Neural correlates of refixation saccades and antisaccades in normal and schizophrenia subjects

McDowell, Jennifer E.; Brown, Gregory G.; Paulus, Martin P.; Martı́nez, Antı́gona; Stewart, Sara E.; Dubowitz, David J.; Braff, David L.

doi:10.1016/s0006-3223(01)01204-5

Cited by 151 publications

(136 citation statements)

References 49 publications

Supporting

Mentioning

115

Contrasting

Unclassified

Order By: Relevance

“…It has been argued that both of these processes depend on working memory resources mediated by the dorsolateral prefrontal cortex (DLPFC) (Roberts et al 1994;Stuyven et al 2000;Hutton et al 2002). This is supported by imaging studies which have found that, in addition to activation of the oculomotor circuitry described above, the DLPFC is activated during antisaccades but not pro-saccades performance (Sweeney et al 1996;Dorricchi et al 1997;Muri et al 1998;McDowell et al 2002) and evidence showing increased antisaccade errors following DLPFC damage (Guitton et al 1985;Pierrot-Deseilligny et al 1991;Fukushima et al 1994). Thus one hypothesis is that a signal from DLPFC to FEF activates an inhibitory mechanism within FEF, which results in suppression of a reflex pro-saccade and generation of an antisaccade (Munoz and Everling, 2004).…”

Section: Discussionmentioning

confidence: 97%

Structural neural networks subserving oculomotor function in first-episode schizophrenia

Bagary

Hutton

Symms

et al. 2004

Biological Psychiatry

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 97%

Structural neural networks subserving oculomotor function in first-episode schizophrenia

Bagary

Hutton

Symms

et al. 2004

Biological Psychiatry

View full text Add to dashboard Cite

show abstract

“…We relied on the antisaccade task, used widely in the human literature for its simplicity, as performance of the task does not require mastery of complex rules requiring extensive instruction but rather the ability to resist a prepotent stimulus and plan a movement away from it (3,4,(35)(36)(37). Our longitudinal study was designed to track the same individuals at different stages to minimize interindividual variability, which is considerable around puberty (38).…”

Section: Discussionmentioning

confidence: 99%

“…Performance on the antisaccade task exhibits significant improvements in adolescence in humans (3,4) and is impaired in childhood conditions such as attention deficit/hyperactivity disorder (35) and mental illnesses such as schizophrenia, which typically manifest in early adulthood (36,37). Young monkeys are able to master tasks that require response inhibition, such as the stop signal task and the object retrieval detour, and performance has been shown to improve with age around the time of puberty (38).…”

Section: Discussionmentioning

confidence: 99%

Behavioral response inhibition and maturation of goal representation in prefrontal cortex after puberty

Zhou

Zhu

King

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Executive functions including behavioral response inhibition mature after puberty, in tandem with structural changes in the prefrontal cortex. Little is known about how activity of prefrontal neurons relates to this profound cognitive development. To examine this, we tracked neuronal responses of the prefrontal cortex in monkeys as they transitioned from puberty into adulthood and compared activity at different developmental stages. Performance of the antisaccade task greatly improved in this period. Among neural mechanisms that could facilitate it, reduction of stimulus-driven activity, increased saccadic activity, or enhanced representation of the opposing goal location, only the latter was evident in adulthood. Greatly accentuated in adults, this neural correlate of vector inversion may be a prerequisite to the formation of a motor plan to look away from the stimulus. Our results suggest that the prefrontal mechanisms that underlie mature performance on the antisaccade task are more strongly associated with forming an alternative plan of action than with suppressing the neural impact of the prepotent stimulus.prefrontal | antisaccade | monkey | neurophysiology | adolescence B ehavioral response inhibition, and cognitive task performance more generally, improves substantially between the time of puberty and adulthood (1-4). Risky decision-making peaks in adolescence, the time period between puberty and adulthood that is most closely linked to delinquent behavior in humans (5-7). Performance in tasks that assay response inhibition, such as the antisaccade task, improves into adulthood, reflecting the progressive development of behavioral control (3). This period of cognitive enhancement parallels the maturation of the prefrontal cortex (8-11). Anatomical changes in the prefrontal cortex continue during adolescence, involving gray and white matter volumes and myelination of axon fibers within the prefrontal cortex and between the prefrontal cortex and other areas (8-15). Changes in prefrontal activation, including increases (12,(16)(17)(18)(19)(20) and decreases (21, 22), have been documented in imaging studies for tasks that require inhibition of prepotent behavioral responses and filtering of distractors.Much less is known about how the physiological properties of prefrontal neurons develop after puberty. Similar to the human pattern of development, the monkey prefrontal cortex undergoes anatomical maturation in adolescence and early adulthood (23,24). Male monkeys enter puberty at ∼3.5 y of age and reach full sexual maturity at 5 y, approximately equivalent to the human ages of 11 y and 16 y, respectively (25,26). By some accounts, biochemical and anatomical changes characteristic of adolescence in humans occur at an earlier, prepubertal age in the monkey prefrontal cortex (27, 28), so it is not known if cognitive maturation or neurophysiological changes occur in monkeys after puberty. The contribution of prefrontal cortex to antisaccade performance has also been a matter of debate, with contrasting views fav...

show abstract

“…Patients with prefrontal lesions that involve Brodmann's area 46 (Guitton et al, 1985;Pierrot-Deseilligny et al, 1991Walker et al, 1998;Ploner et al, 2005) and disorders that impair prefrontal functions, like schizophrenia, have longer reaction times for antisaccades and often fail to suppress a saccade toward the flashed stimulus (Fukushima et al, 1988(Fukushima et al, , 1990. Moreover, functional imaging studies in humans (Sweeney et al, 1996;DeSouza et al, 2003;Ford et al, 2005;Dyckman et al, 2007;Brown et al, 2008) have found higher activations in the dlPFC, in particular in Brodmann's area 46, for the performance of antisaccades compared with saccades toward visual stimuli (prosaccades), a pattern that is absent in patients with schizophrenia (McDowell et al, 2002). A unilateral pharmacological deactivation study of sites in the ventral bank of the principal sulcus in monkeys has reported impairments in the antisaccade task (Condy et al, 2007), and single-unit recording studies in monkeys have found taskselective activity task in dlPFC neurons in this task (Funahashi et al, 1993;Everling and Desouza, 2005).…”

Section: Introductionmentioning

confidence: 99%

Prefrontal Cortex Deactivation in Macaques Alters Activity in the Superior Colliculus and Impairs Voluntary Control of Saccades

Koval

Lomber²,

Everling³

2011

Journal of Neuroscience

View full text Add to dashboard Cite

The cognitive control of action requires both the suppression of automatic responses to sudden stimuli and the generation of behavior specified by abstract instructions. Though patient, functional imaging and neurophysiological studies have implicated the dorsolateral prefrontal cortex (dlPFC) in these abilities, the mechanism by which the dlPFC exerts this control remains unknown. Here we examined the functional interaction of the dlPFC with the saccade circuitry by deactivating area 46 of the dlPFC and measuring its effects on the activity of single superior colliculus neurons in monkeys performing a cognitive saccade task. Deactivation of the dlPFC reduced preparatory activity and increased stimulus-related activity in these neurons. These changes in neural activity were accompanied by marked decreases in task performance as evidenced by longer reaction times and more task errors. The results suggest that the dlPFC participates in the cognitive control of gaze by suppressing stimulus-evoked automatic saccade programs.

show abstract

Neural correlates of refixation saccades and antisaccades in normal and schizophrenia subjects

Cited by 151 publications

References 49 publications

Structural neural networks subserving oculomotor function in first-episode schizophrenia

Structural neural networks subserving oculomotor function in first-episode schizophrenia

Behavioral response inhibition and maturation of goal representation in prefrontal cortex after puberty

Prefrontal Cortex Deactivation in Macaques Alters Activity in the Superior Colliculus and Impairs Voluntary Control of Saccades

Contact Info

Product

Resources

About