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      Highly impulsive rats: modelling an endophenotype to determine the neurobiological, genetic and environmental mechanisms of addiction

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          Abstract

          Impulsivity describes the tendency of an individual to act prematurely without foresight and is associated with a number of neuropsychiatric co-morbidities, including drug addiction. As such, there is increasing interest in the neurobiological mechanisms of impulsivity, as well as the genetic and environmental influences that govern the expression of this behaviour. Tests used on rodent models of impulsivity share strong parallels with tasks used to assess this trait in humans, and studies in both suggest a crucial role of monoaminergic corticostriatal systems in the expression of this behavioural trait. Furthermore, rodent models have enabled investigation of the causal relationship between drug abuse and impulsivity. Here, we review the use of rodent models of impulsivity for investigating the mechanisms involved in this trait, and how these mechanisms could contribute to the pathogenesis of addiction.

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          Varieties of impulsivity.

          J Evenden (1999)
          The concept of impulsivity covers a wide range of "actions that are poorly conceived, prematurely expressed, unduly risky, or inappropriate to the situation and that often result in undesirable outcomes". As such it plays an important role in normal behaviour, as well as, in a pathological form, in many kinds of mental illness such as mania, personality disorders, substance abuse disorders and attention deficit/hyperactivity disorder. Although evidence from psychological studies of human personality suggests that impulsivity may be made up of several independent factors, this has not made a major impact on biological studies of impulsivity. This may be because there is little unanimity as to which these factors are. The present review summarises evidence for varieties of impulsivity from several different areas of research: human psychology, psychiatry and animal behaviour. Recently, a series of psychopharmacological studies has been carried out by the present author and colleagues using methods proposed to measure selectively different aspects of impulsivity. The results of these studies suggest that several neurochemical mechanisms can influence impulsivity, and that impulsive behaviour has no unique neurobiological basis. Consideration of impulsivity as the result of several different, independent factors which interact to modulate behaviour may provide better insight into the pathology than current hypotheses based on serotonergic underactivity.
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            Impulsivity as a vulnerability marker for substance-use disorders: review of findings from high-risk research, problem gamblers and genetic association studies.

            Antonio Verdejo-Garcia, Andrew Lawrence, Luke Clark (2008)
            There is a longstanding association between substance-use disorders (SUDs) and the psychological construct of impulsivity. In the first section of this review, personality and neurocognitive data pertaining to impulsivity will be summarised in regular users of four classes of substance: stimulants, opiates, alcohol and 3,4-methylenedioxymethamphetamine (MDMA). Impulsivity in these groups may arise via two alternative mechanisms, which are not mutually exclusive. By one account, impulsivity may occur as a consequence of chronic exposure to substances causing harmful effects on the brain. By the alternative account, impulsivity pre-dates SUDs and is associated with the vulnerability to addiction. We will review the evidence that impulsivity is associated with addiction vulnerability by considering three lines of evidence: (i) studies of groups at high-risk for development of SUDs; (ii) studies of pathological gamblers, where the harmful consequences of the addiction on brain structure are minimised, and (iii) genetic association studies linking impulsivity to genetic risk factors for addiction. Within each of these three lines of enquiry, there is accumulating evidence that impulsivity is a pre-existing vulnerability marker for SUDs.
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              The 5-choice serial reaction time task: behavioural pharmacology and functional neurochemistry.

              T. W. Robbins (2002)
              The developmental history and application of the 5-choice serial reaction time task (5CSRTT) for measuring effects of drugs and other manipulations on attentional performance (and stimulus control) in rats is reviewed. The 5CSRTT has been used for measuring effects of systemic drug treatments and also central manipulations such as neurochemical lesions on various aspects of attentional control, including sustained, selective and divided attention--and is relevant to the definition of neural systems of attention and applications to human disorders such as attention deficit/hyperactivity disorder (ADHD) and Alzheimer's disease. The 5CSRTT is implemented in a specially designed operant chamber with multiple response locations ('nine-hole box') using food reinforcers to maintain performance on baseline sessions (about 100 trials) at criterion levels of accuracy and trials completed. The 5CSRTT can be used for measuring various aspects of attentional control over performance with its main measures of accuracy, premature responding, correct response latencies and latency to collect earned food pellets. The data reviewed include studies mainly of systemic and intra-cerebral effects of adrenoceptor, dopamine receptor, serotoninergic receptor and cholinergic receptor agents. These are compared with investigations of effects of selective chemical neurotoxins and excitotoxins applied to discrete parts of the forebrain, in order to define the neural and neurochemical substrates of attentional function. Furthermore, these results are integrated with findings from in vivo microdialysis in freely moving rats or metabolic studies. The monoaminergic and cholinergic systems appear to play separable roles in different aspects of performance controlled by the 5CSRTT, in neural systems centred on the prefrontal cortex, cingulate cortex and striatum. These conclusions are considered in the methodological and theoretical context of other psychopharmacological studies of attention in animals and humans.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Dis Model Mech
                Journal ID (iso-abbrev): Dis Model Mech
                Journal ID (hwp): dmm
                Journal ID (publisher-id): DMM
                Title: Disease Models & Mechanisms
                Publisher: The Company of Biologists Limited
                ISSN (Print): 1754-8403
                ISSN (Electronic): 1754-8411
                Publication date (Print): March 2013
                Publication date (Electronic): 25 January 2013
                Volume: 6
                Issue: 2
                Pages: 302-311
                Affiliations
                [1 ]Behavioural and Cognitive Neurosciences Institute and The Department of Psychology, University of Cambridge, Downing Street, Cambridge, CB2 3EB, UK
                [2 ]Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria 3010, Australia
                [3 ]Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK
                Author notes
                [* ]Author for correspondence ( jwd20@ 123456cam.ac.uk )
                Article
                Publisher ID: 0060302
                DOI: 10.1242/dmm.010934
                PMC ID: 3597013
                PubMed ID: 23355644
                SO-VID: 709e6ec5-a9c3-4c14-bb5e-803fdca8ce6a
                Copyright © © 2013. Published by The Company of Biologists Ltd
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License ( http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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                Subject: Review
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                cover-date March 2013

                ScienceOpen disciplines: Molecular medicine
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                ScienceOpen disciplines: Molecular medicine

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