Quantitative effects of typical and atypical neuroleptics on smooth pursuit eye tracking in schizophrenia

Litman, Robert E.; Hommer, Daniel W.; Radant, Allen D.; Clem, Thomas R.; Pickar, David

doi:10.1016/0920-9964(94)90068-x

Cited by 56 publications

(36 citation statements)

References 47 publications

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“…Thus, leading saccades appear to have both spatial and temporal dysmetric components, and are therefore more likely to reflect abnormalities in the integration of saccadic and pursuit eye movements during visual tracking rather than simple saccadic hypermetria. This is consistent with previous descriptions of leading saccades as 'contextinappropriate' or 'intrusive' saccades, which may be related to loss of inhibitory control over saccadic eye movements during pursuit (Litman et al, 1994;Ross et al, 1996;Lencer et al, 1999a).…”

Section: Neurophysiological Basis Of Leading Saccadessupporting

confidence: 80%

“…Experimental administration of a particular pharmacological agent is one means of identifying receptor systems of interest, and in fact a number of drug-probe studies involving SPEM performance in schizophrenia have been conducted (eg Thaker et al, 1991;Friedman et al, 1992;Litman et al, 1994;Radant et al, 1998;Weiler et al, 2000;Avila et al, 2002c). Results of several drug-probe studies involving nicotine suggest that neuronal nicotinic receptors (nAChRs) may be involved (Olincy et al, , 2003Sherr et al, 2002;Depatie et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…Abnormalities include (1) a failure of eye velocity to match target velocity during sustained visual tracking (ie low closed-loop gain) (eg Clementz and McDowell, 1994;Sweeney et al, 1999;Levy et al, 2000; see Levy et al, 1993 for a review), which is thought to reflect deficits in predictive components of the SPEM response (Thaker et al, , 1999; (2) an increase in catch-up saccades, which is secondary to low gain (Abel and Ziegler, 1988;Sweeney et al, 1994); (3) decreased acceleration during pursuit initiation (Clementz et al, 1995;Ross et al, 1996), which may reflect retinal motion processing and/or anticipatory learning deficits (Chen et al, 1999;Avila et al, 2002a); and (4) an increased frequency of leading saccadic eye movements (Avila et al, 2002b;Levy et al, 2000;Ross et al, 2000), which may reflect a loss of cortical inhibitory control over saccades during pursuit (Litman et al, 1994;Ross et al, 1998;Lencer et al, 1999a).…”

Section: Introductionmentioning

confidence: 99%

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

Avila

Sherr

Hong

et al. 2003

Neuropsychopharmacol

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Several studies have shown that schizophrenic patients and their biological relatives generate a greater number of leading saccades during smooth pursuit eye movement (SPEM) tasks. This abnormality may reflect a failure of cortical and/or cerebellar areas to coordinate saccadic and pursuit eye movements during visual tracking. The pharmacology of this phenomenon is not known. Here, we sought to replicate and extend the findings of Olincy et al (1998), who found that nicotine transiently reduced the number of leading saccades during SPEMs. A total of 27 subjects with schizophrenia (17 males; 14 smokers), and 25 healthy comparison subjects (nine males; 14 smokers) completed an eye-tracking task after receiving a 1.0 mg nasal spray of nicotine and during drug-free conditions. Results confirm that nicotine reduces the number of leading saccadic eye movements during visual tracking in schizophrenic patients. Baseline impairments and the beneficial effects of nicotine were not restricted to patient smokers, as nonsmoker patients exhibited the greatest number of leading saccades in the no drug condition and exhibited the most pronounced improvements after nicotine administration. Improvement in patient nonsmokers was not a function of previous smoking history. No effect of nicotine was observed in control nonsmokers. In contrast to the previous study, nicotine appeared to improve performance in control smokers. Overall, the study results support a functional role of nACh receptors in improving eye-tracking performance, and are consistent with the hypothesis, articulated by several investigators, that nACh receptor system abnormalities are responsible for a number of schizophrenia-related neurophysiological deficits.

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Section: Neurophysiological Basis Of Leading Saccadessupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Avila

Sherr

Hong

et al. 2003

Neuropsychopharmacol

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“…Our techniques for presentation of oculomotor stimuli, acquisition and recording of horizontal eye movements, and data analysis have been reported in detail in recent publications (Roy-Byrne et al 1995;Radant and Hommer 1992;Litman et al 1994;Ross et al 1994). Softwaregenerated dependent measures for the smooth pursuit, visually guided saccade, antisaccade, and step ramp tasks have excellent test-retest reliability in our laboratory (Roy-Byrne et al 1995).…”

Section: Eye Movement Recording and Initial Analysismentioning

confidence: 95%

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Radant

Bowdle

Cowley

et al. 1998

Neuropsychopharmacology

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“…However, negative symptoms, even in responsive patients, are not cured by clozapine and some symptoms, e.g. most cognitive deÞcts (Goldberg et al 1993) or eye-tracking abnormalities (Litman et al 1994), are not a¤ected at all.…”

Section: Introductionmentioning

confidence: 99%

Neonatal lesions of the rat ventral hippocampus result in hyperlocomotion and deficits in social behaviour in adulthood

Sams-Dodd¹,

1997

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The neonatal ibotenic acid lesion of the ventral hippocampus in the rat is an animal model of several aspects of schizophrenia. This lesion produces a number of behavioural abnormalities, such as hyperlocomotion and deficits in prepulse inhibition of startle, that present themselves relatively late in development, i.e. after puberty. Some of these abnormalities, which are thought to model the positive symptoms of schizophrenia, can be normalized by chronic treatment with neuroleptics. In the present study, we examined the effects of the neonatal hippocampal lesion on social behaviour. Social withdrawal and isolation are key components of the negative symptoms of schizophrenia that have not been previously addressed in this model. Rats were lesioned on postnatal day 7 (PD7) and tested for social interaction on PD35 and PD65. They were then treated with clozapine (1.9 and 7.4 micromol/kg or 0.63 and 2.5 mg/kg) for 21 days and retested. The results show that although, as previously reported, spontaneous hyperlocomotion emerged in the lesioned rats only after puberty (PD65), social interaction deficits and behaviors that may reflect anxiety were present at both PD35 and PD65. Clozapine normalized locomotion, but did not ameliorate putative anxiety or social interaction deficits in the neonatally lesioned rats. Our results indicate that the neonatal hippocampal lesion in the rat models some aspects of both positive and negative symptoms of schizophrenia. The effects of clozapine appear inconsistent with its putative benefit for negative symptoms.

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Quantitative effects of typical and atypical neuroleptics on smooth pursuit eye tracking in schizophrenia

Cited by 56 publications

References 47 publications

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

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

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Neonatal lesions of the rat ventral hippocampus result in hyperlocomotion and deficits in social behaviour in adulthood

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