Evidence from rats that morphine tolerance is a learned response.

Siegel, Shepard

doi:10.1037/h0077058

Cited by 653 publications

(379 citation statements)

References 16 publications

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“…Animals that had ethanol reliably paired with a distinctive context displayed more tolerance when tested in that environment than animals that were administered ethanol unpaired with this context. The apparent contextual specificity of this tolerance is consistent with theories that contend that salient environmental cues that are reliably paired with drug administration can come to elicit processes that attenuate a drug's direct effects (Siegel 1975;Baker and Tiffany 1985).…”

Section: Discussionsupporting

confidence: 57%

“…Classical conditioning processes have also been invoked to describe the acquisition of drug tolerance (Siegel 1975;Baker and Tiffany 1985). For instance, the Pavlovian model of drug tolerance (Siegel 1975) states that environmental cues routinely paired with drug administration will become conditioned stimuli (CS), which elicit a conditioned response (CR) that is opposite in direction to, or compensatory for, the direct effects of drug.…”

mentioning

confidence: 99%

“…For instance, the Pavlovian model of drug tolerance (Siegel 1975) states that environmental cues routinely paired with drug administration will become conditioned stimuli (CS), which elicit a conditioned response (CR) that is opposite in direction to, or compensatory for, the direct effects of drug. Over conditioning trials the compensatory CR grows in magnitude and counteracts the direct drug effects, i.e., tolerance develops.…”

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confidence: 99%

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The contribution of classical conditioning to tolerance to the antinociceptive effects of ethanol

1987

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In rats, ethanol increases the latency of the tail-flick reflex to radiant heat. Three experiments examined the contribution of classical conditioning to the acquisition of tolerance to this antinociception. Experiment 1 showed that the antinociception produced by ethanol was dose dependent. The results of Experiment 2 demonstrated that rats exposed to a series of ethanol injections paired with a distinctive environment developed tolerance to this antinociception. In Experiment 3, tolerance was more pronounced in animals that had been exposed to ethanol and tested in the distinctive environment than in animals that had received ethanol in a nondistinctive environment. In contrast to previous reports in the literature, these results show that animals need not practice the tail-flick reflex while intoxicated in order to develop tolerance. Additionally, the data suggest that classical conditioning may contribute to tolerance to the antinociceptive effects of ethanol.

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Section: Discussionsupporting

confidence: 57%

mentioning

confidence: 99%

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confidence: 99%

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The contribution of classical conditioning to tolerance to the antinociceptive effects of ethanol

1987

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“…signals of carisoprodol administration, elicited a conditioned compensatory response. Cue-elicited drug-compensatory responses are suggestive of a homoeostatic mechanism: the effect of the drug represents a perturbation of homoeostatic levels, and physiological reactions that compensate for and reduce the drug response are elicited by the drug or stimuli that signal the drug [63,64].…”

Section: Why Not a Compensatory Response?mentioning

confidence: 99%

The relation of emotions to placebo responses

Flaten

Aslaksen

Lyby

et al. 2011

Phil. Trans. R. Soc. B

122

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The hypothesis put forth is that expectations of treatment effects reduce negative emotions and thereby reduce symptoms, e.g. pain. Negative emotions increase pain, and it is hypothesized that placebos reduce pain by reducing negative emotions, i.e. feelings of nervousness, fear and anxiety. Placebo analgesia has been shown to be mediated via opioid activity, and relaxation increases opioid activity. The placebo acquires its relaxing effect due to verbal information that pain will be reduced, or due to associations between the placebo and the reduction in pain after effective treatment. Thus, the placebo signals that unpleasantness will be less after administration of the placebo. This involves negative reinforcement which is due to activation of a dopaminergic system that has been found to be activated during placebo analgesia and is involved in positive emotions. The nocebo effect of increased pain is, consistent with this model, because of increased fear and anxiety. The new aspect of the presented model is the hypothesis that expectations reduce negative emotions, and that negative reinforcement that involves the dopaminergic reinforcement system should be a contributor to placebo responses.

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“…From a drug-taking perspective of brain motivational systems, the initial acute effect of a drug (the a-process or positive hedonic response) was hypothesized to be opposed or counteracted by the b-process as homeostatic changes in brain systems (figure 2). This affect control system was conceptualized as a single negative feedback or opponent loop that opposes the stimulus-aroused affective state and suppresses or reduces all departures from hedonic neutrality (Solomon & Corbit 1974;Siegel 1975;Poulos & Cappell 1991). Affective states, pleasant or aversive, were hypothesized to be automatically opposed by centrally mediated mechanisms that reduce the intensity of these affective states.…”

Section: Opponent Process and Addiction (A) Motivation And Opponent Pmentioning

confidence: 99%

Neurobiological mechanisms for opponent motivational processes in addiction

Koob

Moal

2008

Phil. Trans. R. Soc. B

622

430

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The conceptualization of drug addiction as a compulsive disorder with excessive drug intake and loss of control over intake requires motivational mechanisms. Opponent process as a motivational theory for the negative reinforcement of drug dependence has long required a neurobiological explanation. Key neurochemical elements involved in reward and stress within basal forebrain structures involving the ventral striatum and extended amygdala are hypothesized to be dysregulated in addiction to convey the opponent motivational processes that drive dependence. Specific neurochemical elements in these structures include not only decreases in reward neurotransmission such as dopamine and opioid peptides in the ventral striatum, but also recruitment of brain stress systems such as corticotropinreleasing factor (CRF), noradrenaline and dynorphin in the extended amygdala. Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, anxiety-like responses and extracellular levels of CRF in the central nucleus of the amygdala. CRF receptor antagonists 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 stress-induced relapse. The combination of loss of reward function and recruitment of brain stress systems provides a powerful neurochemical basis for the long hypothesized opponent motivational processes responsible for the negative reinforcement driving addiction.

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Evidence from rats that morphine tolerance is a learned response.

Cited by 653 publications

References 16 publications

The contribution of classical conditioning to tolerance to the antinociceptive effects of ethanol

The contribution of classical conditioning to tolerance to the antinociceptive effects of ethanol

The relation of emotions to placebo responses

Neurobiological mechanisms for opponent motivational processes in addiction

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