The last two decades have witnessed substantial advances in identifying synaptic plasticity responsible for behavioral changes in animal models of substance use disorder. We have learned the most about cocaine-induced plasticity in the nucleus accumbens and its relationship to cocaine seeking, so that is the focus in this review. Synaptic plasticity pointing to potential therapeutic targets has been identified mainly using two drug self-administration models: extinction-reinstatement and abstinence models. A relationship between cocaine seeking and potentiated AMPAR transmission in nucleus accumbens is indicated by both models. In particular, an atypical subpopulation-Ca2+-permeable or CP-AMPARs-mediates cue-induced seeking that persists even after long periods of abstinence, modeling the persistent vulnerability to relapse that represents a major challenge in treating substance use disorder. We review strategies to reverse CP-AMPAR plasticity; strategies targeting other components of excitatory synapses, including dysregulated glutamate uptake and release; and behavioral interventions that can be augmented by harnessing synaptic plasticity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1146/annurev-pharmtox-061724-080548 | DOI Listing |
Publication Analysis
Top Keywords
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 PDFNeurobehavioral plasticity in the rodent gustatory system induced by regular consumption of a low-calorie sweetener during adolescence.
Sci Rep
January 2025
Department of Biological Sciences, University of Southern California, 3616 Trousdale Parkway, AHF 252, Los Angeles, CA, 90089-0372, USA.
Habitual consumption of low-calorie sweeteners (LCS) during juvenile-adolescence can lead to greater sugar intake later in life. Here, we investigated if exposure to the LCS Acesulfame Potassium (Ace-K) during this critical period of development reprograms the taste system in a way that would alter hedonic responding for common dietary compounds. Results revealed that early-life LCS intake not only enhanced the avidity for a caloric sugar (fructose) when rats were in a state of caloric need, it increased acceptance of a bitterant (quinine) in Ace-K-exposed rats tested when middle-aged.
View Article and Find Full Text PDFMuscarinic cannabinoid suppression of excitation, a novel form of coincidence detection.
Pharmacol Res
January 2025
Gill Institute for Neuroscience; Dept. of Psychological and Brain Sciences, Indiana University, Bloomington, IN 47405. Electronic address:
Δ-tetrahydrocannabinol (THC), the chief psychoactive ingredient of cannabis, acts in the brain primarily via cannabinoid CB1 receptors. These receptors are implicated in several forms of synaptic plasticity - depolarization-induced suppression of excitation (DSE), metabotropic suppression of excitation (MSE), long term depression (LTD) and activation-dependent desensitization. Cultured autaptic hippocampal neurons express all of these, illustrating the rich functional and temporal heterogeneity of CB1 at a single set of synapses.
View Article and Find Full Text PDFInvolvement of ROS signal in aging and regulation of brain functions.
J Physiol Sci
December 2024
Department of Memory Neuroscience, Tokyo Metropolitan Institute for Geriatrics and Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo 173-0015, Japan; Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Yoshida-Shimoadachi-cho, Sakyo-ku, Kyoto-city, Kyoto 606-8501, Japan. Electronic address:
Reactive oxygen species (ROS) are redox-signaling molecules involved in aging and lifestyle-related diseases. In the brain, in addition to the production of ROS as byproducts of metabolism, expression of ROS synthases has recently been demonstrated, suggesting possible involvement of ROS in various brain functions. This review highlights current knowledge on the relationship between ROS and brain functions, including their contribution to age-related decline in synaptic plasticity and cognitive function.
View Article and Find Full Text PDFColistin treatment causes neuronal loss and cognitive impairment via ros accumulation and neuronal plasticity alterations.
Biomed Pharmacother
January 2025
Departament de Farmacologia, Toxicologia i Química Terapèutica, Facultat de Farmàcia i Ciències de l'Alimentació, Universitat de Barcelona (UB), Av. de Joan XXIII, 27-31, Barcelona 08028, Spain; Institut de Neurociències, Universitat de Barcelona (UB), Passeig de la Vall d'Hebron, 171, Barcelona 08035, Spain; Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Instituto de Carlos III, Av. Monforte de Lemos, 3-5, Madrid 28029, Spain; Institut d'Investigació Sanitària Pere Virgili (IISPV), Hospital Universitari Sant Joan de Reus, Av. Josep Laporte, 2, Reus 43204, Spain. Electronic address:
The rise of antimicrobial resistance has made necessary the increase of the antibacterial arsenal against multidrug-resistant bacteria. In this context, colistin has re-emerged as a first-line antibiotic in critical situations despite its nephro- and neuro- toxicity at peripheral level. However, the mechanism underlying its toxicity remains unknown, particularly in relation to the central nervous system (CNS).
View Article and Find Full Text PDFWant 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!