Neural correlates of antisaccade deficits in schizophrenia, an fMRI study

Tu, Pei Chi; Yang, Tsui-Fen; Kuo, Wen Jui; Hsieh, Jen-Chuen; Su, Tung‐Ping

doi:10.1016/j.jpsychires.2006.05.012

Cited by 54 publications

(40 citation statements)

References 32 publications

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“…In particular, we are aware that our recording sites in the rostral part of the paralaminar VL thalamus receive inputs from both the basal ganglia and the cerebellum, but the projection from the latter is dominant (DeVito and Anderson, 1982;Anderson and Turner, 1991;Middleton and Strick, 2000). To our knowledge, however, there is no previous study suggesting the roles of the cerebello-thalamocortical pathways in antisaccades, except for a few imaging studies showing enhanced activity in the cerebellum (Luna et al, 2001;Tu et al, 2006).…”

Section: Enhancement Of Neuronal Firing During Antisaccadesmentioning

confidence: 91%

“…The previous functional imaging studies have revealed the enhanced activity in many cortical and subcortical areas during antisaccades compared with prosaccades (for humans, Matsuda et al, 2004;Tu et al, 2006;for monkeys, Ford et al, 2009). However, direct analyses of individual neuronal firing in monkeys have shown that the magnitude of firing modulation in these structures was not necessarily enhanced during antisaccades, possibly because the blood-oxygen-level-dependent signal reflects both the synaptic potentials (Logothetis et al, 2001;Viswanathan and Freeman, 2007) and the non-neuronal vascular elements that can change in a few seconds (Sirotin and Das, 2009).…”

Section: Enhancement Of Neuronal Firing During Antisaccadesmentioning

confidence: 99%

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Roles of the Primate Motor Thalamus in the Generation of Antisaccades

Kunimatsu¹,

Tanaka²

2010

J. Neurosci.

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In response to changes in our environment, we select from possible actions depending on the given situation. The underlying neural mechanisms for this flexible behavioral control have been examined using the antisaccade paradigm. In this task, subjects suppress saccades to the sudden appearance of visual stimuli (prosaccade) and make a saccade in the opposite direction. Because recent imaging studies showed enhanced activity in the thalamus and basal ganglia during antisaccades, we hypothesized that the corticobasal ganglia loop may be involved. To test this, we recorded from neurons in the paralaminar part of the ventroanterior (VA), ventrolateral (VL) and mediodorsal (MD) nuclei of the thalamus when 3 monkeys performed pro/antisaccade tasks. For many VL and some VA neurons, the firing rate was greater during anti-than prosaccades. In contrast, neurons in the MD thalamus showed much variety of responses. For the population as a whole, neuronal activity in the VA/VL thalamus was strongly enhanced during antisaccades compared with prosaccades, while activity in the MD nucleus was not. Inactivation of the VA/VL thalamus resulted in an increase in the number of error trials in the antisaccade tasks, indicating that signals in the motor thalamus play roles in the generation of antisaccades. Enhancement of firing modulation during antisaccades found in the thalamus and those reported previously in the supplementary eye field and the basal ganglia suggest a strong functional linkage between these structures. The neuronal processes through the thalamocortical pathways might be essential for the volitional control of saccades.

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Section: Enhancement Of Neuronal Firing During Antisaccadesmentioning

confidence: 91%

Section: Enhancement Of Neuronal Firing During Antisaccadesmentioning

confidence: 99%

Roles of the Primate Motor Thalamus in the Generation of Antisaccades

Kunimatsu¹,

Tanaka²

2010

J. Neurosci.

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“…Cerebellar Crus I and II constitute a large portion of the primate cerebellar hemispheres, and send outputs to the ventral part of the dentate nucleus, which in turn transmits signals to the frontal and parietal cortices via the thalamus (for review, see Ramnani, 2006;Strick et al, 2009;Prevosto et al, 2010;Lu et al, 2012). This portion of the cerebellum appears to be involved in higher-order cognitive functions, such as executive function and motor planning, rather than the on-line adjustment of movement parameters (Leiner et al, 1986;Ito, 2002;Bellebaum et al, 2012;Stoodley et al, 2012). In this study, we found many saccade-related neurons in the ventral posterior portion of the dentate nucleus that might transmit signals from the lateral cerebellum to the medial and lateral prefrontal cortex.…”

Section: Roles Of the Lateral Cerebellum In Anti-saccadesmentioning

confidence: 99%

Implications of Lateral Cerebellum in Proactive Control of Saccades

Kunimatsu

Suzuki

Tanaka

2016

Journal of Neuroscience

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Although several lines of evidence establish the involvement of the medial and vestibular parts of the cerebellum in the adaptive control of eye movements, the role of the lateral hemisphere of the cerebellum in eye movements remains unclear. Ascending projections from the lateral cerebellum to the frontal and parietal association cortices via the thalamus are consistent with a role of these pathways in higher-order oculomotor control. In support of this, previous functional imaging studies and recent analyses in subjects with cerebellar lesions have indicated a role for the lateral cerebellum in volitional eye movements such as anti-saccades. To elucidate the underlying mechanisms, we recorded from single neurons in the dentate nucleus of the cerebellum in monkeys performing anti-saccade/pro-saccade tasks. We found that neurons in the posterior part of the dentate nucleus showed higher firing rates during the preparation of antisaccades compared with pro-saccades. When the animals made erroneous saccades to the visual stimuli in the anti-saccade trials, the firing rate during the preparatory period decreased. Furthermore, local inactivation of the recording sites with muscimol moderately increased the proportion of error trials, while successful anti-saccades were more variable and often had shorter latency during inactivation. Thus, our results show that neuronal activity in the cerebellar dentate nucleus causally regulates anti-saccade performance. Neuronal signals from the lateral cerebellum to the frontal cortex might modulate the proactive control signals in the corticobasal ganglia circuitry that inhibit early reactive responses and possibly optimize the speed and accuracy of anti-saccades.

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“…In addition, such deficits in goal maintenance are found in the first-degree relatives of individuals with schizophrenia [56,57], as well as in individuals with schizotypal personality disorder [58,59]. Individuals with schizophrenia also show strong evidence of impairment on other tasks that may tap into goal maintenance, such as the Stroop task [e.g., 60] and the antisaccade task [e.g., 61], as do their first degree relatives [58] Individuals with schizophrenia also show consistent evidence of impaired prefrontal activity, particularly in dorsolateral regions, during tasks that require goal maintenance [e.g., 55,62,63]. Again, the first-degree relatives of individuals with schizophrenia also show evidence of impaired prefrontal activation during goal maintenance [57,64].…”

Section: Strong Evidence Of Impairment In Schizophreniamentioning

confidence: 99%

The Cognitive Neuroscience of Working Memory: Relevance to CNTRICS and Schizophrenia

Deanna

Smith

2008

Biological Psychiatry

156

129

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Working memory is one of the central constructs in cognitive science and has received enormous attention in the theoretical and empirical literature. Similarly, working memory deficits have long been thought to be one of the core cognitive deficits in schizophrenia, making it a ripe area for translation. The current article provides a brief overview of the current theories and data on the psychological and neural mechanisms involved in working memory, which is a summary of the presentation and discussion on working memory that occurred at the first CNTRICS meeting in Washington, D.C. At this meeting, the consensus was that the constructs of goal maintenance and interference control were the most ready to be pursued as part of a translational cognitive neuroscience effort in the remaining CNTRICS meetings. The group felt that the constructs of longterm memory reactivation, capacity, and strategic encoding were of great clinical interest, but required more basic research. In addition, the group felt that the constructs of maintenance over time and updating in working memory had growing construct validity at the psychological and neural levels, but required more research in schizophrenia before knowing whether they should be targets for a clinical trials setting.Working memory is perhaps one of the most frequently studied domains in both cognitive science and cognitive neuroscience, with a wealth of accumulated theoretical and empirical work at both the psychological and neural level [1]. Further, a large body of work has demonstrated that individuals with schizophrenia have deficits on a varied set of working memory tasks [e.g., 2,3] that are associated with impairments in a range of neural mechanisms [4]. There is some data to suggest that the degree of impairment in certain aspects of working memory predicts later onset of schizophrenia [5,6]. In addition, the level of working memory impairment predicts the degree of social and occupational impairment in individuals with schizophrenia [e.g., 7,8]. Further, individuals who share unexpressed genetic components of vulnerability to schizophrenia also experience impairments in working memory function [e.g., 9,10].

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Neural correlates of antisaccade deficits in schizophrenia, an fMRI study

Cited by 54 publications

References 32 publications

Roles of the Primate Motor Thalamus in the Generation of Antisaccades

Roles of the Primate Motor Thalamus in the Generation of Antisaccades

Implications of Lateral Cerebellum in Proactive Control of Saccades

The Cognitive Neuroscience of Working Memory: Relevance to CNTRICS and Schizophrenia

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