Alcohol-specific transcriptional dynamics of memory reconsolidation and relapse.

Relapse, a critical issue in alcohol addiction, can be attenuated by disruption of alcohol-associated memories. Memories are thought to temporarily destabilize upon retrieval during the reconsolidation process. Here, we provide evidence for unique transcriptional dynamics underpinning alcohol memory reconsolidation.

New Approaches for Alcohol Use Disorder Treatment via Memory Retrieval and Reconsolidation Manipulations.

Relapse to alcohol seeking and drinking is a major clinical challenge in alcohol use disorder and is frequently brought about by cue-induced craving, caused by exposure to cues that evoke alcohol-related memories. It has been postulated that memories become labile for manipulation shortly after their retrieval and then restabilize in a "memory reconsolidation" process. Disruption or interference with the reconsolidation of drug-associated memories has been suggested as a possible strategy to reduce or even prevent cue-induced craving and relapse.

Targeting the Reconsolidation of Licit Drug Memories to Prevent Relapse: Focus on Alcohol and Nicotine.

Alcohol and nicotine are widely abused legal substances worldwide. Relapse to alcohol or tobacco seeking and consumption after abstinence is a major clinical challenge, and is often evoked by cue-induced craving. Therefore, disruption of the memory for the cue-drug association is expected to suppress relapse.

Disruption of relapse to alcohol seeking by aversive counterconditioning following memory retrieval.

Relapse to alcohol abuse is often caused by exposure to potent alcohol-associated cues. Therefore, disruption of the cue-alcohol memory can prevent relapse. It is believed that memories destabilize and become prone for updating upon their reactivation through retrieval and then restabilize within 6 h during a "reconsolidation" process.

Alcohol consumption alters Gdnf promoter methylation and expression in rats.

Alcohol use disorder is one of the most disabling diseases worldwide. Glial-cell derived neurotrophic factor (Gdnf) shows promising results concerning the inhibition of alcohol consumption in rodent models. We investigated the epigenetic regulation of Gdnf following ethanol consumption and withdrawal in a rat model.

Advances in behavioral animal models of alcohol use disorder.

Alcohol use disorder (AUD) is a multifaceted neuropsychiatric disease that combines behavioral, psychosocial, and neurobiological aspects. Over the previous decade, animal models have advanced in modeling the major psychological constructs that characterize AUD. These advances pave the road for more sophisticated behavioral models that capture addiction-related aspects, such as alcohol craving, compulsive seeking and intake, dependence, and relapse.

Flood-conditioned place aversion as a novel non-pharmacological aversive learning procedure in mice.

The place conditioning paradigm is an efficient, widely-used method to study mechanisms that underlie appetitive or aversive learning and memory processes. However, pharmacological agents used to induce conditioned place preference (CPP) or aversion (CPA) can per se interfere with learning and memory processing, hence confounding the results. Therefore, non-pharmacological place conditioning procedures are of high importance.

Re-exposure to nicotine-associated context from adolescence enhances alcohol intake in adulthood.

Alcohol and nicotine are the two most commonly-abused substances and are often used together. Nicotine enhances alcohol-drinking behaviors in humans and in animals, and was suggested to enhance the reinforcing properties of other reinforcers. Here, we show that nicotine-associated environment, rather than nicotine itself, enhances alcohol intake in rats.

Counterconditioning During Reconsolidation Prevents Relapse of Cocaine Memories.

Relapse to drug abuse is often caused by exposure to drug-associated cues that evoke craving. Therefore, disruption of the cue-drug memory can prevent relapse. Memories destabilize and become temporarily labile upon their retrieval, and re-stabilize in a process termed reconsolidation.

Signal attenuation as a rat model of obsessive compulsive disorder.

In the signal attenuation rat model of obsessive-compulsive disorder (OCD), lever-pressing for food is followed by the presentation of a compound stimulus which serves as a feedback cue. This feedback is later attenuated by repeated presentations of the stimulus without food (without the rat emitting the lever-press response). In the next stage, lever-pressing is assessed under extinction conditions (i.