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Suche nach „[R.] [Weber]“ hat 4 Publikationen gefunden
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    GesundEuropan Campus Rottal-Inn

    Zeitschriftenartikel

    M. Steffens, C. Neumann, Anna-Maria Kasparbauer, B. Becker, B. Weber, M. Mehta, R. Hurlemann, U. Ettinger

    Effects of ketamine on brain function during response inhibition

    Psychopharmacology, vol. 235, pp. 3559-3571

    2018

    DOI: 10.1007/s00213-018-5081-7

    Abstract anzeigen

    Introduction The uncompetitive N-methyl-D-aspartate (NMDA) receptor (NMDAR) antagonist ketamine has been proposed to model symptoms of psychosis. Inhibitory deficits in the schizophrenia spectrum have been reliably reported using the antisaccade task. Interestingly, although similar antisaccade deficits have been reported following ketamine in non-human primates, ketamine-induced deficits have not been observed in healthy human volunteers. Methods To investigate the effects of ketamine on brain function during an antisaccade task, we conducted a double-blind, placebo-controlled, within-subjects study on n = 15 healthy males. We measured the blood oxygen level dependent (BOLD) response and eye movements during a mixed antisaccade/prosaccade task while participants received a subanesthetic dose of intravenous ketamine (target plasma level 100 ng/ml) on one occasion and placebo on the other occasion. Results While ketamine significantly increased self-ratings of psychosis-like experiences, it did not induce antisaccade or prosaccade performance deficits. At the level of BOLD, we observed an interaction between treatment and task condition in somatosensory cortex, suggesting recruitment of additional neural resources in the antisaccade condition under NMDAR blockage. Discussion Given the robust evidence of antisaccade deficits in schizophrenia spectrum populations, the current findings suggest that ketamine may not mimic all features of psychosis at the dose used in this study. Our findings underline the importance of a more detailed research to further understand and define effects of NMDAR hypofunction on human brain function and behavior, with a view to applying ketamine administration as a model system of psychosis. Future studies with varying doses will be of importance in this context.

    GesundEuropan Campus Rottal-Inn

    Zeitschriftenartikel

    M. Steffens, B. Becker, C. Neumann, Anna-Maria Kasparbauer, I. Meyhöfer, B. Weber, M. Mehta, R. Hurlemann, U. Ettinger

    Effects of Ketamine on Brain Function During Smooth Pursuit Eye Movements

    Human Brain Mapping, vol. 37, no. 11, pp. 4047-4060

    2016

    DOI: 10.1002/hbm.23294

    Abstract anzeigen

    The uncompetitive NMDA receptor antagonist ketamine has been proposed to model symptoms of psychosis. Smooth pursuit eye movements (SPEM) are an established biomarker of schizophrenia. SPEM performance has been shown to be impaired in the schizophrenia spectrum and during ketamine administration in healthy volunteers. However, the neural mechanisms mediating SPEM impairments during ketamine administration are unknown. In a counter‐balanced, placebo‐controlled, double‐blind, within‐subjects design, 27 healthy participants received intravenous racemic ketamine (100 ng/mL target plasma concentration) on one of two assessment days and placebo (intravenous saline) on the other. Participants performed a block‐design SPEM task during functional magnetic resonance imaging (fMRI) at 3 Tesla field strength. Self‐ratings of psychosis‐like experiences were obtained using the Psychotomimetic States Inventory (PSI). Ketamine administration induced psychosis‐like symptoms, during ketamine infusion, participants showed increased ratings on the PSI dimensions cognitive disorganization, delusional thinking, perceptual distortion and mania. Ketamine led to robust deficits in SPEM performance, which were accompanied by reduced blood oxygen level dependent (BOLD) signal in the SPEM network including primary visual cortex, area V5 and the right frontal eye field (FEF), compared to placebo. A measure of connectivity with V5 and FEF as seed regions, however, was not significantly affected by ketamine. These results are similar to the deviations found in schizophrenia patients. Our findings support the role of glutamate dysfunction in impaired smooth pursuit performance and the use of ketamine as a pharmacological model of psychosis, especially when combined with oculomotor biomarkers.

    GesundEuropan Campus Rottal-Inn

    Zeitschriftenartikel

    Anna-Maria Kasparbauer, I. Meyhöfer, M. Steffens, B. Weber, M. Aydine, V. Kumari, R. Hurlemann, U. Ettinger

    Neural Effects of Methylphenidate and Nicotine During Smooth Pursuit Eye Movements

    NeuroImage, vol. 141, no. November, pp. 52-59

    2016

    DOI: 10.1016/j.neuroimage.2016.07.012

    Abstract anzeigen

    Introduction Nicotine and methylphenidate are putative cognitive enhancers in healthy and patient populations. Although they stimulate different neurotransmitter systems, they have been shown to enhance performance on overlapping measures of attention. So far, there has been no direct comparison of the effects of these two stimulants on behavioural performance or brain function in healthy humans. Here, we directly compare the two compounds using a well-established oculomotor biomarker in order to explore common and distinct behavioural and neural effects. Methods Eighty-two healthy male non-smokers performed a smooth pursuit eye movement task while lying in an fMRI scanner. In a between-subjects, double-blind design, subjects either received placebo (placebo patch and capsule), nicotine (7 mg nicotine patch and placebo capsule), or methylphenidate (placebo patch and 40 mg methylphenidate capsule). Results There were no significant drug effects on behavioural measures. At the neural level, methylphenidate elicited higher activation in left frontal eye field compared to nicotine, with an intermediate response under placebo. Discussion The reduced activation of task-related regions under nicotine could be associated with more efficient neural processing, while increased hemodynamic response under methylphenidate is interpretable as enhanced processing of task-relevant networks. Together, these findings suggest dissociable neural effects of these putative cognitive enhancers.

    DigitalGesundEuropan Campus Rottal-Inn

    Beitrag (Sammelband oder Tagungsband)

    P. Friedrich, J. Kneitz, P. Martius, R. Weber, Thomas Spittler, B. Wolf

    Telemedizinische Anwendungsbeobachtung mit COMES® im klinischen und heimischen Umfeld.

    Tagungsband des 6. Deutschen AAL-Kongresses "Lebensqualität im Wandel von Demografie und Technik", Berlin

    2013