Laboratory for Perception & Cognition and Clinical Neuroscience (LPCCN)#

LPCCN is one of the first Hungarian research centers applying a multidisciplinary approach to cognitive and clinical neuroscience. The laboratory was established in 1999 on the ground of the University of Szeged, Department of Physiology (Szeged, Hungary) in close collaborations with Bács-Kiskun County Hospital (Kecskemét, Hungary) and Department of Psychiatry (Szeged). Currently, LPCCN is integrated into the National Psychiatry Center, hosted by the Semmelweis University (Budapest, Hungary), with laboratories at Szeged, Kecskemét, and Budapest.

LPCCN studies neurocognitive and molecular mechanisms of psychotic disorders (e.g., schizophrenia), Parkinson’s disease, memory disorders, and other clinical conditions characterized by perceptual and cognitive dysfunctions.

Research is focused on three major domains:#

  1. Functional organization of parallel visual processing systems (magnocellular and parvocellular retino-striatal pathways and their cortical targets) and sensory gating
  2. Basic mechanisms of reinforcement learning
  3. Social cognition of cooperation and trust

The methodological background includes a wide range of tools from neuropsychology, psychophysics, social psychology, molecular biology/genetics, and electrophysiology.

Current staff members and collaborators working on active projects:#

Szabolcs Kéri, M.D., Ph.D., D.Sc. (psychiatrist, professor of physiology, chief of the LPCCN)
Oguz Kelemen, M.D., Ph.D. (psychiatrist, chief physician, clinical director of the LPCCN)
Boglárka Bánsági, M.D. (neurologist, Ph.D. student, Semmelweis University)
Sándor Beniczky, M.D., Ph.D. (neurologist, chief physician, Danish Epilepsy Center, Dianalund, Denmark)
Nikoletta Bódi, M.D. (psychiatrist, Ph.D. student, Semmelweis University)
Gábor Braunitzer, M.Sc., Ph.D. (research fellow, University of Szeged)
Tamás Gyüre (graduate student, psychology, University of Szeged)
Imre Kiss, M.Sc. (psychologist, research fellow, National Psychiatry Center)
Einat Levy-Gigi, Ph.D. (psychologist, postdoctoral fellow, Rutgers University, Center for Molecular and Behavioral Neuroscience, Newark, USA; director: Prof. Mark A. Gluck)
Helga Nagy, M.D., Ph.D. (neurologist, Semmelweis University and Medical Rehabilitation Institute)
Renáta Németh (graduate student, psychology, University of Szeged)
Imola Seres, M.D. (staff physician, Semmelweis University)
Zsuzsanna Somali, M.D. (psychiatrist, Ph.D. student, Semmelweis University)

Representative publications illustrating research projects:#

1. Kéri S, Beniczky S, Kelemen O. Suppression of the P50 evoked response and neuregulin 1-induced AKT phosphorylation in first-episode schizophrenia. American Journal of Psychiatry 2010;167:444-450.
This study demonstrates a relationship between diminished suppression of the P50 auditory evoked potential, a sensory gating phenotype of schizophrenia, and neuregulin 1-induced activation of the phosphoinositide 3'-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3β system.

2. Kéri S, Moustafa AA, Myers CE, Benedek G, Gluck MA. α-Synuclein gene duplication impairs reward learning. Proceedings of the National Academy of Sciences of the USA 2010;107:15992-15994.
Duplication status of the α-Synuclein gene (a putative risk factor for Parkinson’s disease) is associated with impaired reward learning. Reward learning deficits precede the appearance of motor symptoms and major cognitive decline.

3. Kiss I, Fábián A, Benedek G, Kéri S. When doors of perception open: visual contrast sensitivity in never-medicated, first-episode schizophrenia. Journal of Abnormal Psychology 2010;119:586-593.
Patients with newly diagnosed schizophrenia exhibit increased contrast sensitivity on tasks biasing information processing towards the magnocellular visual pathway. Increased sensitivity is associated with anomalous perceptual experiences (illusions, distortions, and sensory overload).

4. Bódi N, Kéri S, Nagy H, Moustafa A, Myers CE, Daw N, Dibó G, Takáts A, Bereczki D, Gluck MA. Reward-learning and the novelty-seeking personality: a between- and within-subjects study of the effects of dopamine agonists on young Parkinson's patients. Brain 2009;132:2385-2395.
Dopamine agonists induce increased reward learning and diminished punishment learning in Parkinson’s disease. Increased reward learning is associated with more pronounced novelty-seeking personality traits after medication.

5. Kéri S, Kiss I, Kelemen O. Sharing secrets: oxytocin and trust in schizophrenia. Social Neuroscience 2009;4:287-293.
Patients with schizophrenia display social withdrawal in interpersonal situations requiring intimate trust (e.g., sharing personal secrets). Decreased trust is associated with lower oxytocin release.

University of Szeged, Faculty of Medicine, Department of Physiology:
http://www.phys.szote.u-szeged.hu/index.php?lap=0&id=en

National Psychiatry Center:
http://193.225.50.35/opk
http://gyemszi.hu/index_en.php



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