Prof. Dr. Stefan Remy
Assistant Professor, Group Leader
German Center for Neurodegenerative Diseases (DZNE)
BMZ 1 - Building 344
Sigmund-Freud-Str. 25
53105 Bonn
stefan.remy(at)dzne.de
+49 (0) 228 / 287-51605
+49 (0) 228 / 287-51619
More information
Areas of investigation/research focus
We study how neurons process neural input signals from upstream cells and convert them into output signals. This is an important step in understanding the function of neuronal networks and thus ultimately the healthy and diseased brain.
Signal processing in dendrites
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 imaging techniques and electrophysiology. With the help of the 2-photon uncaging of neurotransmitter molecules, we can simulate synaptic events with high spatial and temporal resolution.
The role of interneurons
The neurotransmitter GABA is released from different types of interneurons and has an inhibitory effect on the signal processing in the dendrites. The interplay of different interneurons leads to a temporally and spatially precise control of local GABA release at the dendritic tree of the target cell. Clinically relevant is a selective loss of specific types and of interneurons as well as neuromodulatory afferents in a variety of diseases of the central nervous system. It is therefore important to understand the impact of localized dendritic and somatic inhibition on the dendritic signal processing and to identify the underlying interneuron networks.
Disturbed signal processing in Alzheimer's disease
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 a neuronal network. It is very likely that such changes contribute to the cognitive deficits associated with neurodegenerative diseases.
Publications
Dendritic integration in hippocampal dentate granule cells.
Roland Krueppel, Stefan Remy, and Heinz Beck, Neuron, Volume 71, Issue 3, 512-528, 11 August 2011, DOI: 10.1016/j.neuron.2011.05.043
Upregulation of persistent Na+ current contributes to plasticity of intrinsic neuronal firing mode in hippocampal epileptogenesis.
Chen, S., Su, H., Yue, C., Remy, S.,, Sochivko, D., Beck, H., Yaari, Y, Journal of Neurophysiology 2010, October 27, doi:10.1152/jn.00184.2010
A Post-Burst Afterdepolarization Is Mediated by Group I Metabotropic Glutamate Receptor-Dependent Upregulation of Cav2.3 R-Type Calcium Channels in CA1 Pyramidal Neurons.
Park, J., Remy, S., Varela, J., Cooper D., Chung, S., Spruston N, PLoS Biology 2010, 8(11): e1000534. doi:10.137
Plasticity of voltage-gated ion channels in pyramidal cell dendrites
S Remy, H Beck, Y Yaari; Curr Opin Neurobiol. 2010 Aug;20(4):503-9. Epub 2010 Aug 4.
Intrinsic plasticity of dendritic excitability.
Remy, S., Beck, H., Yaari, Y, Current Opinion in Neurobiology, 2010 Aug;20(4):503-9. Übersichtsarbeit
Activity-dependent control of neuronal output by local and global dendritic spike attenuation.
Remy, S., Csicsvari, J., Beck, H, Neuron, 2009 ;61(6):906-16.
Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons.
Royeck, M., Horstmann, MT, Remy, S., Reitze, M.,Yaari, Y. Beck, H, Journal of Neurophysiology, 2008, 100(4):2361-80
Dendritic spikes induce single-burst long-term potentiation.
Remy, S. and Spruston, N, Proceedings of the National Academy of Sciences (PNAS) 2007, 104(43):17192-7
Molecular and cellular mechanisms of pharmacoresistance in epilepsy.
Remy, S., Beck H., 2006, Brain, 2006, 129:18-35. (Übersichtsarbeit)
Novel mechanisms underlying drug resistance in temporal lobe epilepsy.
Heinemann U., Kann O., Remy, S., Beck H. 2005, In Blume, WT (Editor): Intractable Epilepsies 1st edition, Lippincott Williams and Wilkins. (Buchkapitel)
Proximal persistent Na+ channels drive spike afterdepolarizations and associated bursting in adult rat CA1 pyramidal cells.
Yue C.*, Remy, S.*, Beck, H., Yaari, Y, Journal of Neuroscience 2005, 25(42):9704-20. *geteilte Erstautorenschaft
Mechanisms underlying drug resistance in epilepsy: Altered Pharmacosensitivity of Drug Targets.
Beck, H., Remy S, Epilepsy Research, 2004, 60,103. (Uebersichtsarbeit in Sonderbeitrag: W. Loescher, D. Schmidt: New Horizons in the Develeopment of antiepileptic drugs)
Modulation of voltage-dependent Na+ channels by the delta-agonist SNC80 in acutely isolated rat hippocampal neurons.
Remy, C., Remy, S., Beck, H., Swandulla, D., Hans, M, Neuropharmacology 2004, 47(12)
Molecular and functional changes in voltage-dependent Na+ channels following pilocarpine-induced status epilepticus in rat dentate granule cells.
Ellerkmann, R.K.*, Remy, S.*, Chen J., Sochivko D., Elger C.E., Urban B.W., Becker A., Beck, H, Neuroscience 2003, 119(2):323-33. *geteilte Erstautorenschaft
Anticonvulsant pharmacology of voltage-gated sodium channels in hippocampal pyramidal neurons of control and chronically epileptic rats.
Remy, S., Urban, B.W., Elger, C.E., Beck, H, European Journal of Neuroscience 2003, 17(12):2648-58
A novel mechanism underlying drug-resistance in chronic epilepsy.
Remy, S., Gabriel, S., Urban, B.W., Dietrich, D., Lehmann, T.N., Elger, C.E., Heinemann, U., Beck, H, Annals of Neurology 2003, 53(4):469-79