Power Point Slides Alcohol - Meagher Lab
Power Point Slides Alcohol - Meagher Lab Power Point Slides Alcohol - Meagher Lab
Figure 1 Opponent process model of addiction. According to the opponent process theory the affective (hedonic or emotional) response to a stimulus (a drug in this case) is the underlying a-process, which in turn elicits the opponent b-process (bottom). The underlying processes add together to cause the initial pleasant A-state, which is actually experienced, followed by an opponent unpleasant B-state. Initially the pleasant A-state is large, followed by a small B-state. With repeated drug use and in addiction, however, the opponent b-process increases in magnitude and duration, leading to an experience dominated by the unpleasant symptoms associated with withdrawal. (Adapted from Solomon 1977 and Solomon & Corbit 1973.)
Koob’ Model (2004) Animal studies indicate that drug use leads to dysregulation of distinct neurochemical mechanisms in specific reward and stress neural circuits that provide the negative motivational state that drives addiction. An extension of Solomon and Corbit’s opponent-process model. Here both panels represent the affective response to the presentation of a drug. The top represents the initial experience of a drug with no prior drug history. The a-process represents a positive mood state, and the b-process represents the negative mood state. An individual experiencing a positive mood state from a drug of abuse is hypothesized to retain the a-process. In other words, an appropriate counteradaptive opponent-process (b-process) that balances the activational process (a-process) does not lead to an allostatic state. The bottom panel represents changes in the affective stimulus (state) in an individual with repeated frequent drug use that may represent a transition to an allostatic state in the brain reward systems and, by extrapolation, a transition to addiction. Note that the b-process never returns to the original homeostatic level before drug-taking is reinitiated, thus creating a greater and greater allostatic state in the brain reward system. Thus, the counteradaptive opponent process (b-process) does not balance the activational process (a-process) but in fact shows a residual hysteresis. The hypothesis here is that even during post-detoxification, a period of ‘protracted abstinence’, the reward system is still bearing allostatic changes. In the non-dependent state, reward experiences are normal, and the brain stress systems are not greatly engaged. During the transition to the state known as addiction, the brain reward system is in a major underactivated state while the brain stress system is highly activated. DA, dopamine; CRF, corticotropin-releasing factor; GABA, g-aminobutyric acid; NPY, neuropeptide. The following definitions apply: allostasis, the process of achieving stability through change; allostatic state, a state of chronic deviation of the regulatory system from its normal (homeostatic) operating level; allostatic load, the cost to the brain and body of the deviation, accumulating over time, and reflecting in many cases pathological states and accumulation of damage.
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- Page 5 and 6: What Is Substance Dependence? ! Phy
- Page 7 and 8: Addiction Theories (a) The opponent
- Page 9 and 10: Opponent Process Theory
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- Page 19 and 20: DSM-IV Definitions ! ALCOHOL ABUSE:
- Page 21 and 22: EPIDEMIOLOGY ! Stats: ! 1 out of 10
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Figure 1 Opponent process model of addiction. According to the opponent process theory<br />
the affective (hedonic or emotional) response to a stimulus (a drug in this case) is the<br />
underlying a-process, which in turn elicits the opponent b-process (bottom). The underlying<br />
processes add together to cause the initial pleasant A-state, which is actually experienced,<br />
followed by an opponent unpleasant B-state. Initially the pleasant A-state is large, followed<br />
by a small B-state. With repeated drug use and in addiction, however, the opponent b-process<br />
increases in magnitude and duration, leading to an experience dominated by the unpleasant<br />
symptoms associated with withdrawal. (Adapted from Solomon 1977 and Solomon & Corbit<br />
1973.)
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