The Addiction Cycle: What Are The Stages of Addiction?

In contrast, stress-induced reinstatement of drug-related responding in animal models appears to depend on the activation of both CRF and norepinephrine in elements of the extended amygdala (both the CeA and BNST; for reviews, see Shaham et al, 2003; Shalev et al, 2002). Protracted abstinence, largely described in alcohol dependence models, appears to involve overactive glutamatergic and CRF systems, presumably in the extended amygdala, although to a large extent this remains to be explored (de Witte et al, 2005; Valdez et al, 2002). Data with knockout mice also provide key insights into the role of dopamine in the rewarding effects of drugs of abuse. Genetically altered mice homozygous with a lack of the dopamine D1 receptor do not self-administer cocaine (Caine et al, 2007). These results support the hypothesis of a crucial role of the DAT in cocaine’s reinforcing effects.

A person’s ability to resist strong urges is compromised, leading to compulsive behaviors that can be so powerful as to cause an individual to obtain more drug by whatever means necessary, including stealing. These changes in higher https://ecosoberhouse.com/ brain function can also interfere with the person’s ability to follow through with decisions to discontinue drug use. This stage also involves changes in neurocircuitry underlying how we think, learn, plan, and make decisions.

Sources of Reinforcement: Motivation, Opponent Process, Incentive Salience

Compulsive drug use defined by increased intake of drug with extended access is accompanied by a chronic perturbation in brain reward homeostasis using measures of brain stimulation reward thresholds. The differential exposure to drug self-administration has dramatic effects on reward thresholds that progressively increase (ie, decreased reward) in extended-access, but not in limited-access, rats across successive self-administration sessions (Ahmed et al, 2002; Kenny et al, 2006; Wee et al, unpublished results). This mechanism could underlie the benefit of methadone and buprenorphine treatment in heroin addiction.

In summary, multiple brain regions and circuits are disrupted in drug addiction and are likely to contribute differentially to the complex phenotype observed in addicted individuals (Figure 5). Although some of these functional abnormalities may be present to a greater or lesser extent across all classes of drug addictions, some of the changes may be specific to certain types of drugs. For example, long-lasting decrements in the DAT in the striatum are observed in methamphetamine but not in alcohol or cocaine addictions. Conversely, decrements in get out of addiction cycle dopamine D2 receptors in the striatum are observed in subjects addicted to all of the drugs of abuse that have been investigated, and increased activation of brain stress systems such as CRF has been observed in animal models during acute withdrawal for all types of drugs. Evidence from rodent studies suggests that drug-induced reinstatement is mediated by the circuit that links the prelimbic prefrontal cortex to the ventral striatum94 (for correspondence with humans, see figure ​figure2;2; tables ​tables1,1, ​,2,2, circuits 12 and possibly 13).