Neurobiological substrates for the dark side of compulsivity in addiction.
paper
Cited
Public
- Authors
- Koob, George F
- Year
- 2009
- Journal
- Neuropharmacology
- PMID
- 18725236
- DOI
- 10.1016/j.neuropharm.2008.07.043
- PMCID
- PMC2637927
Drug addiction can be defined by a compulsion to seek and take drug, loss of control in limiting intake, and the emergence of a negative emotional state when access to the drug is prevented. Drug addiction impacts multiple motivational mechanisms and can be conceptualized as a disorder that progresses from impulsivity (positive reinforcement) to compulsivity (negative reinforcement). The construct of negative reinforcement is defined as drug taking that alleviates a negative emotional state. The negative emotional state that drives such negative reinforcement is hypothesized to derive from dysregulation of key neurochemical elements involved in reward and stress within the basal forebrain structures involving the ventral striatum and extended amygdala. Specific neurochemical elements in these structures include not only decreases in reward neurotransmission, such as decreases in dopamine and opioid peptide function in the ventral striatum, but also recruitment of brain stress systems, such as corticotropin-releasing factor (CRF), in the extended amygdala. Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, increases in anxiety-like responses, and increases in extracellular levels of CRF in the central nucleus of the amygdala. CRF receptor antagonists also block excessive drug intake produced by dependence. A brain stress response system is hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence, and to contribute to the compulsivity of addiction. Other components of brain stress systems in the extended amygdala that interact with CRF and may contribute to the negative motivational state of withdrawal include norepinephrine, dynorphin, and neuropeptide Y. The combination of loss of reward function and recruitment of brain stress systems provides a powerful neurochemical basis for a negative emotional state that is responsible for the negative reinforcement driving, at least in part, the compulsivity of addiction.
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| 20 | 1. Definitions and conceptual framework for compulsivity in addiction β 1.3. Animal models of compulsivity in addiction as defined by increased drug taking: Escalation in drug self-administration with prolonged access | cocaine intake, but the LgA rats consistently self-administered almost twice as much cocaine at anyβ¦ |
| 21 | 1. Definitions and conceptual framework for compulsivity in addiction β 1.3. Animal models of compulsivity in addiction as defined by increased drug taking: Escalation in drug self-administration with prolonged access | incentive effects of cocaine as drug intake have been observed following extended access and includeβ¦ |
| 22 | 1. Definitions and conceptual framework for compulsivity in addiction β 1.3. Animal models of compulsivity in addiction as defined by increased drug taking: Escalation in drug self-administration with prolonged access | The hypothesis that compulsive cocaine use is accompanied by a chronic perturbation in brain rewardβ¦ |
| 23 | 1. Definitions and conceptual framework for compulsivity in addiction β 1.3. Animal models of compulsivity in addiction as defined by increased drug taking: Escalation in drug self-administration with prolonged access | before the onset of each subsequent self-administration session, thereby deviating more and moreβ¦ |
| 24 | 2. Neural substrates for the negative emotional state associated with addiction β 2.1. Within-system neuroadaptations that contribute to the negative emotional state component of compulsivity | Electrical brain stimulation reward or intracranial self-stimulation has a long history as a measureβ¦ |
| 25 | 2. Neural substrates for the negative emotional state associated with addiction β 2.1. Within-system neuroadaptations that contribute to the negative emotional state component of compulsivity | Within-system neuroadaptations to chronic drug exposure include decreases in function of the sameβ¦ |
| 26 | 2. Neural substrates for the negative emotional state associated with addiction β 2.1. Within-system neuroadaptations that contribute to the negative emotional state component of compulsivity | et al., 1992, 1996). Imaging studies in drug-addicted humans have consistently shown long-lastingβ¦ |
| 27 | 2. Neural substrates for the negative emotional state associated with addiction β 2.1. Within-system neuroadaptations that contribute to the negative emotional state component of compulsivity | Psychostimulant withdrawal in humans is associated with fatigue, decreased mood, and psychomotorβ¦ |
| 28 | 2. Neural substrates for the negative emotional state associated with addiction β 2.1. Within-system neuroadaptations that contribute to the negative emotional state component of compulsivity | Under this conceptual framework, other within-system neuroadaptations would include increasedβ¦ |
| 29 | 2. Neural substrates for the negative emotional state associated with addiction β 2.2. Between-system neuroadaptations that contribute to the negative emotional state component of compulsivity | Brain neurochemical systems involved in arousal-stress modulation also may be engaged within theβ¦ |
| 30 | 2. Neural substrates for the negative emotional state associated with addiction β 2.2. Between-system neuroadaptations that contribute to the negative emotional state component of compulsivity | The neuroanatomical entity termed the extended amygdala (Heimer and Alheid, 1991) may represent aβ¦ |
| 31 | 2. Neural substrates for the negative emotional state associated with addiction β 2.3. Neuropharmacological studies of the aversive stimulus effects of drug withdrawal | Place aversion has been used to measure the aversive stimulus effects of withdrawal, mostly in theβ¦ |
| 32 | 2. Neural substrates for the negative emotional state associated with addiction β 2.3. Neuropharmacological studies of the aversive stimulus effects of drug withdrawal | with doses of naloxone below which somatic signs of withdrawal are observed (Schulteis et al.,β¦ |
| 33 | 2. Neural substrates for the negative emotional state associated with addiction β 2.3. Neuropharmacological studies of the aversive stimulus effects of drug withdrawal | Acute opioid dependence has been defined as the precipitation of withdrawal-like signs by opioidβ¦ |
| 34 | 2. Neural substrates for the negative emotional state associated with addiction β 2.3. Neuropharmacological studies of the aversive stimulus effects of drug withdrawal | Another candidate for the aversive effects of drug withdrawal is dynorphin. Much evidence shows thatβ¦ |
| 35 | 2. Neural substrates for the negative emotional state associated with addiction β 2.4. Neuropharmacological studies of the anxiety-like effects of drug withdrawal | Another common response to acute withdrawal and protracted abstinence from all major drugs of abuseβ¦ |
| 36 | 2. Neural substrates for the negative emotional state associated with addiction β 2.4. Neuropharmacological studies of the anxiety-like effects of drug withdrawal | administration of CRF1/CRF2 peptidergic antagonists (Baldwin et al., 1991), small molecule CRF1β¦ |
| 37 | 3. Neural Substrates for Increased Drug-taking with Extended Access β 3.1. Within-system neuroadaptations | In a series of studies, dopamine partial agonists have not only been shown to reverseβ¦ |
| 38 | 3. Neural Substrates for Increased Drug-taking with Extended Access β 3.1. Within-system neuroadaptations | Similar results have been observed in opioid dependence with the opioid partial agonistβ¦ |
| 39 | 3. Neural Substrates for Increased Drug-taking with Extended Access β 3.2. Between-system neuroadaptations | The ability of CRF antagonists to block the anxiogenic-like and aversive-like motivational effectsβ¦ |
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