Effects of Nicotine on Leading Saccades during Smooth Pursuit Eye Movements in Smokers and Nonsmokers with Schizophrenia

Avila, Matthew T.; Sherr, Jay D.; Hong, Elliot; Myers, Carolyn M.; Thaker, Gunvant K.

doi:10.1038/sj.npp.1300265

Cited by 77 publications

(51 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example several authors have linked increased antisaccade errors to dysfunctional working memory processes (Roberts et al, 1994, Hutton et al 20022004). Similarly intrusive anticipatory saccades that can occur during smooth pursuit eye movements have been argued to reflect a failure of inhibitory control mechanisms [Avila et al 2003]. Studies in patients with schizophrenia, who demonstrate both increased antisaccade errors and impaired smooth pursuit have found that nicotine can significantly ameliorate both of these deficits [Olincy et al, 2003;Larrison Briand and Sereno, 2004).…”

Section: Discussionmentioning

confidence: 99%

Acute effects of nicotine on visual search tasks in young adult smokers

2005

View full text Add to dashboard Cite

Rationale Nicotine is known to improve performance on tests involving sustained attention and recent research suggests that nicotine may also improve performance on tests involving the strategic allocation of attention and working memory. Objectives We used traditional measures and eye tracking techniques to examine the effects of nicotine on visual search tasks. Methods In experiment 1 smokers and non-smokers performed pop-out and serial search tasks. Experiment 2 used a within subject design and a more demanding search task for multiple targets. In both studies, 2-hour abstinent smokers were asked to smoke one of their own cigarettes between baseline and post-tests. Results In experiment 1, Pop-out search times were faster after nicotine, without a loss in accuracy. Similar effects were observed for serial searches, but these were significant only at a trend level. In experiment 2, nicotine facilitated a strategic change in eyemovements resulting in a higher proportion of fixations on target letters. If the cigarette was smoked on the first trial (when the task was novel), nicotine additionally reduced the total number of fixations and refixations on all letters in the display. Conclusions Nicotine improves visual search performance by speeding up search time and enabling a better focus of attention on task relevant items. This appears to reflect more efficient inhibition of eye-movements towards task irrelevant stimuli, and better active maintenance of task goals. When the task is novel, and therefore more difficult, nicotine lessens the need to refixate previously seen letters, suggesting an improvement in working memory.

show abstract

Section: Discussionmentioning

confidence: 99%

Acute effects of nicotine on visual search tasks in young adult smokers

2005

View full text Add to dashboard Cite

show abstract

“…Deficient P50 auditory sensory gating has been linked to polymorphisms at the site of the a7nAChR gene on chromosome 15q14 and is transiently reversed by nicotine administration in smokers with schizophrenia and in nonsmoking first-degree relatives of patients with schizophrenia (Adler et al, 1992(Adler et al, , 1993Freedman et al, 1997;Leonard et al, 2002). Nicotine also improves diseaseassociated deficits in prepulse inhibition (PPI) of the acoustic startle response (Kumari et al, 2001) and oculomotor function, with improvements reported in smooth pursuit eye movement (SPEM) and antisaccade error rates (Olincy et al, 1998(Olincy et al, , 2003Depatie et al, 2002;Sherr et al, 2002;Avila et al, 2003). These findings, combined with the observation that the prevalence of cigarette smoking is much higher in schizophrenia compared with the general population, (Hughes, 1986;de Leon et al, 2002) have led to the hypothesis that smoking represents a form of self-medication for patients with psychiatric illness, particularly schizophrenia (Glassman, 1993;Dalack et al, 1998;Kumari and Postma, 2005).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

Barr

Culhane

Jubelt

et al. 2007

Neuropsychopharmacol

215

151

View full text Add to dashboard Cite

Abundant evidence indicates that the neuronal nicotinic acetylcholine receptor (nAChR) system is integral to regulation of attentional processes and is dysregulated in schizophrenia. Nicotinic agonists may have potential for the treatment of cognitive impairment in this disease. This study investigated the effects of transdermal nicotine on attention in individuals with schizophrenia (n ¼ 28) and healthy controls (n ¼ 32). All participants were nonsmokers in order to eliminate confounding effects of nicotine withdrawal and reinstatement that may occur in the study of smokers. Subjects received 14 mg transdermal nicotine and identical placebo in a randomized, placebocontrolled, crossover design. A cognitive battery was conducted before and 3 h after each patch application. The primary outcome measure was performance on the Continuous Performance Test Identical Pairs (CPT-IP) Version. Nicotine significantly improved the performance on the CPT-IP as measured by hit reaction time, hit reaction time standard deviation and random errors in both groups. In addition, nicotine reduced commission errors on the CPT-IP and improved the performance on a Card Stroop task to a greater extent in those with schizophrenia vs controls. In summary, nicotine improved attentional performance in both groups and was associated with greater improvements in inhibition of impulsive responses in subjects with schizophrenia. These results confirm previous findings that a single dose of nicotine improves attention and suggest that nicotine may specifically improve response inhibition in nonsmokers with schizophrenia.

show abstract

“…Since brain KYNA levels are decreased 4 and 6 days after repeated nicotine administration, excessive smoking in the schizophrenic population could constitute an attempt to self-medicate (cf Introduction). Indeed, a reduction in brain KYNA enhances nicotinic and glutamatergic transmission (Alkondon et al, 2004) and could thus normalize gating (Adler et al, 1993) and eye-tracking Avila et al, 2003), deficit, and improve cognitive function (Mori and Mishina, 2003). However, the present data suggest that more prolonged exposure to nicotine may have the opposite, detrimental effects on sensory and cognitive modalities since brain KYNA levels are elevated (cf Shepard et al, 2003).…”

Section: Discussionmentioning

confidence: 62%

Prolonged Nicotine Administration Results in Biphasic, Brain-Specific Changes in Kynurenate Levels in the Rat

Rassoulpour

Albuquerque

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

The content of the endogenous NMDA and a7 nicotinic acetylcholine receptor antagonist kynurenate (KYNA) is increased in the cerebral cortex and cerebrospinal fluid of patients with schizophrenia. In view of the very high incidence of smoking in schizophrenic individuals, a study was designed to examine the effect of acute and prolonged nicotine administration on brain KYNA levels in experimental animals. Adult male rats received subcutaneous nicotine injections twice daily for up to 10 days, and animals were routinely killed 1 h after the last injection. Neither acute treatment nor a 2-day regimen with 1 mg/kg nicotine ( ¼ 0.35 mg/kg pure base) caused changes in cerebral KYNA levels. Four-or 6 day-treatment with this dose resulted in 20-40% decreases in cerebral KYNA content. Animals treated with 1 or 10 mg/kg nicotine for 10 days showed dose-dependent, significant increases in KYNA in hippocampus, striatum, and cortex, but not in the serum. Discontinuation of nicotine treatment for 7 days restored brain KYNA to control levels. Separate animals, implanted with osmotic minipumps delivering 2 mg/kg of nicotine/day for 10 days also showed significant elevations in brain KYNA. Hippocampal microdialysis, performed in animals receiving nicotine (1 mg/kg) for 10 days, revealed a significant increase in basal extracellular KYNA levels compared to controls, whereas acute treatment with this dose produced no such change. Measurements of KYNA's bioprecursor kynurenine in brain or blood did not reveal any nicotine-induced changes. These results indicate that nicotine has a brain-specific, biphasic effect on the transamination of kynurenine to KYNA. Such nicotine-induced fluctuations in brain KYNA may cause functional changes in processes that regulate glutamatergic and cholinergic neurotransmission in the normal and diseased brain.

show abstract

Effects of Nicotine on Leading Saccades during Smooth Pursuit Eye Movements in Smokers and Nonsmokers with Schizophrenia

Cited by 77 publications

References 75 publications

Acute effects of nicotine on visual search tasks in young adult smokers

Acute effects of nicotine on visual search tasks in young adult smokers

The Effects of Transdermal Nicotine on Cognition in Nonsmokers with Schizophrenia and Nonpsychiatric Controls

Prolonged Nicotine Administration Results in Biphasic, Brain-Specific Changes in Kynurenate Levels in the Rat

Contact Info

Product

Resources

About