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Features of compulsive checking behavior mediated by nucleus accumbens and orbital frontal cortex

Authors

  • Anna Dvorkin,

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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  • Charmaine Silva,

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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  • Thomas McMurran,

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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  • Liane Bisnaire,

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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  • Jane Foster,

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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  • Henry Szechtman

    1. Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West, Health Science Centre, Room 4N82, Hamilton, ON L8N 3Z5, Canada
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Dr Henry Szechtman, as above.
E-mail: szechtma@mcmaster.ca

Abstract

The quinpirole sensitization model of obsessive-compulsive disorder was used to investigate the functional role that brain regions implicated in a neuroanatomical circuit of obsessive-compulsive disorder may play in compulsive checking behavior. Following repeated injections of saline or quinpirole (0.5 mg/kg, twice per week, ×8 injections) to induce compulsive checking, rats received N-methyl-d-aspartate lesions of the nucleus accumbens core (NAc), orbital frontal cortex (OFC) and basolateral amygdala, or sham lesions. When retested at 17 days post-surgery, the results showed effects of NAc and OFC but not basolateral amygdala lesion. NAc lesions affected measures indicative of the amount of checking behavior, whereas OFC lesions affected indices of staying away from checking. The pattern of results suggested that the functional roles of the NAc and OFC in checking behavior are to control the vigor of motor performance and focus on goal-directed activity, respectively. Furthermore, similarities in behavior between quinpirole sham rats and saline NAc lesion rats suggested that quinpirole may drive the vigor of checking by inhibition of NAc neurons, and that the NAc may be a site for the negative feedback control of checking.

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