Mini Review - Addiction & Criminology (2023) Volume 6, Issue 3
Neuroplasticity and drug-seeking behavior: Mechanisms and therapeutic targets.
Christopher Kalivas*
Department of addiction neurobiology, Medical University of South Carolina, Carolina, USA
- *Corresponding Author:
- Christopher Kalivas
Department of addiction neurobiology, Medical University of South Carolina, USA
E-mail: christopherkalivas@slu.edu
Received: 30-May -2023, Manuscript No. AARA-23-103243; Editor assigned: 01-June-2023, PreQC No. AARA-23-103243 (PQ); Reviewed:15-June-2023, QC No. AARA-23-103243; Revised:20-June-2023, Manuscript No. AARA-23-103243 (R); Published:27-June-2023, DOI:10.35841/aara-6.3.146
Citation: Kalivas C. Neuroplasticity and drug-seeking behavior: Mechanisms and therapeutic targets. Addict Criminol. 2023;6(3):146
Abstract
Drug addiction is a complex and chronic disorder characterized by compulsive drug-seeking behavior despite adverse consequences. The persistence of drug-seeking behavior is believed to arise from maladaptive changes in the brain's neural circuitry, particularly in regions involved in reward, motivation, and decision-making. Neuroplasticity, the brain's ability to reorganize and modify its structure and function in response to experience, plays a pivotal role in the development and maintenance of drug addiction.Introduction
Drug addiction is a chronic and complex disorder characterized by compulsive drug-seeking behavior despite negative consequences. It is widely recognized that the brain's neural circuitry undergoes profound changes in response to chronic drug exposure, leading to persistent drug-seeking behavior and a high risk of relapse. Neuroplasticity, the brain's ability to reorganize and modify its structure and function, plays a central role in the development and maintenance of addiction. This review aims to explore the intricate relationship between neuroplasticity and drug-seeking behavior, elucidating the underlying mechanisms and potential therapeutic targets for the treatment of addiction [1].
Chronic drug exposure induces long-lasting changes in synaptic plasticity, which refers to the ability of synapses to undergo modifications in their strength and structure. These neuro adaptations occur in several brain regions, including the mesocorticolimbic system, which is critical for reward and motivation, and the prefrontal cortex, involved in decision-making and inhibitory control [2].
Drug-induced synaptic plasticity involves alterations in neurotransmitter release, receptor expression, and intracellular signaling pathways. For example, drugs of abuse, such as cocaine and opioids, increase dopamine release in the nucleus accumbens, leading to reinforcement of drug-seeking behavior. These changes in synaptic plasticity contribute to the heightened salience of drug-related cues and the dysregulation of reward processing, reinforcing drug-seeking behavior [3].
In addition to synaptic plasticity, structural plasticity and neurogenesis are implicated in drug addiction. Structural plasticity refers to changes in the physical structure of neurons, including dendritic arborization and spine density. Chronic drug exposure can lead to structural remodeling in the prefrontal cortex and the hippocampus, regions critical for cognitive function and memory formation. These changes may contribute to the cognitive impairments observed in individuals with addiction. Multiple neurotransmitter systems, including dopamine, glutamate, and GABA, interact to modulate the neuroplastic changes associated with addiction. Dopamine, a key neurotransmitter involved in reward processing, is central to the reinforcing effects of drugs of abuse [4].
Understanding the mechanisms underlying neuroplasticity in addiction opens avenues for the development of novel therapeutic interventions. Several potential targets have been identified, including modulating receptor function, targeting intracellular signaling pathways, promoting synaptic remodeling, and enhancing neurogenesis. For instance, medications that modulate glutamate receptors, such as NMDA receptor antagonists, have shown promise in reducing drug craving and relapse. Modulating intracellular signaling pathways, such as the protein kinase cascade, may also be a viable target for therapeutic intervention. Furthermore, promoting synaptic remodeling and neurogenesis through environmental enrichment and pharmacological interventions could potentially restore normal neuroplasticity processes and facilitate recovery from addiction [5].
Conclusion
Neuroplasticity plays a central role in the development and maintenance of drug-seeking behavior in addiction. Chronic drug exposure induces long-lasting changes in synaptic plasticity, structural plasticity, and neurogenesis, leading to dysregulation of reward processing and cognitive control. Understanding the intricate interplay between neuroplasticity and addiction provides valuable insights into potential therapeutic targets. Modulating neuroplasticity processes through pharmacological and environmental interventions holds promise for the treatment of drug addiction.
References
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