Tolerance as a Behavioral Phenomenon: Evidence from Two Experimental Paradigms

Blanc, Le; Cx, Poulos; Hd, Cappell

doi:10.1037/e497412006-006

Cited by 12 publications

(2 citation statements)

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“…Tolerance refers to a reduction of the effects of a drug due to repeated drug exposure. It can therefore be viewed as a form of adaptation, and similarities with other forms of adaptation have been noted (LeBlanc, Poulos & Cappell, 1978).…”

mentioning

confidence: 99%

A homeostatic model of Pavlovian conditioning: Tolerance to scopolamine-induced adipsia.

Poulos¹,

Hinson²

1984

Journal of Experimental Psychology: Animal Behavior Processes

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Several experiments support a model proposing that tolerance to scopolamine-induced adipsia involves an interplay between processes of homeostatic regulation and Pavlovian conditioning. In Experiment 1a, rats given access to water while under the influence of scopolamine developed adipsic tolerance, whereas rats denied access to water in the drug state did not. In Experiment 1b, rats displayed adipsic tolerance only when scopolamine was administered with cues associated with previous drug injections. In Experiment 1c, adipsic-tolerant rats showed a polydipsic response to an injection of phenobarbital (which unconditionally augments water consumption) relative to nontolerant animals with the same pharmacological history. Experiment 2 assessed the effect of deprivation level on the Pavlovian extinction of adipsic tolerance. Rats satiated with water during extinction showed a loss of adipsic tolerance, whereas water-deprived rats did not. The present model is discussed in relation to (a) tolerance in other response systems such as morphine analgesia, (b) theories of extinction for nonpharmacological Pavlovian conditioning, and (c) homeostatic regulation and incentive motivation.

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mentioning

confidence: 99%

A homeostatic model of Pavlovian conditioning: Tolerance to scopolamine-induced adipsia.

Poulos¹,

Hinson²

1984

Journal of Experimental Psychology: Animal Behavior Processes

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“…Moreover, it was also found t hat arginine vasopressin administration exacerbated the convulsions characteristic to withdrawal syndrome (Rigter and Crabbe, 1980). The involvement of learning components in development and decay of ethanol tolerance and withdrawal has been demonstrated in both human and animal experiments (Le Blanc et al, 1978;Hinson and Siegel, 1980;Riger and Crabbe, 1980). It seems to be well-documented that learning plays a role in the development of tolerance and physical dependence which may be regarded as the substrate of facilitation to either vasopressin, ACTH-like peptides and adrenaline.…”

Section: Discussionmentioning

confidence: 96%

Effect of 1-Desannino-D-Arginine Vasopressin, ACTH 4–10 and Adrenaline on Acquisition of Active Avoidance Response in Prenatally Ethanol-Treated Rats

Markel¹,

Korányi²,

Lévay³

et al. 2009

Exp Clin Endocrinol Diabetes

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The acquisition of active avoidance response was studied in 45 to 50-day old rats exposed to ethanol during pregnancy. The offsprings showed no retardation in somatic development although there was a marked deficit in learning of avoidance response. Daily administration of 1-desamino-D-arginine vasopressin (0.1 to 5 micrograms/100 g b.w.), ACTH 4-10 (0.1 to 2 micrograms/100 g b.w.) and adrenaline (0.2 to 2.0 micrograms/100 g b.w.) facilitated the learning performance in a dose-dependent manner. The retention of responding was tested after the interruption of training for 7 days. The prenatally ethanol-exposed rats with DDAVP pretreatment during the 5-day training procedure showed a better performance than that of the vehicle-treated ethanol-exposed rats but they were inferior to the controls. The present data indicate a complexity of biochemical changes due to the prenatal exposure to ethanol and the learning deficit can be modified by either neuropeptides or catecholamines, by such humoral mediators which are known to influence learning behavior and memory consolidation under different experimental conditions and due to different noxious stimuli from noxious stimuli from either external or internal environment.

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