State Dependent Learning and Drug Discriminations

Overton, Donald A.

doi:10.1007/978-1-4615-7178-0_2

Cited by 80 publications

(65 citation statements)

References 255 publications

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“…This result is contrary to most theoretical formulations of state-dependency that predict a symmetrical effect of shifting drug states. Some researchers have reported asymmetrical patterns in which only the shift from drug to no drug produces the deficit (e.g., [2,27]). Unfortunately, these asymmetrical state dependency accounts get theoretically burdensome (see [32] for a similar conclusion).…”

Section: Discussionmentioning

confidence: 99%

“…Although there is a very rich theoretical and empirical literature on state-dependent learning with such drugs as ethanol, chlordiazepoxide, pentobarbital, and midazolam [11,17,18,19,[24][25][26][27]30,37], such an extant literature does not exist for nicotine. In fact, the only replicated demonstration that nicotine might have a state-dependent effect used human smokers and recall of word lists [21,29,35].…”

Section: Discussionmentioning

confidence: 99%

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Nicotine does not produce state-dependent effects on learning in a Pavlovian appetitive goal tracking task with rats

Bevins

Penrod

Reichel

2007

Behavioural Brain Research

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Past research has shown that when rats received 0.4 mg base/kg nicotine paired reliably with intermittent sucrose delivery that anticipatory sucrose-seeking behavior (i.e., goal tracking) was differentially displayed in the nicotine state relative to intermixed saline sessions in which no sucrose was delivered. The present research extended this observation to a lower dose of nicotine (i.e., 0.2 mg base/kg) and tested a state-dependent learning account of differential conditioned responding. According to this account, the increase in goal tracking on nicotine sessions reflects a chambersucrose association that is only recalled when in the nicotine state. We used a 2 × 2 factorial design in which rats received sucrose deliveries in one drug state (nicotine or saline) and were then tested in the same state (Nic→Nic or Sal→Sal) or a different state (Nic→Sal or Sal→Nic) after acquiring the conditioned response. A state-dependency account predicts disruption in conditioned goal tracking for rats that receive a shift in drug state on the test day. This disruption did not occur suggesting that differential control of conditioned responding by nicotine is more likely due to a direct excitatory association between the interoceptive cueing effects of nicotine and the appetitive qualities of sucrose.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nicotine does not produce state-dependent effects on learning in a Pavlovian appetitive goal tracking task with rats

Bevins

Penrod

Reichel

2007

Behavioural Brain Research

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“…With regard to drug discrimination, it has been hypothesized that perceptual masking might occur whereby one compound exerts distinctive stimulus effects that render an otherwise readily identified training compound no longer detectable (Colpaert, 1977). Masking has generally been ignored or assumed irrelevant in most drug-discrimination studies (Overton, 1984); jpet.aspetjournals.org however, dopaminergic compounds have been suggested to alter the morphine discriminative stimulus under some conditions by masking (Gauvin and Young, 1989). Although the effects of cocaine and amphetamine on the naltrexone discriminative stimulus in opioid-dependent monkeys might reflect perceptual masking, if this procedure was generally susceptible to masking then it might be expected that a similar effect would be obtained with a wider variety of compounds.…”

Section: Figmentioning

confidence: 99%

Cocaine and Amphetamine Attenuate the Discriminative Stimulus Effects of Naltrexone in Opioid-Dependent Rhesus Monkeys

Sell

2002

J Pharmacol Exp Ther

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This study tested the hypothesis that stimulants (indirect dopamine agonists) attenuate the discriminative stimulus of naltrexone in monkeys chronically treated with L-␣-acetylmethadol (LAAM). Four rhesus monkeys (Macaca mulatta) received LAAM (1.0 mg/kg s.c.) twice daily and discriminated a withdrawalprecipitating dose of naltrexone (0.0178 mg/kg s.c.) from saline. Cocaine (0.1-1.78 mg/kg), amphetamine (0.32-1.78 mg/kg), haloperidol (0.01-0.1 mg/kg), sulpiride (1.0 -10.0 mg/kg), propranolol (0.32-3.2 mg/kg), clonidine (0.001-0.1 mg/kg), desipramine (0.32-3.2 mg/kg), and imipramine (1.0 -10.0 mg/kg) were given s.c. before cumulative doses of naltrexone. Cocaine and amphetamine antagonized the discriminative stimulus effects of naltrexone, each shifting the naltrexone dose-effect curve significantly (e.g., 100-fold) rightward or downward. In contrast, the dopamine antagonist haloperidol shifted the naltrexone dose-effect curve 5-fold leftward. Sulpiride, desipramine, clonidine, and propranolol had comparatively less effect on the naltrexone discriminative stimulus, whereas some doses of imipramine attenuated the naltrexone stimulus in a manner similar to that of cocaine and amphetamine. These results support the notion that multiple neurotransmitter systems are involved in the discriminative stimulus effects of opioid withdrawal. Furthermore, these data are consistent with reports that dopamine levels decrease during opioid withdrawal and provide evidence that enhancing dopamine or other monoamine levels may attenuate subjective effects of opioid withdrawal.

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“…Five different groups were compared: (A) controls (n -8), injected with 5 ml of saline (0.9%) 30 min prior to training (day 1 ); (B) MCPGh (n = 8), injected 30 min prior to training (day 1); (C) statedependency 1 (n = 8), injected with MCPGh 30 min prior to retention test (day 2); (D) state-dependency 2 (n = 9), injected with MCPGh 30 min prior to training (day 1 ) and prior to retention test (day 2); (E) MCPGI (n= 10), injected 30 min prior to training (day 1 ). We had to control for state dependency, because MCPGh significantly impaired retention in the spatial alternation task, and we thus had to exclude possible drug-induced side effects on performance (Overton 1984;Poling and Cross 1993).…”

Section: Animalsmentioning

confidence: 99%

Metabotropic glutamate receptors in spatial and nonspatial learning in rats studied by means of agonist and antagonist application.

Riedel¹,

Wetzel²,

Reymann³

1995

Learn. Mem.

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We examined the effects of both the metabotropic glutamate receptor (mGluR) antagonist MCPG and the agonist tADA in two behavioral paradigms in rats: (1) brightness discrimination and (2) spatial alternation. Compounds were applied intracerebroventricularly at different times, either 30 min prior to training or immediately after training, and rats were tested for retention 24 hr later in the same paradigms. Both MCPG and tADA caused amnesia in the spatial alternation test, when applied pretraining, but no effect was obtained in the brightness discrimination paradigm. Drug-induced amnesia was shown not to be attributable to state-dependent effects of MCPG or tADA. Moreover, the memory inhibiting effect of MCPG was dose dependent, with a low dose (20 raM/5 ml) having no effect on learning and memory and a 10 times higher concentration (200 mM/5 ml) causing complete amnesia. Application of both saline and MCPG immediately post-training prevented memory formation, which may be attributable to an interference by the injection procedure with the process of memory formation. The mGluR agonist tADA, however, facilitated memory formation in the spatial alternation task, when injected immediately after training. 3Corresponding author. Present address:

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State Dependent Learning and Drug Discriminations

Cited by 80 publications

References 255 publications

Nicotine does not produce state-dependent effects on learning in a Pavlovian appetitive goal tracking task with rats

Nicotine does not produce state-dependent effects on learning in a Pavlovian appetitive goal tracking task with rats

Cocaine and Amphetamine Attenuate the Discriminative Stimulus Effects of Naltrexone in Opioid-Dependent Rhesus Monkeys

Metabotropic glutamate receptors in spatial and nonspatial learning in rats studied by means of agonist and antagonist application.

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