Effects of methylphenidate on working memory in pigeons

Wright, Fiona K.; White, K. Geoffrey

doi:10.3758/cabn.3.4.300

Cited by 14 publications

(14 citation statements)

References 56 publications

(81 reference statements)

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“…The latter interpretation seems consistent with instances in which sample-stimulus conditions are held constant, but accuracy is lowered through drug administration and consequential distraction from competing alternatives. For example, administration of the drug scopolamine increases the overall difficulty of discrimination, as reflected in a reduction in the intercept of the forgetting function, consistent with much prior research on the effects of drugs on delayed matching performance in pigeons and rats (Parkes & White, 2000;White & Ruske, 2002;Wright & White, 2003). Ruske, Fisher, and compared the effects of scopolamine with a vehicle control on delayed matching performance in pigeons.…”

Section: Forgetting Functions Differing In Interceptsupporting

confidence: 70%

Forgetting from Short-Term Memory in Delayed Matching to Sample: A Reinforcement Context Model

White¹,

Brown²

2014

CCBR

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Short-term memory in nonhuman animals is typically studied in delayed matching to sample, with variation in the retention interval or delay between the to-be-remembered sample and subsequently presented choice or comparison stimuli. The forgetting function, which relates the systematic decrease in discriminability to increasing delay, is well described by an exponential in the square root of time, with an intercept and slope that vary systematically with different conditions, such as sample-stimulus disparity, retention-interval conditions, and reward parameters. We argue that the rewards for accurate matching are relative to the reinforcement context, which includes rewards R o for extraneous or other behaviors. Forgetting results from competition between R o and rewards for the delayed matching task. We suggest that R o acts to shift attention from the memory task to extraneous behavior, and that R o grows as a linear function of time in the retention interval. By incorporating these assumptions in the model proposed by White and Wixted (1999), we accurately predict the time course of forgetting under a variety of different conditions for delayed matching.

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Section: Forgetting Functions Differing In Interceptsupporting

confidence: 70%

Forgetting from Short-Term Memory in Delayed Matching to Sample: A Reinforcement Context Model

White¹,

Brown²

2014

CCBR

Self Cite

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“…As a second test of a moderate dose of MPH, we ran mice through a hippocampal dependent, delayed non-match to sample T-maze task designed to test spatial working memory, a type of memory that MPH is specifically known to enhance (Repantis et al, 2010; Wright and White, 2003). A boost in T-maze performance should mean we have a moderate therapeutic dose, as indicated in the literature by behavioral experiments in mice (Heredia et al, 2013; Huang and Huang, 2012; Lloyd et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

Dopamine and norepinephrine receptors participate in methylphenidate enhancement of in vivo hippocampal synaptic plasticity

Jenson

Yang²,

Acevedo-Rodriguez

et al. 2015

Neuropharmacology

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Attention-deficit hyperactive disorder (ADHD) is the most commonly studied and diagnosed psychiatric disorder in children. Methylphenidate (MPH, e.g., Ritalin) has been used to treat ADHD for over 50 years. It is the most commonly prescribed treatment for ADHD, and in the past decade it was the drug most commonly prescribed to teenagers. In addition, MPH has become one of the most widely abused drugs on college campuses. In this study, we examined the effects of MPH on hippocampal synaptic plasticity, which serves as a measurable quantification of memory mechanisms. Field potentials were recorded with permanently implanted electrodes in freely-moving mice to quantify MPH modulation of perforant path synaptic transmission onto granule cells of the dentate gyrus. Our hypothesis was that MPH affects hippocampal synaptic plasticity underlying learning because MPH boosts catecholamine signaling by blocking the dopamine and norepinephrine transporters (DAT and NET respectively). In vitro hippocampal slice experiments indicated MPH enhances perforant path plasticity, and this MPH enhancement arose from action via D1-type dopamine receptors and β-type adrenergic receptors. Similarly, MPH boosted in vivo initiation of long-term potentiation (LTP). While there was an effect via both dopamine and adrenergic receptors in vivo, LTP induction was more dependent on the MPH-induced action via D1-type dopamine receptors. Under biologically reasonable experimental conditions, MPH enhances hippocampal synaptic plasticity via catecholamine receptors.

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“…Its major mechanism of action is stimulation of dopamine release and dopamine-reuptake inhibition. Although amphetamines enhance memory in both animal models [4][5][6][7] and humans [6,8], their clinical use is limited by such side effects as hyperactivity, agitation, psychosis, and addiction [9,10]. These adverse effects are thought to be due to increase in dopamine in the subcortical areas, such as the nucleus accumens [11].…”

Section: Introductionmentioning

confidence: 94%

The effects of l-amphetamine sulfate on cognition in MS patients: results of a randomized controlled trial

Morrow

Kaushik²,

Zarevics

et al. 2009

J Neurol

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Defects in processing speed and memory are common in multiple sclerosis (MS) patients. In other populations, amphetamines have been shown to enhance cognition, but their use is limited by adverse behavioral effects. The L-isomer may have equivalent cognition enhancement with less adverse effects due to decreased potency in subcortical areas. The aim of this study was to assess the safety and efficacy of L-amphetamine sulfate in the treatment of cognitive dysfunction in MS. This was a 2:1 randomized, placebo-controlled, double-blind trial, involving 33 MS clinics across the USA. One hundred and fifty-one clinically definite MS patients with documented cognitive dysfunction who were relapse free for >or=90 days, with an Expanded Disability Status Scale (EDSS)

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Effects of methylphenidate on working memory in pigeons

Cited by 14 publications

References 56 publications

Forgetting from Short-Term Memory in Delayed Matching to Sample: A Reinforcement Context Model

Forgetting from Short-Term Memory in Delayed Matching to Sample: A Reinforcement Context Model

Dopamine and norepinephrine receptors participate in methylphenidate enhancement of in vivo hippocampal synaptic plasticity

The effects of l-amphetamine sulfate on cognition in MS patients: results of a randomized controlled trial

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