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Is It a European Car Or a Japanese Car? an ERP Study of Diagnostic Information Use in Visual Expertise

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Is It a European Car Or a Japanese Car? an ERP Study of Diagnostic Information Use in Visual Expertise Wright State University CORE Scholar Psychology Faculty Publications Psychology 11-2007 Is it a European car or a Japanese car? An ERP Study of Diagnostic Information Use in Visual Expertise Assaf Harel Wright State University - Main Campus, [email protected] Shlomo Bentin Follow this and additional works at: https://corescholar.libraries.wright.edu/psychology Part of the Cognition and Perception Commons, and the Cognitive Psychology Commons Repository Citation Harel, A., & Bentin, S. (2007). Is it a European car or a Japanese car? An ERP Study of Diagnostic Information Use in Visual Expertise. Neural Plasticity, 2007, 30585, 52. https://corescholar.libraries.wright.edu/psychology/254 This Abstract is brought to you for free and open access by the Psychology at CORE Scholar. It has been accepted for inclusion in Psychology Faculty Publications by an authorized administrator of CORE Scholar. For more information, please contact [email protected]. Hindawi Publishing Corporation Neural Plasticity Volume 2007, Article ID 30585, 168 pages doi:10.1155/2007/30585 Meeting Abstracts Abstracts of the 16th Annual Meeting of The Israel Society for Neuroscience Eilat, Israel, November 25–27, 2007 Received 9 October 2007; Accepted 9 October 2007 The Israel Society for Neuroscience—ISFN—was founded in 1993 by a group of Israeli leading scientists conducting research in the area of neurobiology. The primary goal of the society was to promote and disseminate the knowledge and understanding acquired by its members, and to strengthen interactions between them. Since then, the society holds its annual meeting every year in Eilat usually during December. At this annual meetings, the senior Israeli neurobiologists, their teams, and their graduate students, as well as foreign scientists and students, present their recent research findings in platform and poster presentations, and the program of the meeting is mainly based on the 338 received abstracts which are published in this volume. The meeting also offers the opportunity for the researchers to exchange information with each other, often leading to the initiation of collaborative studies. Both the number of members of the society and those participating in the annual meeting is constantly increasing, and it is anticipated that this year about 600 scientists will convene at the Princess Hotel in Eilat, Israel. Further information concerning the Israel Society for Neuroscience can be found at http://www.isfn.org.il. Committee: Shlomo Rotshenker (President) Hebrew University of Jerusalem Talma Brenner Hadassah–Hebrew University Medical Center Yoram Rami Grossman Ben Gurion University of the Negev Mmouna Maroun University of Haifa Yoel Yaari Hebrew University of Jerusalem Gal Yadid Bar-Ilan University Zvi Wollberg (Past President) Tel Aviv University Lili Anglister (Treasurer) Michal Gilady (Administrator) Hebrew University of Jerusalem Rishon Le Zion Copyright © 2007 Israel Society for Neuroscience. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 2 Neural Plasticity Amyloid-beta peptide modulates the pattern of study was to gain insight into the role of L-Carnosine and N- transmitter release in hippocampal synapses Acetyl-L-Carnosine (NACar), a lipophilic synthetic deriva- tive of L-Carnosine, on NO synthesis in microglia. It is shown Abramov E. and Slutsky I. here for the first time that L-Carnosine (10–20 mM) can in- hibit LPS-induced NO synthesis by 75% in microglia. NACar Department of Physiology & Pharmacology, Sackler Faculty was even more potent than its parent drug, L-Carnosine, in of Medicine, Tel Aviv University, Israel inhibiting LPS-induced NO synthesis. It inhibits NO release by 40% to 80% at concentration as low as 0.5 mM. Our re- Aggregation of the amyloid-beta (A-beta) peptide in the ex- sults suggest that L-Carnosine and NACar may play a pro- tracellular space of the brain is central to Alzheimer’s dis- tective role in oxidative stress process in the brain. Further ease (AD) pathogenesis. Recent findings have shown that studies are needed aiming to understand the mechanism by synaptic activity promotes release of A-beta through vesi- which L-Carnosine and NACar act and to use these com- cle exocytosis. However, the relationship between vesicu- pounds as a potential treatment strategy for strategy for neu- lar release of A-beta and neurotransmitter release remains rodegenerative diseases. obscure. Current hypothesis of AD suggests that elevated neuronal activity leads to increased extracellular concen- Enhanced stress-induced responses in tration of A-beta, which in turn triggers reduction in the an atroglial NOS2 mouse mutant number, strength, and plasticity of synaptic connections, eventually resulting in memory impairments. According Abu-Ghanem Y.,1 Cohen H.,2 Amitai Y.,1 and Grauer E.3 to this hypothesis, decreased synaptic activity should pro- 1 mote memory function through reducing A-beta level. How- Department of Physiology, Faculty of Health Sciences, Ben-Gurion University Beer-Sheva, Israel ever, on the other hand, memory-related forms of synap- 2 tic plasticity are manifested as increase in synaptic activ- Mental Health Center, Ben-Gurion University, Beer-Sheva, Israel ity. To understand this paradox, we study the relationship 3 between different patterns of synaptic activity, A-beta re- Israel Institute for Biological Research, Ness-Ziona, Israel lease, and synaptic transmission using FM-based functional Nitric oxide (NO) is produced in the brain by both neurons imaging at the level of single synapse and in synaptic net- and astrocytes. Until recently, astrocytic NO production has works. Our results show that acute accumulation of endoge- been demonstrated mainly as a slow reaction to detrimen- nously released A-beta enhances presynaptic activity for sin- tal events through the activity of an inducible NOS isoform gle spikes that mimic background activity through increas- (iNOS). Prior data from our laboratory described for the first ing release probability and the number of functional presy- ff time rapid astrocytic NO release in brains of healthy ani- naptic terminals. However, A-beta does not a ect presy- mals. To further explore the role of astrocytic-produced NO, naptic activity associated with temporally correlated burst we examined the iNOS knockout (KO) mouse. NO imaging of spikes. These results suggest that A-beta might be a key and biochemical assays revealed compensatory NOS activity molecule transforming hippocampal synapses to a low-pass in mutants’ brain, which resulted in 30% higher basal NO filter mode, resulting in decreased short-term facilitation of levels compared with control animals. Evaluation of the mu- transmitter release during bursts. We hypothesize that ele- tants’ behavior in several behavioral tests revealed increased vation of background presynaptic activity by A-beta might anxiety-like responses, with no differences in motor activity be a trigger for homeostatic down-regulation in the number (Buskila et al., 2007). To further characterize the behavioral and plasticity of synapses and, eventually, memory decline phenotype, we compared the performance of mutant mice in AD. to their controls in their response to stress. Seven days af- ter exposure to predator scent stimulation (PSS), mutants Protective effect of N-acetyl-L-Carnosine, exhibited higher anxiety-like behavior in the elevated-plus a lipophilic derivative of L-Carnosine, on maze and stronger acoustic startle response. No such differ- lipopolysaccaride-induced glial oxidative stress ences between groups were observed without the stress expo- sure. Plasma corticosterone levels were significantly higher Abramovitch-Dahan C., Beit-Yannai E., Ben-Shabat S., in mutant mice following PSS, further demonstrating their and Fleisher-Berkovich S. heightened sensitivity to stress. Interestingly, mutant mice performed better on the Morris water maze (MWM) under Department of Clinical Pharmacology, Faculty of Health control conditions. The possibility of improved cognition in Sciences, Ben Gurion University of the Negev, Israel these mice was not supported as these mutants failed to show improved performance in the object recognition test. The Neurodegenerative disorders pathology can be characterized MWM results are probably due to enhanced motivation un- by both chronic inflammation and oxidative stress. The most der water maze stress conditions in mutant mice compared dominant source of inflammatory and oxidative stress me- to controls. Taken together, our results confirm higher sus- diators like nitric oxide (NO), prostaglandins, and cytokines ceptibility to stressful conditions in an astrocytic NOS mouse are activated microglia. We used lipopolysaccharide (LPS) in mutant. order to induce oxidative stress in microglia. L-Carnosine is known as an efficient endgenous antioxidant. The aim of this Supported by a grant from the Israel Science Foundation to Y.A. Israel Society for Neuroscience 3 TheroleofCB1receptorsinthehippocampus some 6q23. Subsequent fine mapping, association, and repli- and nucleus accumbens in extinction learning cation studies identified AHI1 as a putative susceptibility and neural plasticity gene. The same genome scan revealed suggestive evidence for a schizophrenia susceptibility locus in the 10q23-26 region. Abush H. and Akirav I. Methods Department of Psychology, University of Haifa, Israel To refine
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