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Drugs of Abuse and Addiction
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Aarushi Singh
NF-κB transcription factor is linked to synaptic plasticity and evocation in drug addiction. Repeated cocaine administrations lead to induction of this nuclear factor in the nuclear accumbens and also these are analogous to nicotine dependence (Meffert et al., 2003; Russo, 2009; Christoffel, 2011; Robison and Nestler, 2012; Nestler, 2013). Several researches are presently going on to get acquainted with the cellular basis of NF-κB action and the plasticity changes occuring. Many researches have scrutinized that ∆FosB plays a prominent role in mediating these nuclear factors thus it is practicable that there exists a complex transcriptional cascade in this whole drug addiction process (Meffert et al., 2003; Russo, 2009; Christoffel, 2011).
Stimulants and psychedelics
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Genetic variation in a genomic region on chromosome I5q25, which encodes the a5, a3 and b4 subunits of the cholinergic nicotinic receptor genes, confers risk of smoking and nicotine dependence. It also appears that gene cluster-associated variants, which dampen the brain’s response to reward feedback in the right ventral and dorsal anterior cingulate cortex, play a significant role in susceptibility to smoking (Nees et al., 2013). Furthermore, one study has identified 16 single-nucleotide polymorphisms in seven genes that contribute to specific genotypes, and predispose novice adolescent smokers to early smoking and nicotine dependence (O’Loughlin et al., 2014). Regulation of gene expression is also thought to be essential in developing drug addiction, and the transcription factor’s ΔFosB up-regulation may be responsible, at least in part (Nestler, 2013; Ruffle, 2014). Nicotine induces long-term ΔFosB expression in the nucleus accumbens when inhaled or injected at sufficiently high doses, and repeated daily exposure can result in accumbal ΔFosB up-regulation (Marttila et al., 2006; Ruffle, 2014).
The Etiology of Addiction
Published in James MacKillop, George A. Kenna, Lorenzo Leggio, Lara A. Ray, Integrating Psychological and Pharmacological Treatments for Addictive Disorders, 2017
An alternative formulation, the cellular learning model of addiction, makes the case that addiction should be more broadly considered a disorder of learning and memory [8, 9]. From this perspective, sensitization of dopamine neurotransmission is one part of the neurobiology of addiction, but the subsequent downstream learning processes are even more important. Specifically, this account proposes that potent psychoactive drug effects contribute to synaptic plasticity that leads to long-term increases in the salience of drug rewards and, by comparison, decreases in the salience of alternative rewards [8, 9]. This is hypothesized to take place by way of drug-induced remodeling of neuronal dendrites, axons, and synapses, either via up- or down-regulation of gene expression or expression-based effects that lead to morphological synaptic changes. Supporting this thesis, addictive drugs have been robustly found to induce alterations in gene expression associated with synaptic plasticity, including inducing ΔFosB, a relatively long-lasting transcription factor that increases sensitivity to the rewarding and locomotor stimulant effects of addictive drugs [10, 11]. Thus, the highly potent psychoactive effects of addictive drugs are theorized to become deeply instantiated in the brain via potent effects on circuitry for learning new events and remembering important ones from the past.
Effects of escalating versus fixed ethanol exposure on ∆FosB expression in the mesocorticolimbic pathway in adolescent and adult rats
Published in The American Journal of Drug and Alcohol Abuse, 2021
Aranza Wille-Bille, Leonardo Marengo, Andrea Godino, Ricardo Marcos Pautassi
∆FosB is part of a family of transcription factors coded by the fos gene (1). These factors heterodimerize with Jun family’s proteins, to form the activator protein AP-1. This complex recognizes specific DNA sites and regulates target gene expression. Unlike other Fos proteins, ∆FosB is very stable and gradually accumulates after repeated stress or drug exposure. Induction of ∆FosB expression in the brain reward areas after chronic and passive, experimenter-administered, exposure to alcohol (2,3), cocaine (4) and other drugs has been reported, a pattern also found in nucleus accumbens core and shell (AcbSh and AcbC, respectively), striatum and prefrontal cortex after chronic ethanol intake (5). These results are consistent with those of Li et al. (6), who observed greater levels of ∆FosB in AcbC and dorsolateral striatum (DLS) after intermittent access to alcohol (further referred to as ethanol). ∆FosB is also observed after chronic stress exposure and its overexpression in the nucleus accumbens increases cocaine-induced appetitive learning, behavioral stimulation and self-administration (7–9). These and other studies (10) suggest that ∆FosB may act as a molecular trigger, promoting initiation and maintenance of drug use (11,12).
Fat rather than sugar diet leads to binge-type eating, anticipation, effort behavior and activation of the corticolimbic system
Published in Nutritional Neuroscience, 2021
Estefania Espitia-Bautista, Carolina Escobar
After a first episode to the PF diets both groups exhibited elevated levels of ΔFosB. Importantly, after chronic intake, the accumulation of ΔFosB in corticolimbic areas persisted only in the FRD but not in the SRD, indicating the differential influence of the diets on synaptic changes in corticolimbic areas. Other studies have reported that a significant accumulation of ΔFosB can be observed after chronic ad-libitum consumption of high fat and/or high sugar diet [42,43] and after WD of sugar [44]. Nestler et al. [45] suggested that ΔFosB is a transcription factor that enables long-term synaptic changes underlying the development of addiction like behavior. Such changes may also favor the formation of compulsive-like eating behavior, including binge-type eating. The link of ΔFosB accumulation with addiction-like responses is supported by Kaufling, et al. [46] who demonstrated overexpression of ΔFosB after acute administration of cocaine, D-amphetamine, methylphenidate and caffeine. Altogether, data suggest that PF can change the brain by inducing ΔFosB, a factor that triggers neuronal plasticity.
Chronic intermittent ethanol administration differentially alters DeltaFosB immunoreactivity in cortical-limbic structures of rats with high and low alcohol preference
Published in The American Journal of Drug and Alcohol Abuse, 2019
Tatiana Wscieklica, Luciana Le Sueur-Maluf, Leandro Prearo, Rafael Conte, Milena de Barros Viana, Isabel Cristina Céspedes
The changes in the brain that contribute to the phenotype of alcohol use disorder may be related, at least in part, to gene expression alterations that can be evaluated by means of protein DeltaFosB (27). DeltaFosB is a transcription factor from the Fos family, and due to its stability it accumulates in the brain after chronic treatment and mediates long-lasting neural and behavioral plasticity (28). While other members of the Fos family desensitize after a chronic stimulus, DeltaFosB gradually increases its expression (29–31). DeltaFosB expression is being considered as a biomarker of alcohol use disorder and might be used to indicate the stage of its progression (27,32,33). Although the fosb gene expresses two factors, FosB (full length) and DeltaFosB (short form), DeltaFosB is the one that has been related directly to the functional effects of several brain stimuli. The FosB protein and other Fos family proteins are intrinsically unstable and have not been related to chronic stimuli. For this reason, in this work we will use only the term DeltaFosB to refer to the immunohistochemical analyses (34).