Tuesday, 28.03.2023 13:00

Neurobiology Lecture

 

Central neural network to defend life from environmental stresses

Prof. Kazuhiro Nakamura

Department of Integrative Physiology

Nagoya University

Japan

 

 

Hörsaal 2, INF306

ZOOM Meeting ID 880 7727 5856 Passcode 444344

 
29.03.2023 13:00

Neurobiology Lecture

 

From brain development to a disorder: Receptor signaling behind neurodevelopmental psychiatric disorders

Dr. Alena Salašová

Danish Research Institute of Translational Neuroscience

Aarhus, Denmark

 

Hörsaal 2, INF306

Hybrid: no

 

Psychiatric neurodevelopmental disorders (NDDs) is a group of commonly comorbid disorders including autism spectrum disorder, attention-deficit/hyperactivity disorder, Tourette’s syndrome, and some types of schizophrenia. These NDDs are manifested by impairments in social interaction, motor skills, memory, speech and non-verbal communication, and repetitive and often restricted behavior. Pathologically, NDDs are characterized by impaired development of several brain structures such as ventral midbrain, prefrontal cortex, striatum, hippocampus or cerebellum, which is caused by imbalance in neuronal populations, their connectivity, and thus their functionality. Notably, recent studies have reported that especially dysfunction of the dopaminergic system underlies several NDDs endophenotypes.

Recent genome-wide association studies identified VPS10p-D receptors SorCS2 and especially SorCS3 as cross-disorder risk genes for NDDs. These receptors regulate cell fate decisions, neuronal survival, neuronal wiring, and synaptic plasticity in central nervous system. VPS10p-domain receptors have a dual mode of action; either they control cellular signaling at the plasma membrane or they traffic different cargo molecules within the cell.

In this talk, I will present our new, unpublished discoveries on how SorCS2 and SorCS3 signal in embryonic brain and how their dysfunction affects dopaminergic lineage development. I will also discuss how these findings translate into NDDs impairments observed in patients.

Biosketch
I currently work as Assistant Professor at Aarhus University in Denmark. Throughout my carrier, my main scientific focus has been the identification of novel molecular mechanisms involved in cell communication and in the formation of brain circuits in the healthy and diseased brain. Particularly, I am specialized in Wnt signaling during tissue diversification and maturation of dopaminergic neurons. I defended my Bc and MSc degrees in Animal Physiology at Masaryk University (Czech Republic) after which I finalized my PhD degree in Medical Science at Karolinska Institute (Sweden). In 2018, I joined Prof. Anders Nykjaer’s lab in Aarhus University to carry on my research on brain development, SorCS receptor signaling, and psychiatric disorders.

 
Monday, 17.04.23 13:00

Neurobiology Lecture

 

Parallel processing streams through the hippocampus: Pattern separation, pattern completion, and landmark vector coding

James J. Knierim

Professor of Neuroscience, Krieger Mind/Brain Institute

Vice Chair for Education, Solomon H. Snyder Department of Neuroscience

Johns Hopkins University

Baltimore, USA

 

Rm.111, INF366 – please access via INF346

ZOOM Meeting ID 880 7727 5856 Passcode 444344

 
26.04.2023 13:00

Neurobiology Lecture

 

Prefrontal-hippocampal interactions for navigational simulations

Dr. Hiroshi Ito

Max Planck Institute for Brain Research

Frankfurt

 

SR25, INF368

 

Hybrid: no

 
19.07.2023 13.00

Neurobiology Lecture

 

Dr. Simona Lodato

HUNIMED,

Milan, Italy

 

SR25, INF368

 

Welcome to the IZN Home Page

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News...

2023 IZN Competition and Awards:

IZN Art Competition

IZN/Chica and Heinz Schaller Young Investigator Neuroscience Award

Foundation BrainAid IZN Master’s Award

Foundation BrainAid IZN Dissertation Award

 

Full details here Externer Inhalt


Dietmar Hopp Stiftung fördert Erforschung eines neuen Therapiekonzepts bei wiederkehrenden Hirntumoren mit 1,8 Millionen Euro

Neurochirurgische Universitätsklinik Heidelberg startet Projekt zu Kombinationstherapie bei nachgewachsenem Glioblastom: Können die zielgenaue Erhitzung über eine Lasersonde und Medikamententests an Minitumoren dazu beitragen, weiteres Tumorwachstum zu verlangsamen?

Glioblastome sind höchst aggressiHerold Mendeve Hirntumoren, die trotz intensiver Therapie nach wenigen Monaten nachwachsen. Um die Überlebenszeit von Patienten mit einem solchen Rezidiv zu verlängern, prüfen Medizinerinnen, Mediziner und Forschende der Neurochirurgischen Klinik am Universitätsklinikum Heidelberg (UKHD) nun im Rahmen einer klinischen Studie ein neuartiges Therapiekonzept: Der Erhitzung des Tumors mittels einer minimal-invasiv eingebrachten Lasersonde folgen personalisierte Medikamententests an Miniversionen des Patiententumors. An diesen sogenannten Tumororganoiden können mehrere Medikamente gleichzeitig getestet und die wirksamsten identifiziert werden. Das Team um die Projektleiter Privatdozent Dr. Martin Jakobs und Professorin Dr. Christel Herold-Mende entwickelte dazu eigens ein Verfahren, um die Minitumoren aus den geringen Gewebemengen, die im Rahmen der Laserbehandlung entnommen werden, herzustellen. Die Dietmar Hopp Stiftung fördert die nun gestartete Behandlungsstudie, in die bis zu 30 Patientinnen und Patienten eingeschlossen werden sollen, sowie die Medikamententests an den patientenindividuellen Tumororganoiden vier Jahre lang mit insgesamt 1,8 Millionen Euro. Mehr... Externer Inhalt


Spotlight: Using light and sound to see into the brain

Researchers in the Prevedel Group use this spectroscopy setup to test and optimise photoacoustic probes before their usage in mouse neuroscience.

Photoacoustic spectroscopy provides information about the photoacoustic efficiency of probes, which is a measure of how strongly they generate a photoacoustic signal in the presence of calcium. The custom setup built by the Prevedel Lab measures the photoacoustic signal of specially developed calcium-sensitive molecules in order to steer their development, which is performed by the Deo group at EMBL. These molecules can be used to visualise brain activity with photoacoustic imaging, which allows the scientists to go much deeper into a brain region than other light-based neuroimaging methods. More... Externer Inhalt


Drug alleviates autism-associated behavior in mice

The behavioral disorders observed in autism are associated with a multitude of genetic alterations. Scientists from the Hector Institute for Translational Brain Research (HITBR)* have now found another molecular cause for this condition. The transcription factor MYT1L normally protects the molecular identity of nerve cells. If it is genetically switched off in human nerve cells or in mice, the functional changes and symptoms typical of autism occur. A drug that blocks sodium channels in the cell membrane can reverse the consequences of MYT1L failure and alleviate the functional and behavioral abnormalities in mice.

Moritz Mall from the Hector Institute for Translational Brain Research (HITBR) has long been researching the role of the protein MYT1L in various neuronal diseases. The protein is a so-called transcription factor that decides which genes are active in the cell and which are not. Almost all nerve cells in the body produce MYT1L throughout their entire life span.

Mall had already shown a few years ago that MYT1L protects the identity of nerve cells by suppressing other developmental pathways that programme a cell towards muscle or connective tissue, for example. Mutations in MYT1L have been found in several neurological diseases, such as schizophrenia and epilepsy, but also in brain malformations. In their current work, which is funded by the European Research Council ERC, Mall and his team examined the exact role of the "guardian of neuronal identity" in the development of an ASD. To do this, they genetically switched off MYT1L - both in mice and in human nerve cells that had been derived from reprogrammed stem cells in the laboratory. More... Externer Inhalt


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Open positions at the IZN

  • The Department for Molecular and Cellular Cognition Research (Dr. Ana Oliveira) at the Central Institute of Mental Health (Mannheim, Germany) offers a PhD student position in molecular mechanisms of learning and memory. Adobe
    Posted 02.2023

  • The Department for Molecular and Cellular Cognition Research (Dr. Ana Oliveira) at the Central Institute of Mental Health (Mannheim, Germany) offers a Postdoctoral position in molecular mechanisms of learning and memory. Adobe
    Posted 02.2023

  • Prof. Jan Siemens' lab is looking for a motivated Doctoral Student with an interest in studying neuronal pathways and cell-molecular mechanisms of pain sensation. Experimental work will include using the mouse as a model system combined with multidisciplinary ex-vivo and in vivo approaches, such as metabolic analysis / metabolic flux measurements, genetic mouse models, behavior experiments and testing of experimental analgesic drug candidates targeting a metabolic signaling pathway. Adobe
    Posted 11.2022


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Contact

 

IZN Managing Director:
Prof. Dr. Hilmar Bading
IZN-Neurobiology, University of Heidelberg
Im Neuenheimer Feld 366, 1.OG
D-69120 Heidelberg, Germany

Phone:  +49 - 6221 - 54 16500
Fax:  +49 - 6221 - 54 16524
email:  Bading@nbio.uni-heidelberg.de

 

IZN Administration & Information:
Antje König
IZN-Neurobiology, University of Heidelberg
Im Neuenheimer Feld 366, 1.OG
D-69120 Heidelberg, Germany

Phone:  +49 - 6221 - 54 16501
Fax:  +49 - 6221 - 54 16524
email:  Sekretariat@nbio.uni-heidelberg.de

 

IZN Coordinator:
Dr. Anna Hertle
IZN-Neurobiology, University of Heidelberg
Im Neuenheimer Feld 366, 1.OG
D-69120 Heidelberg, Germany

Phone:  +49 - 6221 - 54 16502
Fax:  +49 - 6221 - 54 16524
email:  IZN.Coordinator@uni-heidelberg.de

 

IZN PhD Programme Coordinators:
Prof. Christoph Schuster
IZN Graduate School, University of Heidelberg
Im Neuenheimer Feld 366, 1.OG
D-69120 Heidelberg, Germany

Phone:  +49 - 6221 - 54 16503
Fax:  +49 - 6221 - 54 16524
email:  IZN-GradSchool@uni-heidelberg.de

 

 

Webmaster contact: WebmasterIZN@uni-heidelberg.de
Latest Revision: 2023-03-15
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