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This paper reviews recent developments in the neurocircuitry and neurobiology of addiction from a perspective of allostasis. A model is proposed for brain changes that occur during the development of addiction that explain the persistent vulnerability to relapse long after drug-taking has ceased. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in the compulsive use and loss of control over drug-taking. The development of addiction recruits different sources of reinforcement, different neuroadaptive mechanisms, and different neurochemical changes to dysregulate the brain reward system. Counteradaptive processes such as opponent-process that are part of normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to form an allostatic state. Allostasis from the addiction perspective is defined as the process of maintaining apparent reward function stability by changes in brain reward mechanisms. The allostatic state represents a chronic deviation of reward set point and is fueled not only by dysregulation of reward circuits per se, but also by the activation of brain and hormonal stress responses. The manifestation of this allostatic state as compulsive drug-taking and loss of control over drug-taking is hypothesized to be expressed through activation of brain circuits involved in compulsive behavior such as the cortico-striatal-thalamic loop. The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and relapse.


Every person having a knowledge of the actual commission of any offense punishable by imprisonment in the penitentiary for any other term than for life, who shall take any money or property of another, or any gratuity or reward, or any engagement or promise therefor, upon any agreement or understanding, expressed or implied, to compound or conceal any such crime, or to abstain from any prosecution therefor, or to withhold any evidence thereof shall, upon conviction, be punished by imprisonment in the penitentiary not exceeding three years, or in the county jail not exceeding six months.

When deciding between different options, individuals are guided by the expected (mean) value of the different outcomes and by the associated degrees of uncertainty. We used functional magnetic resonance imaging to identify brain activations coding the key decision parameters of expected value (magnitude and probability) separately from uncertainty (statistical variance) of monetary rewards. Participants discriminated behaviorally between stimuli associated with different expected values and uncertainty. Stimuli associated with higher expected values elicited monotonically increasing activations in distinct regions of the striatum, irrespective of different combinations of magnitude and probability. Stimuli associated with higher uncertainty (variance) elicited increasing activations in the lateral orbitofrontal cortex. Uncertainty-related activations covaried with individual risk aversion in lateral orbitofrontal regions and risk-seeking in more medial areas. Furthermore, activations in expected value-coding regions in prefrontal cortex covaried differentially with uncertainty depending on risk attitudes of individual participants, suggesting that separate prefrontal regions are involved in risk aversion and seeking. These data demonstrate the distinct coding in key reward structures of the two basic and crucial decision parameters, expected value, and uncertainty.

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(A) Relationship between elevations in intracranial self-stimulation (ICSS) reward thresholds and cocaine intake escalation. (Left) Percent change from baseline ICSS thresholds. (Right) Number of cocaine injections earned during the first hour of each session. Rats were first prepared with bipolar electrodes in either the right or left posterior lateral hypothalamus. One week post-surgery, they were trained to respond for electrical brain stimulation. Reward thresholds measured in microamps were assessed according to a modified discrete-trial current-threshold procedure [51]. During the screening phase, the 22 rats that were tested for self-administration were allowed to self-administer cocaine during only 1 h on a fixed-ratio 1 schedule of reinforcement, after which two balanced groups with the same weight, cocaine intake, and reward thresholds were formed. During the escalation phase, one group had access to cocaine self-administration for only 1 h per day (short-access, ShA) and the other group for 6 h per day (long-access, LgA). The remaining eight rats were exposed to the same experimental manipulations as the other rats, with the exception that they were not exposed to cocaine (not shown). Reward thresholds were measured in all rats two times per day, 3 h and 17-22 h after each daily self-administration session (ShA and LgA rats) or the control procedure (drug-naive rats; data not shown). Each reward threshold session lasted about 30 min. *p B) Unlimited daily access to heroin escalated heroin intake and decreased the excitability of brain reward systems. Heroin intake ( SEM; 20 mg per infusion) in rats during limited (1 h) or unlimited (23 h) self-administration sessions. ***p

Neurocircuitry associated with the acute positive reinforcing effects of drugs of abuse and the negative reinforcement of dependence and how it changes in the transition from nondependent drug taking to dependent drug taking. Key elements of the reward circuit are dopamine (DA) and opioid peptide neurons that intersect at both the ventral tegmental area (VTA) and nucleus accumbens and are activated during initial use and the early binge/intoxication stage. Key elements of the stress circuit are corticotropin-releasing factor (CRF) and noradrenergic (norepinephrine, NE) neurons that converge on γ-aminobutyric acid (GABA) interneurons in the central nucleus of the amygdala that are activated during the development of dependence. Taken with permission from [45].

Drugs of abuse act at local cellular-membrane sites, within neurochemical systems that are part of a reward system neurocircuitry. These systems include the dopamine and opioid peptide networks which have many different projection sites. The midbrain dopamine systems have critical roles not only in the reward and motor systems but also in higher-order functions, including cognition and memory (Grant et al. 1996). Opioid peptides have been implicated in pain and emotional processing throughout the neuraxis.

Drug addiction is not a static phenomenon, and as with other biobehavioral dysregulation, such as compulsive gambling and binge eating, there are different components that constitute a cycle or circle of ever-growing pathology (Baumeister et al. 1994). Derived from social psychology and conceptualized as sources of self-regulation failures, the addiction cycle has been described as having three components: preoccupation-anticipation, binge-intoxication, and withdrawal-negative affect (Koob and Le Moal 1997). Spiralling distress describes how, in some cases, the first self-regulation failure can lead to emotional distress, which sets up a cycle of repeated failures to self-regulate, and where each violation brings additional negative affect (Baumeister et al. 1994). Spiralling distress also has been described as the progressive dysregulation of the brain reward system within the context of repeated addiction cycles (Figure 1 ). Psychiatric and experimental psychological constructs address the same addiction cycle, and animal models have been established and validated for different symptoms or constructs associated with elements of the addiction cycle, addiction criteria, and sources of reinforcement associated with addiction (American Psychiatric Association 1994; Koob 1995; Koob et al. 1998a; Markou et al. 1993).

Superimposed on the addiction cycle are multiple sources of reinforcement that can contribute to compulsive use of drugs of abuse during the course of drug addiction. Positive reinforcement occurs when presentation of the drug increases the probability of a response to obtain the drug again. The positive reinforcing effects of drugs when described in the context of reward often are equated with the pleasurable effects of drugs in the absence of a deficit state. Negative reinforcement, in contrast, occurs with alleviation of an existing aversive state or alleviation of a drug-generated aversive state (e.g., withdrawal) (Wikler 1973). Secondary positive reinforcing effects can be obtained through conditioned positive reinforcement (e.g., pairing of previously neutral stimuli with acute positive reinforcing effects of drugs). Secondary negative reinforcing effects can be obtained through removal of the conditioned negative reinforcing effects of conditioned abstinence. Positive reinforcement as a construct is associated largely with the binge intoxication stage outlined in Figure 1, and the construct of negative reinforcement is associated largely with the negative affect/withdrawal stage. Conditioned positive reinforcement and conditioned negative reinforcement can be conceptualized to contribute to the preoccupation/anticipation stage. 041b061a72


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