Max Planck Institute for Brain Research

Frankfurt am Main, Germany

Max Planck Institute for Brain Research

Frankfurt am Main, Germany

The Max Planck Institute for Brain Research is located in Frankfurt, Germany. It was founded as Kaiser Wilhelm Institute for Brain Research in Berlin 1914, moved to Frankfurt-Niederrad in 1962 and more recently in a new building in Frankfurt-Riedberg. It is one of 83 institutes in the Max Planck Society . Wikipedia.

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News Article | December 8, 2016

The German Research Foundation (DFG) will be providing financial support to the Collaborative Research Center (CRC) 1080 on "Molecular and cellular mechanisms of neuronal homeostasis" for four more years. In addition to Johannes Gutenberg University Mainz (JGU), Goethe University Frankfurt as the CRC's speaker university, the Max Planck Institute for Brain Research, and the Mainz-based Institute of Molecular Biology (IMB) are participating in this research center. A total of some EUR 12 million is being made available in the new funding period that will commence on January 1, 2017. CRC 1080 was established on January 1, 2013 with Johannes Gutenberg University Mainz acting as the speaker university. With the commencement of the new funding phase, the speaker role will be transferred to Frankfurt University which, as a member of the Rhine-Main Neuroscience Network (rmn²), is participating in the CRC with its own research projects. The future coordinator of the CRC, Professor Amparo Acker-Palmer, heads up the Frankfurt Institute for Cell Biology and Neurosciences and is also a fellow of the Gutenberg Research College (GRC) at JGU. Professor Heiko Luhmann, Director of the Institute of Physiology at the Mainz University Medical Center, will take up the post of deputy coordinator. The purpose of the CRC on "Molecular and cellular mechanisms of neuronal homeostasis" is to study the molecular and cellular interactions that enable the brain to maintain a state of functional equilibrium, otherwise known as network homeostasis. New findings should contribute to understanding disease processes in the brain, thus providing insights in the development of innovative new therapies. This might even include the creation of new pharmaceutical agents that could be used to treat cerebral disorders in humans. Specifically, the researchers working at the CRC are investigating different classes of molecules, such as those involved in the control of cell-to-cell interactions and signaling processes. "The extension of funding of the Collaborative Research Center 1080, which studies aspects that offer great potential benefits to society, owes much to our very productive and collaborative research endeavors," pointed out the Chief Scientific Officer of the Mainz University Medical Center, Professor Ulrich Förstermann.

Ernsberger U.,Max Planck Institute for Brain Research
Cell and Tissue Research | Year: 2015

With the establishment of the ‘neuron theory’ at the turn of the twentieth century, this remarkably powerful term was introduced to name a breathtaking diversity of cells unified by a characteristic structural compartmentalization and unique information processing and propagating features. At the beginning of the twenty-first century, developmental, stem cell and reprogramming studies converged to suggest a common mechanism involved in the generation of possibly all vertebrate, and at least a significant number of invertebrate, neurons. Sox and, in particular, SoxB and SoxC proteins as well as basic helix-loop-helix proteins play major roles, even though their precise contributions to progenitor programming, proliferation and differentiation are not fully resolved. In addition to neuronal development, these transcription factors also regulate sensory receptor and endocrine cell development, thus specifying a range of cells with regulatory and communicative functions. To what extent microRNAs contribute to the diversification of these cell types is an upcoming question. Understanding the transcriptional and post-transcriptional regulation of genes coding for cell type-specific cytoskeletal and motor proteins as well as synaptic and ion channel proteins, which mark differences but also similarities between the three communicator cell types, will provide a key to the comprehension of their diversification and the signature of ‘generic neuronal’ differentiation. Apart from the general scientific significance of a putative universal core instruction for neuronal development, the impact of this line of research for cell replacement therapy and brain tumor treatment will be of considerable interest. © 2014, Springer-Verlag Berlin Heidelberg.

Analysis of transcription factor function during neurogenesis has provided a huge amount of data on the generation and specification of diverse neuron populations in the central and peripheral nervous systems of vertebrates. However, an understanding of the induction of key neuron functions including electrical information processing and synaptic transmission lags seriously behind. Whereas pan-neuronal markers such as neurofilaments, neuron-specific tubulin and RNA-binding proteins have often been included in developmental analysis, the molecular players underlying electrical activity and transmitter release have been neglected in studies addressing gene expression during neuronal induction. Here, I summarize the evidence for a distinct accumulation pattern of mRNAs for synaptic proteins, a pattern that is delayed compared with pan-neuronal gene expression during neurogenesis. The conservation of this pattern across diverse avian and mammalian neuron populations suggests a common mechanism for the regulation of various sets of neuronal genes during initial neuronal differentiation. The co-regulation of genes coding for synaptic proteins from embryonic to postnatal development indicates that the expression of the players required for synaptic transmission shares common regulatory features. For the ion channels involved in neuronal electrical activity, such as voltage-gated sodium channels, the situation is less clear because of the lack of comparative studies early during neurogenesis. Transcription factors have been characterized that regulate the expression of synaptic proteins in vitro and in vivo. They currently do not explain the co-regulation of these genes across different neuron populations. The neuron-restrictive silencing factor NRSF/REST targets a large gene set, but not all of the genes coding for pan-neuronal, synaptic and ion channel proteins. The discrepancy between NRSF/REST loss-of-function and silencer-to-activator-switch studies leaves the full functional implications of this factor open. Together with microRNAs, splicing regulators, chromatin remodellers and an increasing list of transcriptional regulators, the factor is embedded in feedback circuits with the potential to orchestrate neuronal differentiation. The precise regulation of the coordinated expression of proteins underlying key neuronal functions by these circuits during neuronal induction is a major emerging topic. © 2012 Springer-Verlag.

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.

Fournier J.,Max Planck Institute for Brain Research | Muller C.M.,Max Planck Institute for Brain Research | Laurent G.,Max Planck Institute for Brain Research
Current Opinion in Neurobiology | Year: 2015

Despite considerable effort over a century and the benefit of remarkable technical advances in the past few decades, we are still far from understanding mammalian cerebral neocortex. With its six layers, modular architecture, canonical circuits, innumerable cell types, and computational complexity, isocortex remains a challenging mystery. In this review, we argue that identifying the structural and functional similarities between mammalian piriform cortex and reptilian dorsal cortex could help reveal common organizational and computational principles and by extension, some of the most primordial computations carried out in cortical networks. © 2014 Elsevier Ltd.

Uhlhaas P.J.,University of Glasgow | Singer W.,Max Planck Institute for Brain Research | Singer W.,Ernst Strüngmann Institute (ESI) for Neuroscience | Singer W.,Goethe University Frankfurt
Biological Psychiatry | Year: 2015

A considerable body of work over the last 10 years combining noninvasive electrophysiology (electroencephalography/magnetoencephalography) in patient populations with preclinical research has contributed to the conceptualization of schizophrenia as a disorder associated with aberrant neural dynamics and disturbances in excitation/inhibition balance. This complements previous research that has largely focused on the identification of abnormalities in circumscribed brain regions and on disturbances of dopaminergic mechanisms as a cause of positive symptoms and executive deficits. In the current review, we provide an update on studies focusing on aberrant neural dynamics. First, we discuss the role of rhythmic activity in neural dynamics and in the coordination of distributed neuronal activity into organized neural states. This is followed by an overview on the current evidence for impaired neural oscillations and synchrony in schizophrenia and associated abnormalities in gamma-aminobutyric acidergic and glutamatergic neurotransmission. Finally, we discuss the distinction between fundamental symptoms, which are reflected in cognitive deficits, and psychotic, accessory symptoms, the latter likely constituting a compensatory response for aberrant neuronal dynamics. © 2015 Society of Biological Psychiatry.

Opitz B.,Saarland University | Kotz S.A.,Max Planck Institute for Brain Research
Cortex | Year: 2012

Introduction: Recent functional magnetic resonance imaging (fMRI) evidence shows differential involvement of the inferior frontal gyrus (IFG) and the ventral premotor cortex (PMv) in syntactic processing. Our main goal is to specify the precise role of the PMv in the processing of sequential structures and whether these processes are a necessary prerequisite for the successful acquisition of grammatical structure. Methods: We tested patients with PMv lesions in an artificial grammar (AG) learning task, including correct sentences and sentences with violations of local (referring to adjacent elements within an AG string) and long-distance dependencies (incorporating recursive structures). In addition to performance measures event-related potentials to these violations were recorded. Results and conclusions: Compared to matched controls, patients displayed impaired acquisition of the AG. This impairment was more pronounced for local than for long-distance dependencies. This effect was paralleled by a selective reduction of the P600 component in response to violations of local dependencies. Most importantly, the P600 elicited by violations of long-distance dependencies was comparable between groups. Together, behavioral and ERP results indicate a PMv involvement in processing local sequential information. © 2011 Elsevier Srl.

Cajigas I.J.,Max Planck Institute for Brain Research | Will T.,Max Planck Institute for Brain Research | Schuman E.M.,Max Planck Institute for Brain Research
EMBO Journal | Year: 2010

It is clear that de novo protein synthesis has an important function in synaptic transmission and plasticity. A substantial amount of work has shown that mRNA translation in the hippocampus is spatially controlled and that dendritic protein synthesis is required for different forms of long-term synaptic plasticity. More recently, several studies have highlighted a function for protein degradation by the ubiquitin proteasome system in synaptic plasticity. These observations suggest that changes in synaptic transmission involve extensive regulation of the synaptic proteome. Here, we review experimental data supporting the idea that protein homeostasis is a regulatory motif for synaptic plasticity. © 2010 European Molecular Biology Organization.

Eulenburg V.,Max Planck Institute for Brain Research | Gomeza J.,University of Bonn
Brain Research Reviews | Year: 2010

Synaptic neurotransmission at high temporal and spatial resolutions requires efficient removal and/or inactivation of presynaptically released transmitter to prevent spatial spreading of transmitter by diffusion and allow for fast termination of the postsynaptic response. This action must be carefully regulated to result in the fine tuning of inhibitory and excitatory neurotransmission, necessary for the proper processing of information in the central nervous system. At many synapses, high-affinity neurotransmitter transporters are responsible for transmitter deactivation by removing it from the synaptic cleft. The most prevailing neurotransmitters, glutamate, which mediates excitatory neurotransmission, as well as GABA and glycine, which act as inhibitory neurotransmitters, use these uptake systems. Neurotransmitter transporters have been found in both neuronal and glial cells, thus suggesting high cooperativity between these cell types in the control of extracellular transmitter concentrations. The generation and analysis of animals carrying targeted disruptions of transporter genes together with the use of selective inhibitors have allowed examining the contribution of individual transporter subtypes to synaptic transmission. This revealed the predominant role of glial expressed transporters in maintaining low extrasynaptic neurotransmitter levels. Additionally, transport activity has been shown to be actively regulated on both transcriptional and post-translational levels, which has important implications for synapse function under physiological and pathophysiological conditions. The analysis of these mechanisms will enhance not only our understanding of synapse function but will reveal new therapeutic strategies for the treatment of human neurological diseases. © 2010 Elsevier B.V.

Uhlhaas P.J.,Max Planck Institute for Brain Research
Clinical EEG and Neuroscience | Year: 2011

Neural oscillations and their synchronization may represent a versatile signal to realize flexible communication within and between cortical areas. There is extensive evidence that cognitive functions depending on coordination of distributed neural responses are associated with synchronized oscillatory activity, suggesting a functional mechanism of neural oscillations in cortical networks. In addition to their role in normal brain functioning, there is increasing evidence that altered oscillatory activity may be associated with certain neuropsychiatric disorders, such as schizophrenia, that involve dysfunctional cognition and behavior. In the present paper, the focus is on the role of high-frequency oscillations for cortical computations through establishing correlations between the modulation of oscillations in the β/γ frequency range and specific cognitive processes during normal brain functioning and in schizophrenia. Specifically, it is suggested that in addition to oscillations in the low (30-60 Hz) γ-band range, γ-band oscillations > 60 Hz may have a crucial role for the understanding of cognitive dysfunctions in schizophrenia. Perspectives for future research will be discussed in relationship to methodological issues, the utility of neural oscillations as a biomarker and the neurodevelopmental hypothesis of schizophrenia.

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