The Experimental Reproduction of Amphetamine Psychosis

Bell, David S.

doi:10.1001/archpsyc.1973.04200010020003

Cited by 324 publications

(136 citation statements)

References 30 publications

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“…The initial increase in exploratory locomotion, and later repetitive-focused stereotyped movements observed in rats with progressively increasing drug dose, is in some respects analogous to the evolution of the human behavioral pattern of response to stimulants. Although this description highlights common features shared by rodent behavioral sensitization and the development of psychosis in man (Segal and Mandell, 1974;Segal et al, 1981;Bell, 1973;Segal and Schuckit, 1983;Sato et al, 1983;Lieberman et al, 1997), the rodent brain and behavioral repertoire is far more limited and less complex than its human counterpart, and there is no direct correspondence between rodent behavioral sensitization and human psychiatric disease. There is, however, strong evidence that behavioral sensitization is related in large part to plasticity of limbic neurochemical systems, which also play an important role in a range of psychiatric and substance use disorders.…”

Section: Behavioral Characteristics Of Sensitizationmentioning

confidence: 98%

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Richtand

2006

Neuropsychopharmacol

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Behavioral sensitization, the progressive and enduring augmentation of certain behaviors following repetitive drug use, alters rodent locomotion in a long-standing manner. The same dopamine pathways playing an important role in drug dependence and psychosis also play a critical role in sensitization. Individual dopamine receptor subtypes have markedly different functional responses to stimulation, with D3 dopamine receptor stimulation inhibiting rodent locomotion. The D3 receptor has highest affinity of the dopamine receptor subtypes for dopamine, and is occupied to a greater degree following stimulant drug administration. D3 receptor activity may be regulated through the expression of an alternatively spliced, truncated receptor isoform (termed 'D3nf') altering receptor localization and function via dimerization with the full-length subunit. The expected physiological response to repetitive drug administration is tolerance. Tolerance of D3 receptor inhibition of locomotion would contribute to sensitization to stimulant drugs. We hypothesize that repetitive D3 receptor stimulation contributes to the development of behavioral sensitization through decreased responsivity of D3-receptor-mediated locomotor inhibition. Increased D3nf expression may direct altered receptor localization and subsequent release of D3-receptormediated inhibition, contributing to the expression of sensitization. These hypotheses follow directly from the affinities of the receptor subtypes for dopamine; dopamine concentrations following stimulant administration; the effects of individual dopamine receptor subtype stimulation on locomotion; and the expected homeostatic response of the system to perturbation by drug. Clarifying these mechanisms underlying sensitization may suggest new interventions for neuropsychiatric conditions in which dopamine plays an important role, including psychosis, drug dependence, and Parkinson's disease. This information may also elucidate a previously unrecognized mechanism regulating receptor trafficking and desensitization.

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Section: Behavioral Characteristics Of Sensitizationmentioning

confidence: 98%

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Richtand

2006

Neuropsychopharmacol

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“…Amphetamines and some of its derivatives have been shown to induce psychotic symptoms in experiments in humans (Bell, 1973) and animals (Robinson & Becker, 1986), and they have been known to exacerbate psychotic states in psychiatric patients (Angrist, Rotrosen & Gershon, 1980;Janowsky & Davis, 1976). However, the scientific debate about amphetamine-induced psychosis is ongoing, and it remains unclear whether the use of amphetamine-like substances can actually cause a psychotic disorder in an otherwise healthy individual, or whether it triggers the onset of schizophrenia in an individual with high vulnerability to the disease (Phillips & Johnson, 2001;Poole & Brabbins, 1996).…”

Section: Khat and Psychosis: Theoretical Backgroundmentioning

confidence: 99%

Chronic khat use and psychotic disorders: A review of the literature and future prospects

Odenwald¹

2007

SUCHT

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Aims: In recent decades, the traditional habit of chewing the khat leaves, which contain the amphetamine-like cathinone, has undergone profound changes in African and Arab countries, from a socially regulated use pattern to uncontrolled consumption. This is of special public mental-health concern. In this article, a review of the scientific literature on the relationship between khat use and psychosis is provided. Results: Several case studies, but only a few group and community-based studies, have addressed this topic. The studies show inconsistent results, have methodological problems, and fail to report quantitative results. Many important questions remain unaddressed. Conclusions: The frequently stated association between khat use and psychosis contrasts with the small number of sound studies. Currently, only a few conclusions can be drawn, that excessive khat use can cause brief psychotic disorders and that people with a preexisting vulnerability should be discouraged to use it. The direction of causality between general psychopathology and khat use remains unclear. This review confirms the need for quantitative, controlled, and longitudinal studies,

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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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The Experimental Reproduction of Amphetamine Psychosis

Cited by 324 publications

References 30 publications

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Chronic khat use and psychotic disorders: A review of the literature and future prospects

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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