Drug-induced decrement in spatial reversal learning in the white rat

Wilpizeski, Chester R.; Hamilton, Charles

doi:10.1007/bf00429574

Cited by 7 publications

(4 citation statements)

References 4 publications

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“…This effect was also observed after intra-cortical infusion of dopamine D 1 receptor antagonist (Sokolowski and Salamone 1995). Several elegant studies have also demonstrated that dopamine receptor antagonists and indirect dopamine agonists can produce deficits in reversal learning and responding for delayed reward similar to those produced by frontal lesions in both rodents (Wilpizeski and Hamilton 1964;Charrier and Theibot 1996;Evenden and Ryan 1996) and monkeys (Ridley et al 1981a(Ridley et al , 1981b.…”

Section: Dopamine and Frontal Cortical Cognitive Functionmentioning

confidence: 99%

Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli

Jentsch¹,

Taylor²

1999

Psychopharmacology

1,404

1,037

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Drug abuse and dependence define behavioral states involving increased allocation of behavior towards drug seeking and taking at the expense of more appropriate behavioral patterns. As such, addiction can be viewed as increased control of behavior by the desired drug (due to its unconditioned, rewarding properties). It is also clear that drug-associated (conditioned) stimuli acquire heightened abilities to control behaviors. These phenomena have been linked with dopamine function within the ventral striatum and amygdala and have been described specifically in terms of motivational and incentive learning processes. New data are emerging that suggest that regions of the frontal cortex involved in inhibitory response control are directly affected by long-term exposure to drugs of abuse. The result of chronic drug use may be frontal cortical cognitive dysfunction, resulting in an inability to inhibit inappropriate unconditioned or conditioned responses elicited by drugs, by related stimuli or by internal drive states. Drug-seeking behavior may thus be due to two related phenomena: (1) augmented incentive motivational qualities of the drug and associated stimuli (due to limbic/amygdalar dysfunction) and (2) impaired inhibitory control (due to frontal cortical dysfunction). In this review, we consider the neuro-anatomical and neurochemical substrates subserving inhibitory control and motivational processes in the rodent and primate brain and their putative impact on drug seeking. The evidence for cognitive impulsivity in drug abuse associated with dysfunction of the frontostriatal system will be discussed, and an integrative hypothesis for compulsive reward-seeking in drug abuse will be presented.

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Section: Dopamine and Frontal Cortical Cognitive Functionmentioning

confidence: 99%

Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli

Jentsch¹,

Taylor²

1999

Psychopharmacology

1,404

1,037

View full text Add to dashboard Cite

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“…Administration of methylphenidate in rodents does not affect reversal learning (Seu and Jentsch, 2009; Cheng and Li, 2013), although the latter authors observed beneficial effects in animals with reversal learning impairments (spontaneously hypertensive rats). Effects of amphetamine and methamphetamine on reversal learning have been variable, but possibly dose-dependent: high doses (5 mg/kg) impair reversal learning (Ridley et al, 1981; Arushanian and Baturin, 1982; Idris et al, 2005; Cheng et al, 2007; White et al, 2009; Izquierdo et al, 2010; Kosheleff et al, 2012; Talpos et al, 2012), while intermediate doses 1–2 mg/kg show no effect or improved learning (Wilpizeski and Hamilton, 1964; Kulig and Calhoun, 1972; Mead, 1974; Weiner and Feldon, 1986; Weiner et al, 1986; Daberkow et al, 2008; Pastuzyn et al, 2012; Soto et al, 2012) and low doses again impair reversal performance (Ridley et al, 1981; Idris et al, 2005). These results are compatible with the general idea that cognitive function depends on DA activity in an inverse U-shaped fashion (Cools and D'Esposito, 2011; Arnsten et al, 2012).…”

Section: Pharmacological Manipulations In Animalsmentioning

confidence: 99%

Dopaminergic control of cognitive flexibility in humans and animals

2013

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Striatal dopamine (DA) is thought to code for learned associations between cues and reinforcers and to mediate approach behavior toward a reward. Less is known about the contribution of DA to cognitive flexibility—the ability to adapt behavior in response to changes in the environment. Altered reward processing and impairments in cognitive flexibility are observed in psychiatric disorders such as obsessive compulsive disorder (OCD). Patients with this disorder show a disruption of functioning in the frontostriatal circuit and alterations in DA signaling. In this review we summarize findings from animal and human studies that have investigated the involvement of striatal DA in cognitive flexibility. These findings may provide a better understanding of the role of dopaminergic dysfunction in cognitive inflexibility in psychiatric disorders, such as OCD.

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“…Studies of the effects of amphetamine, or its analogues, on reversal learning in rodent models have generated variable results, including impairments (Idris et al, 2005, McLean et al, 2010), no effect (Wilpizeski and Hamilton, 1964) or improvements (Kulig and Calhoun, 1972, Weiner and Feldon, 1986); the variability in types of reversal used (spatial vs. visual; appetitively-reinforced vs. escape-reinforced; Pavlovian vs. instrumental) and the inconsistency in doses and routes of administration make a direct resolution of these disparate findings challenging.…”

Section: Neurotransmitter Mechanisms In Reversal Learningmentioning

confidence: 99%

Reversal learning as a measure of impulsive and compulsive behavior in addictions

2011

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Background Our ability to measure the cognitive components of complex decision-making across species has greatly facilitated our understanding of its neurobiological mechanisms. One task in particular, reversal learning, has proven valuable in assessing the inhibitory processes that are central to executive control. Reversal learning measures the ability to actively suppress reward-related responding and to disengage from ongoing behavior, phenomena that are biologically and descriptively related to impulsivity and compulsivity. Consequently, reversal learning could index vulnerability for disorders characterized by impulsivity, such as proclivity for initial substance abuse, as well as the compulsive aspects of dependence. Objective Though we describe common variants and similar tasks, we pay particular attention to discrimination reversal learning, its supporting neural circuitry, neuropharmacology and genetic determinants. We also review the utility of this task in measuring impulsivity and compulsivity in addictions. Methods We restrict our review to instrumental, reward-related reversal learning studies, as they are most germane to addiction. Conclusion The research reviewed here suggests that discrimination reversal learning may be used as a diagnostic tool for investigating the neural mechanisms that mediate impulsive and compulsive aspects of pathological reward-seeking and –taking behaviors. Two interrelated mechanisms are posited for the neuroadaptations in addiction that often translate to poor reversal learning: frontocorticostriatal circuitry dysregulation and poor dopamine (D2 receptor) modulation of this circuitry. These data suggest new approaches to targeting inhibitory control mechanisms in addictions.

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Drug-induced decrement in spatial reversal learning in the white rat

Cited by 7 publications

References 4 publications

Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli

Impulsivity resulting from frontostriatal dysfunction in drug abuse: implications for the control of behavior by reward-related stimuli

Dopaminergic control of cognitive flexibility in humans and animals

Reversal learning as a measure of impulsive and compulsive behavior in addictions

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