387 research outputs found

    Modelling Visual Neglect: Computational Insights into Conscious Perception

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    Background: Visual neglect is an attentional deficit typically resulting from parietal cortex lesion and sometimes frontal lesion. Patients fail to attend to objects and events in the visual hemifield contralateral to their lesion during visual search. Methodology/Principal Finding: The aim of this work was to examine the effects of parietal and frontal lesion in an existing computational model of visual attention and search and simulate visual search behaviour under lesion conditions. We find that unilateral parietal lesion in this model leads to symptoms of visual neglect in simulated search scan paths, including an inhibition of return (IOR) deficit, while frontal lesion leads to milder neglect and to more severe deficits in IOR and perseveration in the scan path. During simulations of search under unilateral parietal lesion, the model’s extrastriate ventral stream area exhibits lower activity for stimuli in the neglected hemifield compared to that for stimuli in the normally perceived hemifield. This could represent a computational correlate of differences observed in neuroimaging for unconscious versus conscious perception following parietal lesion. Conclusions/Significance: Our results lead to the prediction, supported by effective connectivity evidence, that connections between the dorsal and ventral visual streams may be an important factor in the explanation of perceptua

    A Neurocomputational Model of the Functional Role of Dopamine in Stimulus-Response Task Learning and Performance

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    Thesis (Ph.D.) - Indiana University, Psychology, 2009The neuromodulatory neurotransmitter dopamine (DA) plays a complex, but central role in the learning and performance of stimulus-response (S-R) behaviors. Studies have implicated DA's role in reward-driven learning and also its role in setting the overall level of vigor or frequency of response. Here, a neurocomputational model is developed which models DA's influence on a set of brain regions believed to be involved in the learning and execution of S-R tasks, including frontal cortex, basal ganglia, and cingulate cortex. An `actor' component of the model is trained, using `babble' (random behavior selection) and `critic' (rewarding and punishing) components of the model, to perform acceptance/rejection responses upon presentation of color stimuli in the context of recently presented auditory tones. The model behaves like an autonomous organism learning (and relearning) through `trial-and-error'. The focus of the study, the impact of hypo- and hyper-normal DA activity on this model, is investigated by three different dopaminergic pathways--two striatal and one prefrontal cortical--being manipulated independently during the learning and performance of the color response task. Hypo-DA conditions, analogous to Parkinsonism, cause slowing and reduction of frequency of learned responses, and, at extremes, degrade the learning (either initial or reversal) of the task. Hyper-DA conditions, analogous to psychostimulant effects, cause more rapid response times, but also can lead to perseveration of incorrect learning of response on the task. The presence of these effects often depends on which DA-ergic pathway is manipulated, however, which has implications for interpretation of the pharmacological experimental data. The proposed model embodies an integrative theory of dopamine function which suggests that the base rate of DA cell activity encodes the overall `activity-oriented motivation' of the organism, with hunger and/or expectation of reward driving both response vigor and tendency to generate an explorative `babble' response. This more `tonic' feature of DA functionality coexists naturally with the more extensively-studied `phasic' reward-learning features. The model may provide better insights on the role of DA system dysfunction in the cognitive and motivational symptoms of disorders such as Parkinsonism, psychostimulant abuse, ADHD, OCD, and schizophrenia, accounting for deficits in both learning and performance of tasks

    The neuropsychopharmacology of reversal learning

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    Reversal learning deficits are a feature of many neuropsychiatric disorders, most notably schizophrenia. These deficits could be due, in part, to altered ability to dissipate either or both associations of previous positive (perseverance) and negative (learned non-reward) valence. Studies reported in this thesis developed an egocentric maze task and a visuospatial operant task for separate assessments of spatial reversal learning, perseverance and learned non-reward in mice. These tasks were subsequently used to assess the cognitive causes for altered performance after manipulations to brain systems recognised to be involved in reversal learning and relevant for human psychopathology, with a specific focus on schizophrenia. NMDA receptor (NMDAr) antagonism through acute phencyclidine did not affect reversal learning in the operant task, but caused general impairments in the maze task. Orbitofrontal (OFC) lesioned mice showed perseverative impairments in the operant task. Mice treated with the 5-HT2C receptor (5-HT2CR) antagonist SB242084 and 5-HT2CR KO mice showed facilitated reversal learning and decreased learned nonreward in the operant task. In the maze task, SB242084 decreased perseverance but increased learned non-reward, while 5-HT2CR KO mice showed perseverance and discrimination learning deficits. The final experimental chapter investigated the effect of SB242084 on touch-screen visual reversal learning in the rat. SB242084 retarded learning in this task. These studies demonstrate that previously non-reinforced associations can be of considerable importance in tasks of cognitive flexibility. The studies also show that the NMDAr, the 5-HT2CR, and the OFC, are involved in reversal learning and can modulate mechanisms related to both perseverance and learned non-reward. Moreover, in reversal learning, few effects of manipulations affecting PFC-functioning, or activity at the NMDAr and 5-HT2CR, generalise across the procedures in the visuospatial, egocentric spatial, and visual domains

    Effects of Subchronic Phencyclidine (PCP) Treatment on Social Behaviors, and Operant Discrimination and Reversal Learning in C57BL/6J Mice

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    Subchronic treatment with the psychotomimetic phencyclidine (PCP) has been proposed as a rodent model of the negative and cognitive/executive symptoms of schizophrenia. There has, however, been a paucity of studies on this model in mice, despite the growing use of the mouse as a subject in genetic and molecular studies of schizophrenia. In the present study, we evaluated the effects of subchronic PCP treatment (5 mg/kg twice daily × 7 days, followed by 7 days withdrawal) in C57BL/6J mice on (1) social behaviors using a sociability/social novelty-preference paradigm, and (2) pairwise visual discrimination and reversal learning using a touchscreen-based operant system. Results showed that mice subchronically treated with PCP made more visits to (but did not spend more time with) a social stimulus relative to an inanimate one, and made more visits and spent more time investigating a novel social stimulus over a familiar one. Subchronic PCP treatment did not significantly affect behavior in either the discrimination or reversal learning tasks. These data encourage further analysis of the potential utility of mouse subchronic PCP treatment for modeling the social withdrawal component of schizophrenia. They also indicate that the treatment regimen employed was insufficient to impair our measures of discrimination and reversal learning in the C57BL/6J strain. Further work will be needed to identify alternative methods (e.g., repeated cycles of subchronic PCP treatment, use of different mouse strains) that reliably produce discrimination and/or reversal impairment, as well as other cognitive/executive measures that are sensitive to chronic PCP treatment in mice

    Dopamine and the development of executive dysfunction in autism spectrum disorders.

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    Persons with autism regularly exhibit executive dysfunction (ED), including problems with deliberate goal-directed behavior, planning, and flexible responding in changing environments. Indeed, this array of deficits is sufficiently prominent to have prompted a theory that executive dysfunction is at the heart of these disorders. A more detailed examination of these behaviors reveals, however, that some aspects of executive function remain developmentaly appropriate. In particular, while people with autism often have difficulty with tasks requiring cognitive flexibility, their fundamental cognitive control capabilities, such as those involved in inhibiting an inappropriate but relatively automatic response, show no significant impairment on many tasks. In this article, an existing computational model of the prefrontal cortex and its role in executive control is shown to explain this dichotomous pattern of behavior by positing abnormalities in the dopamine-based modulation of frontal systems in individuals with autism. This model offers excellent qualitative and quantitative fits to performance on standard tests of cognitive control and cognitive flexibility in this clinical population. By simulating the development of the prefrontal cortex, the computational model also offers a potential explanation for an observed lack of executive dysfunction early in life

    Master of Science

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    thesisIn response to the growing need to understand individual differences in executive functioning (EF) among non-neurologic populations, this study examined two competing theoretical models of EF among healthy, neurologically-intact individuals: the prefrontal convexity model and the hemispheric asymmetry model. A total of 315 neurologically healthy individuals (M = 20.8 years; 50% female) completed two phases of the study. In the first phase (i.e., Model Identification), latent profile analysis was applied to variables measuring the abilities to form, switch, and maintain mental sets under conditions designed to tax the left or right hemisphere (i.e., a modified switching task). In the second phase (i.e., Model Validation), latent clusters from the first phase were compared on a separate EF task (i.e., Attention Network Test; ANT). The Model Identification phase yielded a three-profile solution consistent with the hemispheric asymmetry model. Profile 1 (N=203) was characterized by average EF performances. Profile 2 (N=43) revealed a set maintenance weakness under nonverbal conditions. Profile 3 (N=38) demonstrated a global weakness in cognitive flexibility and a specific weakness on tasks administered under verbal conditions. The Model Validation phase confirmed group/cluster differences (F(4,554) = 5.938, p<.001). Individual differences in EF follow a hemispheric asymmetry model of EF, with approximately 15% of neurologically healthy individuals exhibiting weaknesses in set maintenance and nonverbal processing, and 13% exhibiting weaknesses in set formation/switching and verbal processing
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