Learning and memory in the aetiopathogenesis of addiction: future implications for therapy?

Eur Arch Psychiatry Clin Neurosci

Department of Addictive Behavior and Addiction Medicine, Central Institute of Mental Health (CIMH), University of Heidelberg, J5, 68159 Mannheim, Germany.

Published: November 2009

Addiction is a chronic relapsing disorder. Even after long periods of abstinence from drugs, the risk of relapse, often precipitated by drug-associated cues, remains high. Especially learning processes have been shown to play a major role in the maintenance of addictive behaviour. Humans and animals rapidly learn cues and contexts that predict the availability of addictive drugs. Once learned, these cues and contexts initiate drug seeking, craving and relapse in both animal models and clinical studies. These observations have converged on the hypothesis that addiction represents the pathological usurpation of neural processes that normally serve reward-related learning. In this context, a substantial body of evidence suggests that several types of neuroadaptation occur, including synapse-specific adaptations of the type thought to underlie specific long-term associative memory. Consequently, understanding learning and memory processes in the brain in addiction is an important key for understanding the persistence of addiction, and it is reasonable to hypothesize that the disruption of drug-related memories may help to prevent relapses.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00406-009-0057-6DOI Listing

Publication Analysis

Top Keywords

learning memory
8
cues contexts
8
addiction
5
learning
4
memory aetiopathogenesis
4
aetiopathogenesis addiction
4
addiction future
4
future implications
4
implications therapy?
4
therapy? addiction
4

Similar Publications

Neuronal Plasma Membranes as Supramolecular Assemblies for Biological Memory.

Langmuir

January 2025

Department of Physics and Astronomy, The University of Tennessee, Knoxville, Tennessee 37996, United States.

Biological memory is the ability to develop, retain, and retrieve information over time. Currently, it is widely accepted that memories are stored in synapses (i.e.

View Article and Find Full Text PDF

The Role of SIRT1-BDNF Signaling Pathway in Fluoride-Induced Toxicity for Glial BV-2 Cells.

Biol Trace Elem Res

January 2025

Department of Hematology, Affiliated Hospital of Guizhou Medical University, No. 4 Bei Jing Road, Yunyan District, Guiyang, 550004, Guizhou Province, China.

Chronic fluorosis is often accompanied by neurological symptoms, leading to attention, memory and learning ability decline and causing tension, anxiety, depression, and other mental symptoms. In the present study, we analyzed the molecular mechanisms of SIRT1-BDNF regulation of PI3K-AKT, MAPK, and FOXO1A in F-treated BV2 cells. The cytotoxic effect of sodium fluoride (NaF) on BV2 cells was assessed using Cell Counting Kit-8 (CCK-8), crystal violet, and 5-ethynyl-2'-deoxyuridine (EdU) staining.

View Article and Find Full Text PDF

Histone acetylation is the process by which histone acetyltransferases (HATs) add an acetyl group to the N-terminal lysine residues of histones, resulting in a more open chromatin structure. Histone acetylation tends to increase gene expression more than methylation does. In the central nervous system (CNS), histone acetylation is essential for controlling the expression of genes linked to cognition and learning.

View Article and Find Full Text PDF

Social isolation is a risk factor for cognitive impairment. Adolescents may be particularly vulnerable to these effects, because they are in a critical period of development marked by significant physical, hormonal, and social changes. However, it is unclear if the effects of social isolation on learning and memory are similar in both sexes or if they persist into adulthood after a period of recovery.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!