Acute Psychosis Caused by Dextro-amphetamine

Wallis, Geoffrey; McHarg, James F.; Scott, O. C. A.

doi:10.1136/bmj.2.4641.1394

Cited by 27 publications

(10 citation statements)

References 3 publications

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“…The psychotogenic effects of repeated exposure to psychostimulants, primarily but not exclusively the AMPHs, have been extensively documented (Wallis et al 1949; O’Flanagan and Taylor 1950; Weiner 1964; Bell 1965; Snyder et al 1972, Snyder 1973; Bell 1973; Janowsky and Risch 1979; Kokkinidis and Anisman 1981; LeDuc and Mittleman 1995; Bartlett et al 1997). Generally, the effects of repeated exposure to AMPH reproduce the main features of paranoid schizophrenia (hallucinations in all modalities, paranoid delusions, thought disorder, obsessive and compulsive cognitive activity and behaviors).…”

Section: Repeated Amphetamine Exposure As An Animal Modelmentioning

confidence: 99%

A neurocognitive animal model dissociating between acute illness and remission periods of schizophrenia

2008

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Rationale-The development and validation of animal models of the cognitive impairments of schizophrenia have remained challenging subjects.Objective-We review evidence from a series of experiments concerning an animal model that dissociates between the disruption of attentional capacities during acute illness periods and the cognitive load-dependent impairments that characterize periods of remission. The model focuses on the long-term attentional consequences of an escalating-dosing pretreatment regimen with amphetamine (AMPH).Results-Acute illness periods are modeled by the administration of AMPH challenges. Such challenges result in extensive impairments in attentional performance and the "freezing" of performance-associated cortical acetylcholine (ACh) release at pretask levels. During periods of remission (in the absence of AMPH challenges), AMPH-pretreated animals' attentional performance is associated with abnormally high levels of performance-associated cortical ACh release, indicative of the elevated attentional effort required to maintain performance. Furthermore, and corresponding with clinical evidence, attentional performance during remission periods is exquisitely vulnerable to distractors, reflecting impaired top-down control and abnormalities in fronto-mesolimbic-basal forebrain circuitry. Finally, this animal model detects the moderately beneficial cognitive effects of low-dose treatment with haloperidol and clozapine that were observed in clinical studies.Conclusions-The usefulness and limitations of this model for research on the neuronal mechanisms underlying the cognitive impairments in schizophrenia and for drug-finding efforts are discussed.

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Section: Repeated Amphetamine Exposure As An Animal Modelmentioning

confidence: 99%

A neurocognitive animal model dissociating between acute illness and remission periods of schizophrenia

2008

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“…Adderall ® ) are effective in the treatment of subjects with ADHD (Faraone et al, 2002; Janols et al, 2009; Minzenberg, 2012; Treuer et al, 2013). Psychostimulant treatment in ADHD is often labeled as “paradoxical”, since, as indicated by their categorical definition, ADHD medications, particularly d -amphetamine, can produce motor activation (Glick and Milloy, 1973; Ralph et al, 2001) and disruption of cognitive performance (Ornstein et al, 2000; Sanday et al, 2013; Stefani and Moghaddam, 2002), even psychosis (Bramness et al, 2012; Grant et al, 2012; Segal and Kuczenski, 1997; Wallis et al, 1949). Some researchers discount differences in response between ADHD and normal adolescents to psychostimulants, reporting that pre-pubertal adolescents respond to psychostimulants oppositely to that seen in adults (Rapoport et al, 1978; Zahn et al, 1980), and thus the “paradoxical” effect of psychostimulants in ADHD may be more a bias based on expectations from adult actions of the drugs.…”

Section: Introductionmentioning

confidence: 99%

Genetic targeting of the amphetamine and methylphenidate-sensitive dopamine transporter: On the path to an animal model of attention-deficit hyperactivity disorder

Mergy

Gowrishankar

Davis

et al. 2014

Neurochemistry International

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Alterations in dopamine (DA) signaling underlie the most widely held theories of molecular and circuit level perturbations that lead to risk for attention-deficit hyperactivity disorder (ADHD). The DA transporter (DAT), a presynaptic reuptake protein whose activity provides critical support for DA signaling by limiting DA action at pre- and postsynaptic receptors, has been consistently associated with ADHD through pharmacological, behavioral, brain imaging and genetic studies. Currently, the animal models of ADHD exhibit significant limitations, stemming in large part from their lack of construct validity. To remedy this situation, we have pursued the creation of a mouse model derived from a functional nonsynonymous variant in the DAT gene (SLC6A3) of ADHD probands. We trace our path from the identification of these variants to in vitro biochemical and physiological studies to the production of the DAT Val559 mouse model. We discuss our initial findings with these animals and their promise in the context of existing rodent models of ADHD.

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“…Repeated exposure to psychostimulants has long been known to produce psychotogenic effects in humans (Bell, 1965(Bell, , 1973Kokkinidis and Anisman, 1981;LeDuc and Mittleman, 1995;McDonald, 1964;O'Flanagan and Taylor, 1950;Snyder, 1973;Snyder et al, 1972;Wallis et al, 1949;Weiner, 1964). Furthermore, the effects of repeated psychostimulant exposure in healthy humans and animals model important neurobiological, behavioral, and cognitive aspects of schizophrenia Goldman-Rakic, 1999, 2003;Kapur, 2003;Laruelle, 2000;Lieberman et al, 1997;Robinson and Becker, 1986;Segal et al, 1981;Segal and Janowski, 1978;Strakowski et al, 1997;Yui et al, 1999), including the deficits in sensorimotor gating and attentional processing (Crider et al, 1982;Martinez et al, 2005;Sarter et al, 2005b;Tenn et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Kozak

Martı́nez

Young

et al. 2007

Neuropsychopharmacol

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Impairments in attentional functions and capacities represent core aspects of the cognitive symptoms of schizophrenia. Attentional performance has been demonstrated to depend on the integrity and activity of cortical cholinergic inputs. The neurobiological, behavioral, and cognitive effects of repeated exposure to psychostimulants model important aspects of schizophrenia. In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH. In non-performing rats, pretreatment with AMPH did not affect the increases in ACh release produced by AMPH-challenges. In contrast, attentional task performanceassociated increases in ACh release were attenuated in AMPH-pretreated and AMPH-challenged rats. This effect of repeated AMPH exposure on ACh release was already present before task-onset, suggesting that the loss of cognitive control that characterized these animals' performance was a result of cholinergic dysregulation. The findings indicate that the demonstration of repeated AMPH-induced dysregulation of the prefrontal cholinergic input system depends on interactions between the effects of repeated AMPH exposure and cognitive performance-associated recruitment of this neuronal system. Repeated AMPH-induced disruption of prefrontal cholinergic activity and attentional performance represents a useful model to investigate the cholinergic mechanisms contributing to the cognitive impairments of schizophrenia.

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Acute Psychosis Caused by Dextro-amphetamine

Cited by 27 publications

References 3 publications

A neurocognitive animal model dissociating between acute illness and remission periods of schizophrenia

A neurocognitive animal model dissociating between acute illness and remission periods of schizophrenia

Genetic targeting of the amphetamine and methylphenidate-sensitive dopamine transporter: On the path to an animal model of attention-deficit hyperactivity disorder

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

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