Max Planck Institute of Neurobiology
Max Planck Institute of Neurobiology
The Max Planck Institute of Neurobiology is a research institute of the Max Planck Society located in Martinsried, a suburb of Munich in Germany. Research centers on the basic mechanisms and functions of the developing and adult nervous system. Main focus areas include the mechanisms of information processing and storage. It is one of 80 institute in the Max Planck Society . Wikipedia.
Held K.,Max Planck Institute of Neurobiology
Journal of neurovirology | Year: 2011
Although recurrent Herpes simplex virus type 1 (HSV-1) infections are quite common in humans, little is known about the exact molecular mechanisms involved in latency and reactivation of the virus from its stronghold, the trigeminal ganglion. After primary infection, HSV-1 establishes latency in sensory neurons, a state that lasts for the life of the host. Reactivation of the virus leads to recurrent disease, ranging from relatively harmless cold sores to ocular herpes. If herpes encephalitis-often a devastating disease-is also caused by reactivation or a new infection, is still a matter of debate. It is widely accepted that CD8(+) T cells as well as host cellular factors play a crucial role in maintaining latency. At least in the animal model, IFNγ and Granzyme B secretion of T cells were shown to be important for control of viral latency. Furthermore, the virus itself expresses factors that regulate its own latency-reactivation cycle. In this regard, the latency associated transcript, immediate-early proteins, and viral miRNAs seem to be the key players that control latency and reactivation on the viral side. This review focuses on HSV-1 latency in humans in the light of mechanisms learned from animal models.
Kurschus F.C.,Johannes Gutenberg University Mainz |
Jenne D.E.,Max Planck Institute of Neurobiology
Immunological Reviews | Year: 2010
Granzyme B (GzmB) is used by cytotoxic lymphocytes as a molecular weapon for the defense against virus-infected and malignantly transformed host cells. It belongs to a family of small serine proteases that are stored in secretory vesicles of killer cells. After secretion of these cytolytic granules during killer cell attack, GzmB is translocated into the cytosol of target cells with the help of the pore-forming protein perforin. GzmB has adopted similar protease specificity as caspase-8, and once delivered, it activates major executioner apoptosis pathways. Since GzmB is very effective in killing human tumor cell lines that are otherwise resistant against many cytotoxic drugs and since GzmB of human origin can be recombinantly expressed, its use as part of a 'magic bullet' in tumor therapy is a very tempting idea. In this review, we emphasize the peculiar characteristics of GzmB that make it suited for use as an effector domain in potential immunoconjugates. We discuss what is known about its uptake into target cells and the trials performed with GzmB-armed immunoconjugates, and we assess the prospects of its potential therapeutic value. © 2010 John Wiley & Sons A/S.
Berer K.,Max Planck Institute of Neurobiology |
Krishnamoorthy G.,Max Planck Institute of Neurobiology
Acta Neuropathologica | Year: 2012
Multiple sclerosis (MS) and other chronic inflammatory autoimmune diseases represent major public health challenges in industrialised Western society. MS results from an autoimmune attack against myelin structures by self-reactive lymphocytes, which are normal components of the healthy immune repertoire. The nature of the triggers that convert the innocuous self-reactive lymphocytes into an autoaggressive phenotype is poorly understood. In the past, it was primarily suspected that pathogenic infections trigger MS. However, so far, none of the incriminated pathogenic microbes were firmly associated with the disease. A growing body of evidence in animal models of MS implicates the gut microbiota in the induction of central nervous system (CNS) autoimmunity. The mammalian gut harbors a diverse population of microbial organisms which are essential for our well being. There is an increasing understanding that the gut microbiota not only modulates the local immune functions but also affects the systemic immune system. We are only just beginning to understand the nature of the interactions of the gut microbiota with the host's immune system especially in the context of autoimmune diseases. This review will address the influence of intestinal microbiota on immune homeostasis and on the development of autoimmune responses at sites distal to the intestine with a particular emphasis placed on a discussion about CNS autoimmunity. © Springer-Verlag 2012.
Scheuss V.,Max Planck Institute of Neurobiology |
Bonhoeffer T.,Max Planck Institute of Neurobiology
Cerebral Cortex | Year: 2014
The majority of γ-aminobutyric acid (GABA)ergic interneurons have smooth dendrites with no or only few dendritic spines, but certain types of spiny GABAergic interneurons do actually contain substantial numbers of spines. The explanation for such spines has so far been purely structural: They increase the dendritic surface area and thus provide the opportunity to accommodate larger numbers of synapses. We reasoned that there may be specific functional properties for these spines and therefore, undertook to characterize interneuron spines functionally. We find a remarkable similarity to pyramidal cell spines: They receive excitatory synapses with calcium impermeable α-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors, compartmentalize biochemical signals, and display activity-dependent morphological plasticity. Nevertheless, notable differences in spine density, neck length, and spine-dendrite coupling exist. Thus, dendritic spines on inhibitory interneurons have a number of important functional properties that go substantially beyond simply expanding the dendritic surface area. It therefore seems likely that spiny and aspiny interneurons may have very different roles in neural circuit function and plasticity. © The Author 2013. Published by Oxford University Press.
Borst A.,Max Planck Institute of Neurobiology |
Helmstaedter M.,Max Planck Institute for Brain Research
Nature Neuroscience | Year: 2015
Motion-sensitive neurons have long been studied in both the mammalian retina and the insect optic lobe, yet striking similarities have become obvious only recently. Detailed studies at the circuit level revealed that, in both systems, (i) motion information is extracted from primary visual information in parallel ON and OFF pathways; (ii) in each pathway, the process of elementary motion detection involves the correlation of signals with different temporal dynamics; and (iii) primary motion information from both pathways converges at the next synapse, resulting in four groups of ON-OFF neurons, selective for the four cardinal directions. Given that the last common ancestor of insects and mammals lived about 550 million years ago, this general strategy seems to be a robust solution for how to compute the direction of visual motion with neural hardware. © 2015 Nature America, Inc. All rights reserved.
Borst A.,Max Planck Institute of Neurobiology
European Journal of Neuroscience | Year: 2014
Detecting the direction of image motion is important for visual navigation as well as predator, prey and mate detection and, thus, essential for the survival of all animals that have eyes. However, the direction of motion is not explicitly represented at the level of the photoreceptors: it rather needs to be computed by subsequent neural circuits, involving a comparison of the signals from neighbouring photoreceptors over time. The exact nature of this process as implemented at the neuronal level has been a long-standing question in the field. Only recently, much progress has been made in Drosophila by genetically targeting individual neuron types to block, activate or record from them. The results obtained this way indicate that: (i) luminance information from fly photoreceptors R1-6 is split into two parallel motion circuits, specialized to detect the motion of luminance increments (ON-Channel) and decrements (OFF-Channel) separately; (ii) lamina neurons L1 and L2 are the primary input neurons to these circuits (L1 → ON-channel, L2 → OFF-channel); and (iii) T4 and T5 cells carry their output signals (ON → T4, OFF → T5). © 2014 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
Klein R.,Max Planck Institute of Neurobiology
Development (Cambridge) | Year: 2012
Eph receptors and their membrane-tethered ligands have important functions in development. Trans interactions of Eph receptors with ephrins at cell-cell interfaces promote a variety of cellular responses, including repulsion, attraction and migration. Eph-ephrin signalling can be bi-directional and controls actin cytoskeleton dynamics, thereby leading to changes in cellular shape. This article provides an overview of the general structures and signalling mechanisms, and of typical developmental functions along with cell biological principles. © 2012. Published by The Company of Biologists Ltd.
Hubener M.,Max Planck Institute of Neurobiology |
Bonhoeffer T.,Max Planck Institute of Neurobiology
Cell | Year: 2014
Neuronal plasticity in the brain is greatly enhanced during critical periods early in life and was long thought to be rather limited thereafter. Studies in primary sensory areas of the neocortex have revealed a substantial degree of plasticity in the mature brain, too. Often, plasticity in the adult neocortex lies dormant but can be reactivated by modifications of sensory input or sensory-motor interactions, which alter the level and pattern of activity in cortical circuits. Such interventions, potentially in combination with drugs targeting molecular brakes on plasticity present in the adult brain, might help recovery of function in the injured or diseased brain. ©2014 Elsevier Inc.
Helmstaedter M.,Max Planck Institute of Neurobiology
Nature Methods | Year: 2013
Neuronal networks are high-dimensional graphs that are packed into three-dimensional nervous tissue at extremely high density. Comprehensively mapping these networks is therefore a major challenge. Although recent developments in volume electron microscopy imaging have made data acquisition feasible for circuits comprising a few hundreds to a few thousands of neurons, data analysis is massively lagging behind. The aim of this perspective is to summarize and quantify the challenges for data analysis in cellular-resolution connectomics and describe current solutions involving online crowd-sourcing and machine-learning approaches. © 2013 Nature America, Inc. All rights reserved.
Baier H.,Max Planck Institute of Neurobiology
Annual Review of Cell and Developmental Biology | Year: 2013
Synaptic connections between neurons form the basis for perception and behavior. Synapses are often clustered in space, forming stereotyped layers. In the retina and optic tectum, multiple such synaptic laminae are stacked on top of each other, giving rise to stratified neuropil regions in which each layer combines synapses responsive to a particular sensory feature. Recently, several cellular and molecular mechanisms that underlie the development of multilaminar arrays of synapses have been discovered. These mechanisms include neurite guidance and cell-cell recognition. Molecules of the Slit, Semaphorin, Netrin, and Hedgehog families, binding to their matching receptors, bring axons and dendrites into spatial register. These guidance cues may diffuse over short distances or bind to sheets of extracellular matrix, thus conditioning the local extracellular milieu, or are presented on the surface of cells bordering the future neuropil. In addition, mutual recognition of axons and dendrites through adhesion molecules with immunoglobulin domains ensures cell type-specific connections within a given layer. Thus, an elaborate genetic program assembles the parallel processing channels that underlie visual perception. © 2013 by Annual Reviews. All rights reserved.