Article

Neural correlates of response reversal: Considering acquisition

Department of Psychology, University College London, London WC1E 6BT, UK.
NeuroImage (Impact Factor: 6.36). 03/2007; 34(4):1754-65. DOI: 10.1016/j.neuroimage.2006.08.060
Source: PubMed

ABSTRACT Previous work on response reversal has typically used a single pair of stimuli that serially reverse. This conflation of acquisition and reversal processes has prevented an examination of the functional role of neural systems implicated in response reversal during acquisition despite the relevance of such data in evaluating accounts of response reversal. In the current study, participants encountered 16 independent reversing stimulus pairs in the context of a probabilistic response reversal paradigm. Functional regions of interest identified as involved in response reversal through a contrast used in the previous literature (punished errors made in the reversal phase versus rewarded correct responses), were interrogated across conditions. Consistent with suggestions that middle frontal cortex codes reward, this region showed significantly greater responses to rewarded rather than punished trials irrespective of accuracy or learning phase (acquisition or reversal). Consistent with the suggestion that this coding of the expectation of reinforcement is acquired via input from the amygdala, we observed significant positive connectivity between activity within the amygdala and a region of rostral anterior cingulate cortex highly proximal to this region of middle frontal/mesial prefrontal cortex. In contrast, inferior frontal cortex, anterior cingulate cortex and caudate showed greater responses to punished errors than to the rewarded correct responses. These three regions also showed significant activation to rewarded errors during acquisition, in contrast to positions suggesting that inferior frontal cortex represents punishment or suppresses previously rewarded responses. Moreover, a connectivity analysis with an anterior cingulate cortex seed revealed highly significant positive connectivity among them. The implications of these data for recent accounts of response reversal and of response reversal impairments in specific neuropsychiatric populations are discussed.

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    • "Impaired reversal learning performance by individuals with ventromedial prefrontal cortex damage highlights involvement of this region in this task (Fellows 2003). Individuals with psychopathy show greater response perseveration and during functional magnetic resonance imaging (fMRI) display aberrant activation of ventromedial prefrontal cortex during the reversal phase (Budhani 2007; Finger 2008). Increased ventromedial prefrontal cortex activity to punished error may underpin an inability to respond appropriately to aversive reinforcement in order to regulate behaviour (Rolls 1994). "
    Clinical topics in personality disorder, Edited by Jaydip Sarkar, Gwen Adshead, 07/2012: chapter Differences between psychopathy and other personality disorders: evidence from neuroimaging: pages 21−37; Royal College of Psychiatrists., ISBN: 9781908020390
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    • "Given that reversal learning can be divided in several cognitive processes, such as learning associations between neutral stimuli and their rewarding or punishing value, switching to new associations (inhibiting the selection of the previously rewarded stimulus in favor of the newly rewarded stimulus after contingencies have reversed), and forming learning-sets to improve performance, it is quite possible that several of these processes rely upon distinct sectors of the OFC (Butter, 1969; Iversen and Mishkin, 1970; see for review Roberts, 2006). Such a proposal is consistent with recent functional neuroimaging studies that have identified multiple regions of activation within OFC specifically linked to reversal learning abilities (Budhani et al., 2007; Cools et al., 2002; Kringelbach and Rolls, 2003; Mitchell et al., 2008; O'Doherty et al., 2003; Remijnse et al., 2005). "
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    ABSTRACT: Neither lesions of orbital frontal (OFC) areas 11/13 nor selective amygdala lesions alter the ability to learn stimulus-reinforcer association and reversal discriminations in adult monkeys. Here, we investigated whether the same conclusion will hold true when the same lesions occur in infancy. Infant rhesus monkeys received sham-operations, neurotoxic amygdala lesions, or aspiration OFC 11/13 lesions at 8-15 days of age and were trained on object discrimination reversal (ODR) tasks. Performance on a single pair (1-Pair) ODR was assessed at the age of 3 months and 3 years, and then animals were tested in a 5-Pair ODR task in which they had to concurrently learn and reverse five discrimination problems. The results indicated that the ability to solve a single-pair discrimination problem followed by six reversals appears to be late maturing in monkeys but is spared following selective lesions of either OFC areas 11/13 or amygdala, even with the use of the more challenging 5-object ODR task. Finally, performance in the 1 and 5-Pair ODR at 3 years was comparable to that following adult-onset lesions, indicating that neither OFC areas 11/13 nor amygdala are critical for the development of reversal learning.
    03/2012; 2(3):363-80. DOI:10.1016/j.dcn.2012.03.002
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    • "Impaired reversal learning performance by individuals with ventromedial prefrontal cortex damage highlights involvement of this region in this task (Fellows 2003). Individuals with psychopathy show greater response perseveration and during functional magnetic resonance imaging (fMRI) display aberrant activation of ventromedial prefrontal cortex during the reversal phase (Budhani 2007; Finger 2008). Increased ventromedial prefrontal cortex activity to punished error may underpin an inability to respond appropriately to aversive reinforcement in order to regulate behaviour (Rolls 1994). "
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    ABSTRACT: ICD-1O and DSM-IV-TR diagnostic guidelines do not list psychopathy as a distinct psychiatric entity. However, there are significant overlaps between psychopathy and DSM-IV-TR Cluster B personality disorders. Neuroimaging studies implicate deficits in structure and function of frontal and limbic regions in this group of personality disorders, while highlighting both distinctions and overlaps between syndromes. Here, these data are reviewed and implications for diagnosis and clinical practice are discussed.
    Advances in Psychiatric Treatment 04/2011; 17:119. DOI:10.1192/apt.bp.107.004747
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