Professor Dr. Stefan Remy

Neuronal Networks
German Center for Neurodegenerative Diseases (DZNE) Bonn
Ludwig-Erhard-Allee 2
D- 53175 Bonn
and
Department of Epileptology
University of Bonn Medical School

Office:
c/o Biomedizinisches Zentrum 1
Sigmund-Freud-Str. 25
D- 53127 Bonn

Phone +49  (0) 228 287-51605
Fax: +49 (0) 228 287-51619

Website Remy Group
Website DZNE

Curriculum vitae Professor Dr. Stefan Remy

Research Interests

Dendritic integration of synaptic signals
Neurons form branched extensions, so called dendrites, which receive more than 95% of the input signals from other neurons. Signal processing depends on the properties and structure of these small-caliber   dendrites. Changes in the way in which neurons process synaptic information form the cellular basis of learning and memory. Although the central role of dendrites in signal integration and synaptic plasticity has been recognized for decades, it has only become possible recently to study the properties of even the finest dendrites by modern two-photon and STED imaging techniques and electrophysiology (see Remy and Spruston 2007, Remy et al. 2009, Müller et al, 2012, Siskova et al, 2014).

Neural circuits underlying cognitive map formation
The hippocampal formation is an important part of our memory systems. It receives and processes external information about our environment and our position in space and uses this information to form and retrieve memories. We study the neural circuits that feed spatial information into our memory systems and try to understand the circuit operations that lead to memory formation and retrieval. The brain uses oscillations of hundreds of neurons, which can be visualized in an EEG or local field potential recordings, to coordinate the information flow during processing of spatial information. One important focus of our work is to understand how oscillations are generated and maintained during behavior (see Fuhrmann et al. 2015). We use two-photon GECI imaging,  whole-cell patch-clamp recordings, single-unit tetrode recordings, LFP recordings and fiberoptometry during behavior to address these questions.

Dysfunction of neurons and neural circuits in neurodegenerative diseases
Alzheimer’s disease is the most common form of dementia, the risk for its development increases with each decade of adult life. It affects memory, thinking and behavior. At the present time no satisfying therapeutic approach exists to prevent the disease-related changes. A prerequisite for the development of such therapies is to gain a better understanding of the underlying molecular and structural disease-related changes of individual neuronal compartments such as single synapses on dendritic spines and dendrites. Even the smallest changes in the processing of synaptic signals can easily lead to a change in the output signal and thus cause a disturbance of the function of an entire neuronal network (see Siskova et al, 2014). On the network level, a balanced interplay of excitatory neurons and inhibitory interneurons is required to direct the information flow through our memory systems and to form and retrieve memories. Clinically relevant is a selective loss of specific types and of interneurons as well as neuromodulatory afferents in Alzheimer’s disease and other neurodegenerative diseases. We use computational, imaging and electrophysiological techniques to understand the structural and functional neural circuit remodeling that leads to cognitive dysfunction in neurodegenerative diseases (see Siskova et al, 2014).

Techniques

We are using advanced electrophysiological techniques combined with multiphoton imaging in brain slices and in vivo. We study the functional organization of neural networks in behaving rodents on the single cell and population level in a virtual environment.

5  most important publications

1.    Fuhrmann F*, Justus D*, Sosulina L, Kaneko H, Beutel T, Friedrichs D, Schoch S, Schwarz MK, Fuhrmann M, Remy S. (2015) Locomotion, Theta oscillations, and the speed-correlated firing of hippocampal neurons are controlled by a medial septal glutamatergic circuit. Neuron, 86(5): 1253-1264. (*equal contribution).

2. Šišková Z, Justus D, Kaneko H, Friedrichs D, Henneberg N, Beutel T, Pitsch J, Schoch S, Becker A, von der Kammer H, Remy S. (2014) Dendritic structural degeneration is functionally linked to cellular hyperexcitability in a mouse model of Alzheimer’s Disease. Neuron, 84(5): 1023-1033.

3. Müller C, Beck H, Coulter D, Remy S. (2012) Inhibitory control of linear and supralinear dendritic excitation in CA1 pyramidal neurons. Neuron, 75(5):851-64.

4. Remy S, Csicsvari J, Beck H. (2009) Activity-dependent control of neuronal output by local and global dendritic spike attenuation. Neuron, 61(6): 906-916.

5. Remy S, Spruston N. (2007) Dendritic spikes induce single-burst long-term potentiation. PNAS, 104(43): 17192-17197.