Max Planck Institute for Experimental Medicine
Gottingen, Germany

The Max Planck Institute of Experimental Medicine is located in Göttingen, Germany. It was founded as Kaiser Wilhelm Institute for Medical Research in 1947, and was renamed in 1965. It is one of 80 institutes in the Max Planck Society . Prof. Dr. Klaus-Armin Nave is currently the acting director of the institute. Wikipedia.

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Kawabe H.,Max Planck Institute for Experimental Medicine | Brose N.,Max Planck Institute for Experimental Medicine
Nature Reviews Neuroscience | Year: 2011

Nerve cell development in the brain is a tightly regulated process. The generation of neurons from precursor cells, their migration to the appropriate target sites, their extensive arborization and their integration into functional networks through synapse formation and refinement are governed by multiple interdependent signalling cascades. The function and turnover of proteins involved in these signalling cascades, in turn, are spatially and temporally controlled by ubiquitylation. Recent advances have provided first insights into the highly complex and intricate molecular pathways that regulate ubiquitylation during all stages of neural development and that operate in parallel with other regulatory processes such as phosphorylation or cyclic nucleotide signalling. © 2011 Macmillan Publishers Limited. All rights reserved.

Nave K.-A.,Max Planck Institute for Experimental Medicine
Nature Reviews Neuroscience | Year: 2010

In addition to their role in providing myelin for rapid impulse propagation, the glia that ensheath long axons are required for the maintenance of normal axon transport and long-term survival. This presumably ancestral function seems to be independent of myelin membrane wrapping. Here, I propose that ensheathing glia provide trophic support to axons that are metabolically isolated, and that myelin itself might cause such isolation. This glial support of axonal integrity may be relevant for a number of neurological and psychiatric diseases. © 2010 Macmillan Publishers Limited. All rights reserved.

Mei L.,Georgia Regents University | Mei L.,Charlie Norwood Medical Center | Nave K.-A.,Max Planck Institute for Experimental Medicine
Neuron | Year: 2014

Neuregulins (NRGs) comprise a large family of growth factors that stimulate ERBB receptor tyrosine kinases. NRGs and their receptors, ERBBs, have been identified as susceptibility genes for diseases such as schizophrenia (SZ) and bipolar disorder. Recent studies have revealed complex Nrg/Erbb signaling networks that regulate the assembly of neural circuitry, myelination, neurotransmission, and synaptic plasticity. Evidence indicates there is an optimal level of NRG/ERBB signaling in the brain and deviation from it impairs brain functions. NRGs/ERBBs and downstream signaling pathways may provide therapeutic targets for specific neuropsychiatric symptoms. Neuregulins (NRGs) comprise a family of growth factors that activate ERBB receptor kinases. Mei and Nave review the role of Nrg-Erbb signaling in neural development, myelination, and synaptic plasticity and the possible contribution of abnormal NRG1 signaling to brain disorders. © 2014 Elsevier Inc.

Gutig R.,Max Planck Institute for Experimental Medicine
Science | Year: 2016

The brain routinely discovers sensory clues that predict opportunities or dangers. However, it is unclear how neural learning processes can bridge the typically long delays between sensory clues and behavioral outcomes. Here, I introduce a learning concept, aggregatelabel learning, that enables biologically plausible model neurons to solve this temporal credit assignment problem. Aggregate-label learning matches a neuron's number of output spikes to a feedback signal that is proportional to the number of clues but carries no information about their timing. Aggregate-label learning outperforms stochastic reinforcement learning at identifying predictive clues and is able to solve unsegmented speech-recognition tasks. Furthermore, it allows unsupervised neural networks to discover reoccurring constellations of sensory features even when they are widely dispersed across space and time.

Nave K.-A.,Max Planck Institute for Experimental Medicine | Werner H.B.,Max Planck Institute for Experimental Medicine
Annual review of cell and developmental biology | Year: 2014

Myelination of axons in the nervous system of vertebrates enables fast, saltatory impulse propagation, one of the best-understood concepts in neurophysiology. However, it took a long while to recognize the mechanistic complexity both of myelination by oligodendrocytes and Schwann cells and of their cellular interactions. In this review, we highlight recent advances in our understanding of myelin biogenesis, its lifelong plasticity, and the reciprocal interactions of myelinating glia with the axons they ensheath. In the central nervous system, myelination is also stimulated by axonal activity and astrocytes, whereas myelin clearance involves microglia/macrophages. Once myelinated, the long-term integrity of axons depends on glial supply of metabolites and neurotrophic factors. The relevance of this axoglial symbiosis is illustrated in normal brain aging and human myelin diseases, which can be studied in corresponding mouse models. Thus, myelinating cells serve a key role in preserving the connectivity and functions of a healthy nervous system.

Gutig R.,Max Planck Institute for Experimental Medicine
Current Opinion in Neurobiology | Year: 2014

Recent experimental reports have suggested that cortical networks can operate in regimes were sensory information is encoded by relatively small populations of spikes and their precise relative timing. Combined with the discovery of spike timing dependent plasticity, these findings have sparked growing interest in the capabilities of neurons to encode and decode spike timing based neural representations. To address these questions, a novel family of methodologically diverse supervised learning algorithms for spiking neuron models has been developed. These models have demonstrated the high capacity of simple neural architectures to operate also beyond the regime of the well established independent rate codes and to utilize theoretical advantages of spike timing as an additional coding dimension. © 2014.

Burgalossi A.,Max Planck Institute for Experimental Medicine
Nature protocols | Year: 2012

Neurotransmitter release is triggered by membrane depolarization, Ca(2+) influx and Ca(2+) sensing by the release machinery, causing synaptic vesicle (SV) fusion with the plasma membrane. Interlinked is a complex membrane cycle in which vesicles are tethered to the release site, primed, fused and recycled. As many of these processes are Ca(2+) dependent and simultaneously occurring, it is difficult to dissect them experimentally. This problem can be partially circumvented by controlling synaptic Ca(2+) concentrations via UV photolysis of caged Ca(2+). We developed a culture protocol for Ca(2+) uncaging in small synapses on the basis of the generation of small glia cell islands with single neurons on top, which are sufficiently small to be covered with a UV-light flash. Neurons are loaded with the photolabile Ca(2+)-chelator nitrophenyl-EGTA and Ca(2+) indicators, and a UV flash is used to trigger Ca(2+)-uncaging and SV fusion. The protocol takes three weeks to complete and provides unprecedented insights into the mechanisms of transmitter release.

Bakhti M.,Max Planck Institute for Experimental Medicine
Cellular and molecular life sciences : CMLS | Year: 2014

Rapid nerve conduction requires the coating of axons by a tightly packed multilayered myelin membrane. In the central nervous system, myelin is formed from cellular processes that extend from oligodendrocytes and wrap in a spiral fashion around an axon, resulting in the close apposition of adjacent myelin membrane bilayers. In this review, we discuss the physical principles underlying the zippering of the plasma membrane of oligodendrocytes at the cytoplasmic and extracellular leaflet. We propose that the interaction of the myelin basic protein with the cytoplasmic leaflet of the myelin bilayer triggers its polymerization into a fibrous network that drives membrane zippering and protein extrusion. In contrast, the adhesion of the extracellular surfaces of myelin requires the down-regulation of repulsive components of the glycocalyx, in order to uncover weak and unspecific attractive forces that bring the extracellular surfaces into close contact. Unveiling the mechanisms of myelin membrane assembly at the cytoplasmic and extracelluar sites may help to understand how the myelin bilayers are disrupted and destabilized in the different demyelinating diseases.

Pardo L.A.,Max Planck Institute for Experimental Medicine | Stuhmer W.,Max Planck Institute for Experimental Medicine
Nature Reviews Cancer | Year: 2014

Potassium channels are transmembrane proteins that selectively facilitate the flow of potassium ions down an electrochemical gradient. These molecules have been studied in great detail in the context of cell excitability, but their roles in less cell type-specific functions, such as cell proliferation, angiogenesis or cell migration, have only recently been assessed. Moreover, the importance of these channels for tumour biology has become evident. This, coupled with the fact that they are accessible proteins and that their pharmacology is well characterized, has increased the interest in investigating potassium channels as therapeutic targets in cancer patients.

Nave K.-A.,Max Planck Institute for Experimental Medicine
Nature | Year: 2010

The myelination of axons by glial cells was the last major step in the evolution of cells in the vertebrate nervous system, and white-matter tracts are key to the architecture of the mammalian brain. Cell biology and mouse genetics have provided insight into axon-glia signalling and the molecular architecture of the myelin sheath. Glial cells that myelinate axons were found to have a dual role by also supporting the long-term integrity of those axons. This function may be independent of myelin itself. Myelin abnormalities cause a number of neurological diseases, and may also contribute to complex neuropsychiatric disorders. © 2010 Macmillan Publishers Limited. All rights reserved.

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