins are the agents that modulate the course of brain diseases in a positive or negative manner. Here in this review article, the various aspects of PGs in the disease state have discussed. It appears more studies must be done to understand the exact role of these agents in the pathophysiology of brain diseases. However, the suppression of prostaglandin production may confer the alleviation of some brain diseases.

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“…Alcohol reliably reduces the number of lever presses for water. Because blocking PG production attenuates the behavioral effects of alcohol, it can be inferred that PGs have a role in the development of alcohol addiction . Grupp et al .…”

Section: Lipid Signaling Effects On Ethanol Abusementioning

confidence: 99%

“…Because blocking PG production attenuates the behavioral effects of alcohol, it can be inferred that PGs have a role in the development of alcohol addiction. 90 Grupp et al find that the ␤ 1,2 -adrenergic agonist isoproterenol attenuates alcohol consumption. Isoproterenol raises blood glucose levels, which correlate with a reduction in alcohol intake.…”

Section: Sex Steroids and Alcoholmentioning

confidence: 99%

Lipids and addiction: how sex steroids, prostaglandins, and cannabinoids interact with drugs of abuse

Leishman

Kokesh

Bradshaw

2013

Annals of the New York Academy of Sciences

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Lipidomics aims to identify and characterize all endogenous species of lipids and understand their roles in cellular signaling and, ultimately, the functioning of the organism. We are on the cusp of fully understanding the functions of many of the lipid signaling systems that have been identified for decades (e.g., steroids, prostaglandins), whereas our understanding of newer lipid signaling systems (e.g., endocannabinoids, N-acyl amides) still lags considerably behind. With an emphasis on their roles in the neurophysiology of addiction, we will examine three classes of lipids--sex steroids, prostaglandins, and cannabinoids--and how they work synergistically in the neurocircuitry of motivation. We will first give a brief overview of the biosynthesis for each class of lipid and its receptors, and then summarize what is known about the collective roles of the lipids in cocaine and alcohol abuse. This approach provides a novel view of lipid signaling as a class of molecules and their synergistic roles in addiction.

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Cyclooxygenase inhibitors antagonize the rate-depressant effects of ethanol on fixed-ratio responding

Cited by 7 publications

References 37 publications

Protective effect of cyclooxygenase‐2 (COX‐2) inhibitors but not non‐selective cyclooxygenase (COX)‐inhibitors on ethanol withdrawal‐induced behavioural changes

Protective effect of cyclooxygenase‐2 (COX‐2) inhibitors but not non‐selective cyclooxygenase (COX)‐inhibitors on ethanol withdrawal‐induced behavioural changes

<p>Prostaglandins as the Agents That Modulate the Course of Brain Disorders</p>

Lipids and addiction: how sex steroids, prostaglandins, and cannabinoids interact with drugs of abuse

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