Acute ethanol challenge inhibits glycogen synthase kinase-3beta in the rat prefrontal cortex.

Intracellular signalling pathways emerge as key mediators of the molecular and behavioural effects of addictive drugs including ethanol. Previously, we demonstrated that the innate high ethanol preference in AA rats is driven by dysfunctional endocannabinoid signalling in the medial prefrontal cortex (mPFC). Here, we report that acute ethanol challenge, at a dose commonly regarded as reinforcing, strongly phosphorylates glycogen synthase kinase-3beta (GSK-3beta) in this region with corresponding increased phosphorylation of AKT, a major regulator of GSK-3beta.

[The relationship between the craving for alcohol and relapse of the disease].

The craving for alcohol was studied using 2 Russian and 4 international scales, including ratings of the clinician and self-rating of the patient. Depression and anxiety as well as the content of alcohol in exhaled air were assessed. The data were compared to the scores of the Impulsive Relapse Questionnaire.

Neuroplasticity in brain reward circuitry following a history of ethanol dependence.

Mitogen-activated and extracellular regulated kinase (MEK) and extracellular signal-regulated protein kinase (ERK) pathways may underlie ethanol-induced neuroplasticity. Here, we used the MEK inhibitor 1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene (UO126) to probe the role of MEK/ERK signaling for the cellular response to an acute ethanol challenge in rats with or without a history of ethanol dependence. Ethanol (1.

Effect of memantine on cue-induced alcohol craving in recovering alcohol-dependent patients.

Objective: Ethanol blocks N-methyl-d-aspartic acid (NMDA) glutamate receptors. Increased NMDA receptor function may contribute to motivational disturbances that contribute to alcoholism. The authors assessed whether the NMDA receptor antagonist memantine reduces cue-induced alcohol craving and produces ethanol-like subjective effects.

The NMDA receptor channel blocker memantine and opioid receptor antagonist naltrexone inhibit the saccharin deprivation effect in rats.

Several drugs, such as N-methyl-D-aspartate (NMDA) receptor channel blockers (memantine), naltrexone (but not naloxone) and acamprosate, have previously been reported to attenuate the expression of the alcohol deprivation effect, a phenomenon seen as an increase in post-deprivation alcohol consumption. The present study aimed to evaluate the effects of these drugs on the development and expression of the saccharin deprivation effect in adult male Wistar rats. Memantine (13 mg/kg per day) and naltrexone (5 mg/kg, twice daily), but not naloxone (24 mg/kg per day) or acamprosate (200 mg/kg, twice daily), prevented the increase in the consumption of saccharin after a 1-week deprivation from free-choice, unlimited access to saccharin (0.