Investigation of insight with magic tricks

11/14/12 • 0 min

Graduate School of Systemic Neurosciences - Digitale Hochschulschriften der LMU

This thesis proposes a new approach to investigate insight problem solving. Introducing magic tricks as a problem solving task, we asked participants to find out the secret method used by the magician to create the magic effect. Based on the theoretical framework of the representational change theory, we argue that magic tricks are ideally suited to investigate insight because similar to established insight tasks like puzzles, observers’ prior knowledge activates constraints. In order to see through the magic trick, the constraints must be overcome by changing the problem representation. The aim of the present work is threefold: First, we set out to provide a proof of concept for this novel paradigm by demonstrating that it is actually possible for observers to gain insight into the magician’s secret method and that this can be experienced as a sudden, insightful solution. We therefore aimed at showing that magic tricks can trigger insightful solutions that are accompanied by an Aha! experience. The proposed paradigm could be a useful contribution to the field of insight research where new stimuli beyond traditional puzzle approaches are sorely needed. Second, the present work is aimed at contributing to a better understanding of the subjective Aha! experience that is currently often relied on as important classification criterion in neuroscientific studies of insight, yet remains conceptually vague. The new task will therefore be used to further elucidate the phenomenology of the Aha! experience by assessing participants’ individual solving experiences. As a third question, we investigated the influence of insight on memory. A positive impact of insight on subsequent solution recall is often implicitly assumed, because the representational change underlying insightful solutions is assumed to facilitate the retention of solution knowledge, yet this was never tested. A stimulus set of magic tricks was developed in collaboration with a professional magician, covering a large range of different magic effects and methods. After recording the tricks in a standardized theatre setting, pilot studies were run on 45 participants to identify appropriate tricks and to ensure that they were understandable, surprising and difficult. In the main experiment, 50 participants watched the final set of 34 magic tricks, with the task of trying to figure out how the trick was accomplished. Each trick was presented up to three times. Upon solving the trick, participants had to indicate whether they had found the solution through sudden insight (i.e. with an Aha! experience) or not. Furthermore, we obtained a detailed characterization of the Aha! experience by asking participants for a comprehensive quantitative (ratings on a visual analogue scale with fixed dimensions) and qualitative evaluation (free self-reports) which was repeated after 14 days to control for its reliability. At that time, participants were also required to perform a recall of their solutions. We found that 49% of all magic tricks could be solved and specifically, that insightful solutions were elicited in 41.1% of solved trials. In comparison with noninsight solutions, insightful solutions (brought about by representational change) were more likely to be correct and reached earlier. Quantitative evaluations of individual Aha! experiences turned out to be highly reliable since they remained identical across the time span of 14 days. Qualitatively, participants reported more emotional than cognitive aspects. This primacy of positive emotions was found in qualitative as well as in quantitative evaluations, although two different methods were used. We also found that experiencing insight leads to a facilitated recall of the respective solutions since 64.4% of all insight solutions were recalled correctly, whereas only 52.4% of all noninsight solutions were recalled correctly after a delay of 14 days. We demonstrated the great potential of our new approach by providing a proof of concept for magic tricks as a problem solving task and conclude that magic tricks offer a novel way of inducing problem solving that elicits insight. The reliability of individual evaluations of Aha! experiences indicates that, despite its subjective character, it can be justified to use the Aha! experience as a classification criterion. The present work contributes to a better understanding of the phenomenology of the Aha! experience by providing evidence for the occurrence of strong positive emotions as a prevailing aspect. This work also revealed a memory advantage for solutions that were reached through insight, demonstrating a facilitating effect of previous insight experiences on the recall of solutions. This finding provides support for the assumption that a representational change underlying insightful solving experiences leads to long-lasting changes in the representation of a problem that facilitate the retention of the problem’s solution. In sum, the novel approach ...

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Mechanisms of visual salience and memory on reaching and grasping behavior

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Anti-neurofascin antibodies

Neurofascin (NF) is a cell-adhesion molecule that is found at the nodes of Ranvier. The 186 kDa isoform of neurofascin (NF186) is expressed on the axon in the exposed node, and the 155 kDa isoform (NF155) is expressed on myelinating glia at the paranode. NF186 is essential for clustering of sodium channels to the nodes while NF155 is needed for close paranodal interactions between myelinating glia and axons. The neurofascins are found in both the peripheral and central nervous system (PNS and CNS). NF-specific autoantibodies were identified in serum of multiple sclerosis (MS) patients using a proteomics approach with two-dimensional Western blotting of human myelin glycoproteins. A monoclonal antibody (mAb) specific for NF was shown to induce axonal injury in an animal model of MS, experimental autoimmune encephalomyelitis. This indicated that NF is a relevant autoantibody target in patients with inflammatory diseases of the nervous system (central and peripheral), but actual abundance of anti-NF autoantibodies is unknown. The objectives of the thesis were the following: 1) Develop assays to detect autoantibodies against human NF. 2) Determine the prevalence in patients with MS and with inflammatory diseases of the PNS. 3) Characterize the reactivity by immunoglobulin isotyping, serial dilution, epitope mapping, and staining of nodal structures in tissue sections. 4) Affinity purify anti-NF antibodies from plasma exchange material. 5) Determine possible in vivo effects of anti-NF antibodies in the PNS using a neuritis animal model. First, we expressed the complete human NF155 and NF186 on the surface of stable human cell lines, produced the complete extracellular portion of the NFs in HEK293 cells, and expressed truncated variants of the NFs in E. coli. With these reagents, we set up three antibody detection assays: cell-based assay by flow cytometry, ELISA, and Western blot. These assays were validated using NF-specific monoclonal and polyclonal antibodies, and optimized with a test cohort of serum samples. We screened 687 serum and 48 plasma exchange samples from patients with MS (n = 233), inflammatory diseases in the PNS (n = 294), and controls (n = 208). From serum analysis, we observed low prevalence of anti-NF reactivity (3%) by flow cytometry and/or ELISA despite broad reactivity in almost half of the serum samples analyzed by Western blot. Reactivity observed by flow cytometry and by ELISA were congruent only in the patients with the highest reactivities. The anti-NF antibodies were NF-isoform specific, mainly IgG subclasses, and at high titres in some cases. Using truncated variants of NF fused to super green fluorescence protein (sGFP), we showed that reactivity of anti-NF Abs was largely directed towards the membrane proximal extracellular domains that are unique to each isoform, while the membrane distal immunoglobulin-like domains and fibronectin domains were not recognized. A small proportion (3%; 8/254) of patients with GBS and CIDP showed reactivity to human NF by ELISA. A few showed a particularly high reactivity (up to 1:10 000 dilution) to NF. Two CIDP patients showed a particularly high (up to 1:10 000 dilution) anti-NF155 reactivity by FACS and ELISA, recognized paranodes in tissue sections, and exhibited dominant IgG4 subclass usage. Another CIDP patient who benefited from plasma exchange had a persistent anti-NF155 reactivity by ELISA in serum, and after affinity purification, anti-NF186 and -NF155 reactivity by FACS and ELISA were detected in addition. These antibodies were mainly IgG3, with minor contribution of IgM and IgA. To investigate possible functions of anti-NF antibodies in inflammatory PNS diseases, we injected two different monoclonal antibodies (mAbs) into a P2-peptide induced experimental autoimmune neuritis (EAN) animal model at disease onset. We found that while the anti-NF mAbs prolonged and exacerbated clinical disease in these animals, they could not induce disease on their own. We detected NF-reactivity in a small proportion of MS samples (3%; 7/225) by ELISA and flow cytometry. We obtained follow-up material from two NF-reactive patients and saw a persistent NF reactivity in one of them. To increase detection sensitivity, we affinity purified anti-NF antibodies from plasma exchange material of patients with MS (n = 8). IgG, IgM, and IgA were isolated from most of the samples; they were found to recognize NF155 and to a lower extent NF186 by ELISA and in a few also by flow cytometry. This indicates that low levels of anti-NF antibodies exist in a proportion of MS patients. In conclusion, 3% of serum samples from patients with PNS inflammatory neuropathies (GBS and CIDP) showed reactivity by ELISA and none of the controls. In an animal model of autoimmune peripheral nerve inflammation, we showed, using two anti-NF mAbs, that antibody targeting of NF can enhance and prolong disease course. This suggests t...