Attenuation of pharmacologically-induced attentional impairment by methylphenidate in rats

Rezvani, Amir H.; Kholdebarin, Ehsan; Cauley, Marty; Dawson, Elizabeth; Levin, Edward D.

doi:10.1016/j.pbb.2008.11.005

Cited by 20 publications

(26 citation statements)

References 31 publications

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“…First, ketamine (10.0-18.0 mg/kg) decreased signal detection performance at doses that have been shown to produce antidepressant-like effects in rats (Hillhouse et al, 2014a,b; Koike et al, 2013; Reus et al, 2011; Zhou et al, 2014). The effects of ketamine in the present study are consistent with the effects of the noncompetitive NMDA receptor antagonist MK-801, which also produces a decrease in percent hit and correct rejection accuracy and increases in response latency and trial omissions (Rezvani et al, 2009). The impairments produced by ketamine in the signal detection task parallel findings in other attention tasks.…”

Section: Discussionsupporting

confidence: 83%

“…To thoroughly address the effects of ketamine on sustained attention, we evaluated the dose- and time-dependent effects of ketamine using the visual signal detection procedure in rats. The visual signal detection procedure has been used to evaluate the effects of antipsychotic drugs, nicotinic agonists, muscarinic antagonists, dopamine reuptake inhibitors and other NMDA receptor antagonists on sustained attention (Hillhouse and Prus, 2013; Levin et al, 2011; Rezvani et al 2008, 2009). …”

Section: Introductionmentioning

confidence: 99%

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Effects of the noncompetitive N-methyl-D-aspartate receptor antagonist ketamine on visual signal detection performance in rats

Hillhouse

Merritt²,

Porter³

2015

Behavioural Pharmacology

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The noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist ketamine produces consistent, rapid, and sustained antidepressant effects in patients suffering from treatment-resistant depression. However, ketamine-induced cognitive impairments remain a major concern. The present study sought to extend the preclinical evaluation of ketamine-induced cognitive impairments by evaluating the dose (1.0-18.0 mg/kg) and time-course (10 min-24 hr) of effects of ketamine on sustained attention using a visual signal detection procedure in rats. Overall, ketamine (10.0-18.0 mg/kg) dose dependently decreased percent hit and correct rejection accuracy. Additionally, these same doses of ketamine increased response latency and trial omissions. In the time-course study, treatment with 18.0 mg/kg ketamine produced the greatest decrease in visual signal detection performance at 10 min, when ketamine decreased percent hit and correct rejection accuracy as well as increased response latency and trial omissions, but returned to saline baseline controls by 100 min. In conclusion, acute ketamine inhibited sustained attention in rats performing a visual signal detection task; however, these effects were short in duration, similar to the short duration (< 2 hours) of psychotomimetic effects reported in low-dose ketamine treatment in depressed patients.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Effects of the noncompetitive N-methyl-D-aspartate receptor antagonist ketamine on visual signal detection performance in rats

Hillhouse

Merritt²,

Porter³

2015

Behavioural Pharmacology

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“…Further support for the broad applicability of the model beyond AD comes from a number of studies demonstrating the ability of other cholinergic and non-cholinergic compounds, including caffeine, nicotine, methylphenidate, thyrotropin-releasing hormone, and cycloserine, to reverse scopolamine-induced deficits in animals and humans in similar types of tests as reported here (Bontempi et al 2003;Jones et al 1991;Molchan et al 1990;Rezvani et al 2008;Riedel et al 1995). Furthermore, the construct validity of the scopolamine model is supported by a similarity in the preclinical and clinical scopolamine and donepezil exposures needed to induce and attenuate scopolamine-induced cognitive impairment.…”

Section: Discussionmentioning

confidence: 65%

“…Reversal of scopolamine-induced impairments has been demonstrated in humans and animals with donepezil, an acetylcholinesterase inhibitor that improves cognition in Alzheimer's disease (AD) (Buccafusco et al 2008;Snyder et al 2005), and historically, the scopolamine model has been viewed as a model of AD. Additionally, several other compounds with non-cholinergic mechanisms of action, including methylphenidate, thyrotropin-releasing hormone, D-cycloserine, and caffeine, also effectively reverse scopolamine-induced cognitive deficits in animals and humans, supporting the notion that this model has utility in the assessment of cholinergic as well as non-cholinergic compounds (Jones et al 1991;Molchan et al 1990;Rezvani et al 2008;Riedel et al 1995).…”

Section: Introductionmentioning

confidence: 74%

“…The translational validity of the scopolamine model from animals to humans is supported by the number of compounds shown to be effective in both animal and healthy human scopolamine studies (Bontempi et al 2003;Jones et al 1991;Molchan et al 1990;Rezvani et al 2008;Riedel et al 1995); however, translation from animals or healthy humans to specific disease states is not well studied, primarily due to the limited number of procognitive compounds and mechanisms with proven efficacy in disease states. This additional piece of translational validation will only be obtained as other drugs and mechanisms that prove successful in treating cognitive impairments can be tested in the scopolamine model.…”

Section: Discussionmentioning

confidence: 99%

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The scopolamine model as a pharmacodynamic marker in early drug development

et al. 2011

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Effects of Acute and Sustained Pain Manipulations on Performance in a Visual‐Signal Detection Task of Attention in Rats

Freitas

Hillhouse

Leitl

et al. 2015

Drug Development Research

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Strategy, Management and Health PolicyEnabling Technology, Genomics, ProteomicsPreclinical ResearchPreclinical Development Toxicology, Formulation Drug Delivery, PharmacokineticsClinical Development Phases I–III Regulatory, Quality, ManufacturingPostmarketing Phase IV Patients with pain often display cognitive impairment including deficits in attention. The visual-signal detection task (VSDT) is a behavioral procedure for assessment of attention in rodents. Male Sprague Dawley rats were trained in a VSDT and tested with three different noxious stimuli: (i) intraperitoneal injection of lactic acid; (ii) intraplantar injection of formalin; and (iii) intraplantar injection of complete Freund’s adjuvant (CFA). The muscarinic acetylcholine receptor antagonist, scopolamine was also tested as a positive control. Scopolamine (0.01–1.0 mg/kg) dose dependently reduced accuracy and increased response latencies during completed trials with higher scopolamine doses increasing omissions. Lactic acid (0.56–5.6% ip) also increased response latencies and omissions, although it failed to alter measures of response accuracy. Formalin produced a transient decrease in accuracy while also increasing both response latency and omissions. CFA failed to alter VSDT performance. Although VSDT effects were transient for formalin and absent for CFA, both treatments produced mechanical allodynia and paw edema for up to 7 days. These results support the potential for noxious stimuli to produce a pain-related disruption of attention in rats. However, relatively strong noxious stimulation appears necessary to disrupt performance in this version of the VSDT.

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Attenuation of pharmacologically-induced attentional impairment by methylphenidate in rats

Cited by 20 publications

References 31 publications

Effects of the noncompetitive N-methyl-D-aspartate receptor antagonist ketamine on visual signal detection performance in rats

Effects of the noncompetitive N-methyl-D-aspartate receptor antagonist ketamine on visual signal detection performance in rats

The scopolamine model as a pharmacodynamic marker in early drug development

Effects of Acute and Sustained Pain Manipulations on Performance in a Visual‐Signal Detection Task of Attention in Rats

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