Time-dependent effects of post-trial amphetamine treatment in rats: evidence for enhanced storage of representational memory

Strupp, Barbara J.; Bunsey, Michael; Levitsky, David A.; Kesler, Marilyn

doi:10.1016/0163-1047(91)90291-w

Cited by 29 publications

(16 citation statements)

References 40 publications

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“…Because of its attention-improving properties amphetamine was used to treat ADHD but then this treatment was replaced by drugs with fewer psychoactive side effects (Wilens et al 2008). Animal studies also showed that, similar to other stimulants, acute amphetamine and methamphetamine enhanced hippocampus-dependent learning and memory in the T-maze (Ito and Canseliet 2010), Morris water maze (Packard and McGaugh 1994;Brown et al 2000;Cao et al 2013), radial arm-maze (Strupp et al 1991), and avoidance conditioning (Doty and Doty 1966). However, these procognitive effects were dose-dependent as higher doses of acute amphetamine resulted in deficits in hippocampus-dependent learning and memory (Blokland et al 1998).…”

Section: Amphetaminementioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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It has long been hypothesized that conditioning mechanisms play major roles in addiction. Specifically, the associations between rewarding properties of drugs of abuse and the drug context can contribute to future use and facilitate the transition from initial drug use into drug dependency. On the other hand, the self-medication hypothesis of drug abuse suggests that negative consequences of drug withdrawal result in relapse to drug use as an attempt to alleviate the negative symptoms. In this review, we explored these hypotheses and the involvement of the hippocampus in the development and maintenance of addiction to widely abused drugs such as cocaine, amphetamine, nicotine, alcohol, opiates, and cannabis. Studies suggest that initial exposure to stimulants (i.e., cocaine, nicotine, and amphetamine) and alcohol may enhance hippocampal function and, therefore, the formation of augmented drug-context associations that contribute to the development of addiction. In line with the self-medication hypothesis, withdrawal from stimulants, ethanol, and cannabis results in hippocampus-dependent learning and memory deficits, which suggest that an attempt to alleviate these deficits may contribute to relapse to drug use and maintenance of addiction. Interestingly, opiate withdrawal leads to enhancement of hippocampus-dependent learning and memory. Given that a conditioned aversion to drug context develops during opiate withdrawal, the cognitive enhancement in this case may result in the formation of an augmented association between withdrawalinduced aversion and withdrawal context. Therefore, individuals with opiate addiction may return to opiate use to avoid aversive symptoms triggered by the withdrawal context. Overall, the systematic examination of the role of the hippocampus in drug addiction may help to formulate a better understanding of addiction and underlying neural substrates.Addiction is a major worldwide health problem that results in maladaptive behavioral changes, some that can last a lifetime. This behavioral plasticity, often times maladaptive, must be associated changes in neural plasticity. In fact, it has been noted multiple times that there is a high degree of overlap between the neurobiology of learning and memory and the neurobiology of addiction

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Section: Amphetaminementioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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“…Systemic injections of AMPH have been shown to enhance the consolidation of aversive tasks such as conditioned taste aversion (Fenu & Di Chiara, 2003) and various types of avoidance learning (Doty & Doty, 1966;Haycock, Van Buskirk & Gold, 1977;Janak & Martinez, 1992;Kulkarni, 1968;Martinez, Jensen, Messing, Vasquez, Soumireu-Mourat, Geddes, Liang & McGaugh, 1980). In addition, systemic injections of AMPH have been shown to enhance the consolidation of spatial learning (Brown, Bardo, Mace, Phillips & Kraemer, 2000;Packard & White, 1989;Strupp, Bunsey, Levitsky & Kesler, 1991), visual discrimination learning (Krivanek & McGaugh, 1969), and appetitive conditioning (Oscos, Martinez & McGaugh, 1988;Simon & Setlow, 2006). Systemic injections of AMPH can also enhance the consolidation of verbal learning in humans (Soetens, Casaer, D'Hooge & Hueting, 1995;Soetens, D'Hooge & Hueting, 1993).…”

Section: Introductionmentioning

confidence: 99%

Post-training, but not post-reactivation, administration of amphetamine and anisomycin modulates Pavlovian conditioned approach

Blaiss

Janak

2007

Neurobiology of Learning and Memory

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The psychostimulant, amphetamine (AMPH), and the protein synthesis inhibitor, anisomycin (ANI), have been shown to modulate the consolidation and reconsolidation of several types of learning. To determine whether Pavlovian conditioned approach (PCA) is modulated in a similar manner, we examined the effects of post-training and post-reactivation administration of both AMPH and ANI on memory for PCA. Male Long-Evans rats received PCA training sessions during which presentations of a CS+ were followed by sucrose delivery. AMPH (1 mg/kg, s.c.) injected immediately but not 6 hrs after the first training session enhanced PCA behavior. ANI (150 mg/kg, s.c.) injected immediately but not 3 hrs after the first training session impaired PCA behavior. This impairment was not due to the development of a conditioned taste aversion. To examine whether PCA can also be modulated by post-reactivation administration of AMPH and ANI, rats were given an injection of AMPH, ANI, or vehicle immediately after a memory reactivation session. Upon testing, the behavior of both the AMPH-and the ANI-treated rats was unaffected. This result remained consistent when the experiment was repeated with changes to various behavioral parameters (i.e. amount of training, length of memory reactivation). These findings indicate that AMPH and ANI act during the post-training but not the post-reactivation period to enhance and impair, respectively, the learning of PCA. This suggests that the consolidation of PCA can be modulated in a manner comparable to other types of learned associations, but once learned, the memory appears to be relatively robust and stable.

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“…In rats and mice, amphetamine produces dose-and time-dependent enhancement of memory storage (11)(12)(13)(14)(15)(16)(17). The effects of posttraining injections of amphetamine on memory are attenuated by surgical removal of the adrenal medulla (13), the primary source of circulating epinephrine (18).…”

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confidence: 99%

Adrenocortical suppression blocks the memory-enhancing effects of amphetamine and epinephrine.

Roozendaal

Carmi

McGaugh

1996

Proc. Natl. Acad. Sci. U.S.A.

113

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This study examined glucocorticoidadrenergic interactions in modulating acquisition and memory storage for inhibitory avoidance training. Systemically (s.c.) administered amphetamine (1 mg/kg), but not epinephrine (0.1 mg/kg) or the peripherally acting amphetamine derivative 4-OH amphetamine (2 mg/kg), given to rats shortly before training facilitated acquisition performance in a continuous multiple-trial inhibitory avoidance (CMIA) It is well established that adrenal hormones are released during training in emotionally motivated tasks (1-3) and influence neurobiological mechanisms underlying regulation of memory storage (4-6). Systemic injections of the adrenomedullary hormone epinephrine produce dose-dependent enhancement of retention performance when given to rats and mice shortly after training in aversive and appetitive learning tasks (7-10).Earlier evidence suggesting that peripheral catecholamines modulate memory storage came from experiments examining the effects of systemic injections of amphetamine. In rats and mice, amphetamine produces dose-and time-dependent enhancement of memory storage (11)(12)(13)(14)(15)(16)(17). The effects of posttraining injections of amphetamine on memory are attenuated by surgical removal of the adrenal medulla (13), the primary source of circulating epinephrine (18). This finding suggests that the effects of amphetamine on memory storage are due, at least in part, to an influence on the release of catecholamines from peripheral storage sites (19). This view is supported by evidence that 4-OH amphetamine, a derivative of amphetamine with a limited capacity to enter the brain (20),The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. also facilitates retention when given immediately after training (12,14,17).Training in aversively motivated learning tasks is also known to stimulate the adrenocortical system, resulting in increased plasma levels of corticosterone (3, 21). There is extensive evidence that glucocorticoids modulate memory consolidation (22)(23)(24)(25)(26). Furthermore, findings of experiments using adrenalectomized (ADX) rats indicate that the level of circulating corticosterone is a major factor in determining the sensitivity of epinephrine in modulating memory storage (27,28), suggesting an interaction between sympathoadrenal and adrenocortical systems in the modulation of memory storage for emotionally influenced tasks.The present experiments examined glucocorticoidadrenergic interactions in the regulation of memory storage in adrenally intact rats. The enhancing effects of systemic injections of amphetamine, 4-OH amphetamine, and epinephrine on memory for inhibitory avoidance training were examined in rats pretreated with a vehicle solution or metyrapone, a drug that inhibits 1 1 3-hydroxylase, a rate-limiting enzyme in corticosterone synthesis (29,30 Apparatus and Procedures. Two variants of ...

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Time-dependent effects of post-trial amphetamine treatment in rats: evidence for enhanced storage of representational memory

Cited by 29 publications

References 40 publications

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

Post-training, but not post-reactivation, administration of amphetamine and anisomycin modulates Pavlovian conditioned approach

Adrenocortical suppression blocks the memory-enhancing effects of amphetamine and epinephrine.

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