Neuroadaptational Views of Addiction
Counteradaptation and Opponent Process
Counteradaptation hypotheses have long been proposed in an attempt to explain tolerance and withdrawal and the motivational changes that occur with the development of addiction. The initial acute effects of a drug are opposed or counteracted by homeostatic changes in systems that mediate the primary drug effects. The origins of the counteradaptive hypotheses can be traced back to much earlier work on physical dependence (for further reading of early formulations, see Himmelsbach, 1943) and the counteradaptive changes in physiological measures associated with acute and chronic opioid administration.
The opponent-process theory was developed in the 1970s (for further reading, see Solomon and Corbit, 1974; Solomon, 1980). Since then, it has been applied by many researchers to various situations, including drugs of abuse, fear conditioning, tonic immobility, ulcer formation, eating disorders, jogging, peer separation, glucose preference, and even parachuting.
The theory assumes that the brain contains many affect control mechanisms that serve as a kind of emotional immunization system that counteracts or opposes departures from emotional neutrality or equilibrium, regardless of whether they are aversive or pleasant. The theory is basically a negative feed-forward control construct designed to keep mood in check even though stimulation is strong. The system is conceptualized as being composed of three subparts organized in a temporal manner. Two opposing processes control a summator, which determines the controlling affect at a given moment. First, an unconditioned arousing stimulus triggers a primary affective process, termed the a-process; an unconditional reaction that translates the intensity, quality, and duration of the stimulus (for example, the first, initial use of an opiate). Second, as a consequence of the a-process, the opposing b-process is evoked after a short delay, thus defining the opponent process. The b-process feeds a negative signal into the summator, subtracting the impact of the already existing a-process in the summator. These two responses are consequently and temporally linked (a triggers b) and depend on different neurobiological mechanisms. The b-process has a longer latency, but some data show that it may appear soon after the beginning of the stimulus in the course of the stimulus action and have more inertia, slower recruitment, and a more sluggish decay. At any given moment, the pattern of affect will be simply the algebraic sum of these opposite influences, yielding the net product of the opponent process with the passage of time (Figure 1.8).
Importantly, with repetition of the stimulus, the dynamics or net product is a result of a progressive increase in the b-process. In other words, the b-process itself is sensitized with repeated drug use and appears more and more rapidly after the unconditional stimulus onset. It then persists longer after its initial, intended action (the unconditioned effect) and eventually masks the unconditioned effect (a-process), resulting in apparent tolerance (for further reading, see Colpaert, 1996). Experimental data show that if the development of the b-process is blocked, then no tolerance can develop with drugs. The unconditioned effect of the drug does not change with repeated drug administration. The development of the b-process equals the development of a negative affective state and withdrawal symptoms, in opposition to the hedonic quality of the unconditioned stimulus. Importantly, the nature of the acquired motivation is specified by the nature of the b-process (that is, an aversive affect in the case of drug abuse). The individual will work to reduce, terminate, or prevent the negative affect.
In this opponent-process theory from a drug addiction perspective, tolerance and dependence are inextricably linked. Solomon argued that the first few self-administrations of an opiate drug produce a pattern of motivational changes. The onset of the drug effect produces euphoria (a-process), followed by a subsequent decline in intensity. After the effects of the drug wear off, the b-process emerges as an aversive craving state. The b-process gets progressively stronger over time, in effect contributing to or producing more complete tolerance to the initial euphoric effects of the drug (Figure 1.8).