Erich Seifritz
University of Zurich
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Featured researches published by Erich Seifritz.
The Journal of Neuroscience | 2007
Cyril Herry; Dominik R. Bach; Fabrizio Esposito; Francesco Di Salle; Walter J. Perrig; Klaus Scheffler; Andreas Lüthi; Erich Seifritz
The amygdala has been studied extensively for its critical role in associative fear conditioning in animals and humans. Noxious stimuli, such as those used for fear conditioning, are most effective in eliciting behavioral responses and amygdala activation when experienced in an unpredictable manner. Here, we show, using a translational approach in mice and humans, that unpredictability per se without interaction with motivational information is sufficient to induce sustained neural activity in the amygdala and to elicit anxiety-like behavior. Exposing mice to mere temporal unpredictability within a time series of neutral sound pulses in an otherwise neutral sensory environment increased expression of the immediate-early gene c-fos and prevented rapid habituation of single neuron activity in the basolateral amygdala. At the behavioral level, unpredictable, but not predictable, auditory stimulation induced avoidance and anxiety-like behavior. In humans, functional magnetic resonance imaging revealed that temporal unpredictably causes sustained neural activity in amygdala and anxiety-like behavior as quantified by enhanced attention toward emotional faces. Our findings show that unpredictability per se is an important feature of the sensory environment influencing habituation of neuronal activity in amygdala and emotional behavior and indicate that regulation of amygdala habituation represents an evolutionary-conserved mechanism for adapting behavior in anticipation of temporally unpredictable events.
NeuroImage | 2013
James Sulzer; Sven Haller; Frank Scharnowski; Nikolaus Weiskopf; Niels Birbaumer; Maria Laura Blefari; A. B. Bruehl; Leonardo G. Cohen; R. C. deCharms; Roger Gassert; Rainer Goebel; Uwe Herwig; Stephen M. LaConte; David Edmund Johannes Linden; Andreas R. Luft; Erich Seifritz; Ranganatha Sitaram
In February of 2012, the first international conference on real time functional magnetic resonance imaging (rtfMRI) neurofeedback was held at the Swiss Federal Institute of Technology Zurich (ETHZ), Switzerland. This review summarizes progress in the field, introduces current debates, elucidates open questions, and offers viewpoints derived from the conference. The review offers perspectives on study design, scientific and clinical applications, rtfMRI learning mechanisms and future outlook.
PLOS ONE | 2012
M Scheidegger; Martin Walter; Mick Lehmann; Coraline D. Metzger; Simone Grimm; Heinz Boeker; Peter Boesiger; A Henning; Erich Seifritz
Increasing preclinical and clinical evidence underscores the strong and rapid antidepressant properties of the glutamate-modulating NMDA receptor antagonist ketamine. Targeting the glutamatergic system might thus provide a novel molecular strategy for antidepressant treatment. Since glutamate is the most abundant and major excitatory neurotransmitter in the brain, pathophysiological changes in glutamatergic signaling are likely to affect neurobehavioral plasticity, information processing and large-scale changes in functional brain connectivity underlying certain symptoms of major depressive disorder. Using resting state functional magnetic resonance imaging (rsfMRI), the „dorsal nexus “(DN) was recently identified as a bilateral dorsal medial prefrontal cortex region showing dramatically increased depression-associated functional connectivity with large portions of a cognitive control network (CCN), the default mode network (DMN), and a rostral affective network (AN). Hence, Sheline and colleagues (2010) proposed that reducing increased connectivity of the DN might play a critical role in reducing depression symptomatology and thus represent a potential therapy target for affective disorders. Here, using a randomized, placebo-controlled, double-blind, crossover rsfMRI challenge in healthy subjects we demonstrate that ketamine decreases functional connectivity of the DMN to the DN and to the pregenual anterior cingulate (PACC) and medioprefrontal cortex (MPFC) via its representative hub, the posterior cingulate cortex (PCC). These findings in healthy subjects may serve as a model to elucidate potential biomechanisms that are addressed by successful treatment of major depression. This notion is further supported by the temporal overlap of our observation of subacute functional network modulation after 24 hours with the peak of efficacy following an intravenous ketamine administration in treatment-resistant depression.
Neuropsychopharmacology | 1996
Erich Seifritz; Pierre Baumann; Matthias J. Müller; Oliver Annen; Marlyse Amey; Ulrich Hemmeter; Martin Hatzinger; François Chardon; Edith Holsboer-Trachsler
Pharmacokinetic measurements, neuroendocrine responses, and side effect profiles of intravenous infusions of 20 mg citalopram over 30 minutes during the early afternoon have been studied. Eight healthy male volunteers were enrolled in a placebo- (saline) controlled, single-blind, cross-over protocol. Plasma concentrations of the parent compound showed a double exponential decay. Demethyl and didemethyl metabolites were not detectable, but low concentrations of the propionic acid derivative of citalopram were found. Determination of the citalopram enantiomers yielded a balanced S(+)/R(−) ratio of 0.9 to 1.2. The endocrine response to the drug was characterized by significant increases in plasma prolactin and cortisol. Except for one subject, who developed pronounced side effects, human growth hormone showed a surge following saline that was inhibited following citalopram. Rectal temperature and heart rate were not affected and tolerability was favorable. Because of citaloprams extremely high selectivity for the presynaptic 5-hydroxytryptamine nerve terminals, the present data suggest that it might be a promising tool for the investigation of serotonergic function in the human brain in vivo.
Pharmacology & Therapeutics | 2011
Christopher R. Pryce; Damiano Azzinnari; Simona Spinelli; Erich Seifritz; Marion Tegethoff; Gunther Meinlschmidt
Helplessness is a major concept in depression and a major theme in preclinical and clinical depression research. For example, in rodents and humans, the learned helplessness (LH) effect describes a specific deficit in behaviour to control aversive stimuli that is induced by prior exposure to uncontrollable aversive stimuli. The LH effect is objective and valid in that the cause of the behavioural deficit, namely uncontrollability, is clear; furthermore, the deficit induced is underlain by emotional, motivational and cognitive processes that are relevant to depression psychopathology. As a further example, helplessness, hopelessness, external locus of control and causal attribution are inter-related and major themes in psychological theories (primarily cognitive theories) of depression. Despite this broad interest in helplessness, it can be argued that its potential usefulness as a scientific and clinical concept has so far not been investigated optimally, including with respect to its application in research aimed at development of improved anti-depressant pharmacotherapy. The first aim of this review was to describe and integrate the psychological evidence and the neurobiological evidence for the LH effect in rodents and healthy humans and for helplessness in depressed patients. The second aim was to conduct three systematic reviews, namely of rodent studies of the LH effect, rodent studies of effects of psychopharmacological agents on the LH effect, and human studies of efficacy of pharmacotherapeutic and psychotherapeutic treatment on helplessness in depressed patients. With respect to the first aim, the major findings are: the specificity of the LH effect in otherwise non-manipulated rodents and healthy humans has been under-estimated, and the LH effect is a specific learned aversive uncontrollability (LAU) effect. There is theoretical and empirical support for a model in which a specific LAU effect induced by a life event of major emotional significance can function as an aetiological factor for generalised helplessness which can in turn function as an aetiological and maintenance factor for depression. However, to date such models have focused on cognitive mediating processes whereas it is emotional-motivational-cognitive processes (as proposed for the LAU effect) that need to be invoked and understood. The evidence is for analogous neural processes underlying the LAU effect in rodents and healthy humans and helplessness in depression, with the ventro-medial prefrontal cortex exhibiting aversive uncontrollability-dependent activity. With respect to the second aim, the major findings are: the LAU effect is demonstrated quite consistently using a number of different paradigms in rat but is poorly studied in mouse. The rat LAU effect can be reversed by chronic administration of monoamine reuptake inhibitors. The effects of antidepressants on human helplessness have been scarcely studied to-date. The major conclusion is that the LAU effect and generalised helplessness constitute major neuropsychological concepts of high value to future translational research aimed at increased understanding of depression and development of novel, improved antidepressant treatments.
Biological Psychiatry | 2012
Michael Kometer; André Schmidt; Rosilla Bachmann; Erich Studerus; Erich Seifritz; Franz X. Vollenweider
BACKGROUND Serotonin (5-HT) 1A and 2A receptors have been associated with dysfunctional emotional processing biases in mood disorders. These receptors further predominantly mediate the subjective and behavioral effects of psilocybin and might be important for its recently suggested antidepressive effects. However, the effect of psilocybin on emotional processing biases and the specific contribution of 5-HT2A receptors across different emotional domains is unknown. METHODS In a randomized, double-blind study, 17 healthy human subjects received on 4 separate days placebo, psilocybin (215 μg/kg), the preferential 5-HT2A antagonist ketanserin (50 mg), or psilocybin plus ketanserin. Mood states were assessed by self-report ratings, and behavioral and event-related potential measurements were used to quantify facial emotional recognition and goal-directed behavior toward emotional cues. RESULTS Psilocybin enhanced positive mood and attenuated recognition of negative facial expression. Furthermore, psilocybin increased goal-directed behavior toward positive compared with negative cues, facilitated positive but inhibited negative sequential emotional effects, and valence-dependently attenuated the P300 component. Ketanserin alone had no effects but blocked the psilocybin-induced mood enhancement and decreased recognition of negative facial expression. CONCLUSIONS This study shows that psilocybin shifts the emotional bias across various psychological domains and that activation of 5-HT2A receptors is central in mood regulation and emotional face recognition in healthy subjects. These findings may not only have implications for the pathophysiology of dysfunctional emotional biases but may also provide a framework to delineate the mechanisms underlying psylocybins putative antidepressant effects.
Comprehensive Psychiatry | 2003
Marc Hofmann; Alexander Rösler; Wolfram Schwarz; Franz Müller-Spahn; Kurt Kräuchi; Christoph Hock; Erich Seifritz
The current study sought to evaluate a novel kind of interactive computer-based cognitive training (ICT) in Alzheimers disease (AD). AD patients (N = 9), age- and gender-matched patients with a major depressive episode (N = 9), and healthy control subjects (N = 10) were trained to use an ICT program that relates to activities of daily living (ADL). Digital photographs of a shopping route were implemented in a close-to-reality simulation on a computer touch-screen. The task was to find a predefined shopping route, to buy three items, and to answer correctly 10 multiple-choice questions addressing knowledge related to the virtual tasks. Training performance was rated using the number of mistakes (wrong way), time needed for the tasks, number of correct multiple-choice answers, and of repeat of instruction. Compared to normal controls and depressed patients, AD patients performed significantly worse with regard to all variables. Within a 4-week training period including 12 sessions, however, substantial training gains were observed, including a significant reduction of mistakes. Training effects were sustained until follow-up 3 weeks later. The performance of the depressed patients and the normal controls improved as well, with no difference between the two groups. Self-reported effects revealed that the training was well perceived. Thus, the task performance of AD patients improved substantially and subjects appeared to have liked this approach to ICT. New interactive media, therefore, may yield interesting opportunities for rehabilitation and (psycho)therapeutic interventions.
Addiction Biology | 2014
Katrin H. Preller; Lea M. Hulka; Matthias Vonmoos; Daniela Jenni; Markus R. Baumgartner; Erich Seifritz; Isabel Dziobek; Boris B. Quednow
Chronic cocaine users consistently display neurochemical and functional alterations in brain areas involved in social cognition (e.g. medial and orbitofrontal cortex). Although social functioning plays a crucial role in the development and treatment of drug dependence, studies investigating social cognition in cocaine users are lacking. Therefore, we investigated mental perspective taking (‘theory of mind’) and emotional and cognitive empathy in recreational (RCU) and dependent (DCU) cocaine users. Furthermore, we related these measures to real‐life indicators of social functioning. One‐hundred cocaine users (69 RCU, 31 DCU) and 68 stimulant‐naïve healthy controls were tested with the Multifaceted Empathy Test (MET), Movie for the Assessment of Social Cognition (MASC) and Reading the Mind in the Eyes Test (RMET). The Social Network Questionnaire was conducted to assess social network size. Furthermore, participants provided information on committed criminal offenses. RCU and DCU showed less emotional empathy compared to controls (MET), whereas cognitive empathy was not impaired (MET, RMET). Additionally, DCU made more errors in mental perspective taking (MASC). Notably, cocaine users committed more criminal offenses and displayed a smaller social network and higher cocaine use was correlated with less social contacts. Diminished mental perspective taking was tentatively correlated with more intense cocaine use as well. Finally, younger age of onset of cocaine use was associated with more pronounced empathy impairment. In conclusion, social cognition impairments in cocaine users were related to real‐life social functioning and should therefore be considered in therapy and prevention strategies.
Biological Psychiatry | 2009
Anja Kraus; Fabrizio Esposito; Erich Seifritz; Francesco Di Salle; Matthias Ruf; Gabriele Valerius; Petra Ludaescher; Martin Bohus; Christian Schmahl
BACKGROUND Previous studies have revealed altered affective pain processing in patients with borderline personality disorder (BPD) as well as in patients with posttraumatic stress disorder (PTSD). Reduced levels of activation in the amygdala might be related to antinociceptive mechanisms pertinent to both disorders. This study aimed at clarifying whether central antinoceptive mechanisms discriminate BPD patients with and without co-occurrent PTSD. METHODS We investigated 29 medication-free female outpatients with BPD, 12 with and 17 without co-occurrent PTSD. Psychophysical characteristics were assessed, and functional magnetic resonance imaging was performed during heat stimulation with stimuli adjusted for equal subjective painfulness. RESULTS No difference in pain sensitivity was found between both groups of patients. Amygdala deactivation, however, was more pronounced in BPD patients with co-occurrent PTSD compared with those without PTSD. Amygdala deactivation was independent of BPD symptom severity and dissociation. CONCLUSIONS Amygdala deactivation seems to differentiate patients who meet criteria for both BPD and PTSD from BPD patients without co-occurrent PTSD. On the basis of these preliminary findings it might be speculated that reduced pain sensitivity or at least the emotional component of it is associated with amygdala deactivation in patients with both disorders, whereas BPD patients without PTSD use different yet unknown antinociceptive mechanisms.
Psychological Medicine | 2014
Lea M. Hulka; Christoph Eisenegger; Katrin H. Preller; Matthias Vonmoos; Daniela Jenni; Katharine Bendrick; Markus R. Baumgartner; Erich Seifritz; Boris B. Quednow
BACKGROUND Maladaptive decision-making is assumed to be a core feature of cocaine addiction. Indeed, numerous studies have reported deficits in non-social decision-making tasks and reward-related impulsivity in dependent cocaine users. However, social decision-making has not been examined in cocaine users yet. Moreover, it is unknown if even recreational and non-dependent cocaine use is linked to decision-making deficits. Therefore, we investigated whether recreational and dependent cocaine users exhibit alterations in social and non-social decision-making. METHOD The performance of healthy controls (n = 68), recreational cocaine users (n = 68) and dependent cocaine users (n = 30) in classical decision-making paradigms (Iowa Gambling Task, Delay Discounting) and in social interaction paradigms (Distribution Game, Dictator Game) was assessed. RESULTS Decisions in the social interaction tasks of both cocaine user groups were more self-serving compared with controls as cocaine users preferred higher monetary payoffs for themselves. In the Iowa Gambling Task, only dependent cocaine users were more likely to choose disadvantageous card decks, reflecting worse decision-making. They were also more likely to choose immediate smaller rewards over larger delayed rewards in the Delay Discounting task. CONCLUSIONS Our results imply that both recreational and dependent cocaine users are more concerned with their own monetary gain when interacting with another person. Furthermore, primarily dependent cocaine users are less foresighted and more impulsive regarding immediate reward. Overall, social interaction deficits are already present in recreational users, while non-social decision-making deficits occur predominantly in dependent cocaine users. Thus, social interaction training and cognitive remediation strategies may improve treatment success and quality of life in cocaine dependence.