ADDICTION AND THE BRAIN ANTIREWARD SYSTEM PDF

In this framework, addiction is conceptualized as a cycle of decreased function of brain reward systems and recruitment of antireward systems that progressively worsen, resulting in the compulsive use of drugs. Counteradaptive processes, such as opponent process, that are part of the normal homeostatic limitation of reward function fail to return within the normal homeostatic range and are hypothesized to repeatedly drive the allostatic state. Excessive drug taking thus results in not only the short-term amelioration of the reward deficit but also suppression of the antireward system. However, in the long term, there is worsening of the underlying neurochemical dysregulations that ultimately form an allostatic state decreased dopamine and opioid peptide function, increased corticotropin-releasing factor activity. This allostatic state is hypothesized to be reflected in a chronic deviation of reward set point that is fueled not only by dysregulation of reward circuits per se but also by recruitment of brain and hormonal stress responses. Vulnerability to addiction may involve genetic comorbidity and developmental factors at the molecular, cellular, or neurocircuitry levels that sensitize the brain antireward systems.

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Koob, Ph. Abstract Drug addiction is conceptualized as chronic, relapsing compulsive use of drugs with significant dysregulation of brain hedonic systems.

Compulsive drug use is accompanied by decreased function of brain substrates for drug positive reinforcement and recruitment of brain substrates mediating the negative reinforcement of motivational withdrawal.

These changes, combined with decreased reward function, are hypothesized to persist in the form of an allostatic state that forms a powerful motivational background for relapse. Relapse also involves a key role for the basolateral amygdala in mediating the motivational effects of stimuli previously paired with drug seeking and drug motivational withdrawal. The basolateral amygdala has a key role in mediating emotional memories in general. The hypothesis argued here is that brain stress systems activated by the motivational consequences of drug withdrawal can not only form the basis for negative reinforcement that drives drug seeking, but also potentiate associative mechanisms that perpetuate the emotional state and help drive the allostatic state of addiction.

Conceptual Framework Drug addiction, also known as substance dependence, is a chronically relapsing disorder characterized by 1 compulsion to seek and take the drug, 2 loss of control in limiting intake, and 3 emergence of a negative emotional state e.

Although the emergence of a negative emotional state is not an established criterion of Substance Dependence defined by the Diagnostic and Statistical Manual of Mental Disorder, 4th edition DSM-IV, [ 4 ] , it is a reflection of what has been termed motivational withdrawal. Clinically, the occasional but limited use of an abusable drug is distinct from compulsive drug use and the emergence of chronic drug addiction. An important goal of current neurobiological research is to understand the neuropharmacological and neuroadaptive mechanisms within specific neurocircuits that mediate the transition from occasional, controlled drug use and the loss of behavioral control over drug seeking and drug taking that defines chronic addiction.

Different theoretical perspectives, ranging from experimental and social psychology to neurobiology, can be superimposed on these three stages, which are conceptualized as feeding into each other, becoming more intense, and moving from positive to negative reinforcement. Positive reinforcement can be defined as a situation in which presentation of a stimulus increases the probability of a response, and negative reinforcement can be defined as a situation in which removal of a stimulus increases the probability of a response.

Neural substrates for the positive reinforcing properties of drug taking and drug seeking have dominated the field of the neurobiology of addiction.

Two neurobiological circuits are proposed as key to the hedonic aspects of the motivation to seek drugs: the neurobiological circuitry involved in dysregulation of the positive-reinforcing properties of drugs of abuse ventral striatal-pallidal-thalamic loops and the neurobiological circuitry associated with recruitment of the negative-reinforcing properties of drugs of abuse extended amygdala Figure 1.

The present review will explore the neurobiological mechanisms of addiction that are involved in various stages of the addiction cycle, with a focus on the plasticity of neurocircuits associated with the transition from drug taking to drug addiction, the motivational effects of withdrawal and protracted abstinence, and the parallels with emotional memory that help sustain the addiction process.

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Koob, Ph. Abstract Drug addiction is conceptualized as chronic, relapsing compulsive use of drugs with significant dysregulation of brain hedonic systems. Compulsive drug use is accompanied by decreased function of brain substrates for drug positive reinforcement and recruitment of brain substrates mediating the negative reinforcement of motivational withdrawal. These changes, combined with decreased reward function, are hypothesized to persist in the form of an allostatic state that forms a powerful motivational background for relapse.

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