Tobias Bonhoeffer

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Tobias Bonhoeffer (born January 9, 1960) is a German-American neurobiologist. He is director of the department Synapses – Circuits – Plasticity and current managing director at the Max Planck Institute for Biological Intelligence (formerly Max Planck Institute of Neurobiology) [1] ). His father, the neurobiologist Friedrich Bonhoeffer, was director at the Max Planck Institute for Developmental Biology in Tübingen.


Education and career

Bonhoeffer studied physics at the University of Tübingen. He received his doctorate at the Max Planck Institute for Biological Cybernetics in Tübingen. As a postdoctoral fellow, he worked at Rockefeller University (USA) and at the Max Planck Institute for Brain Research in Frankfurt am Main. He then headed an independent research group at the Max Planck Institute of Psychiatry in Munich and was appointed director at the Max Planck Institute of Neurobiology in 1998.

From 2008 until 2011, Tobias Bonhoeffer was chairman of the Biology & Medicine Section of the Max Planck Society. In mid-2008, he was nominated as founding president of the Institute of Science and Technology Austria (ISTA) in Maria Gugging near Vienna, [2] but announced on July 21, 2008 that he would decline the offered leadership position at the ISTA for personal reasons. [3]

In 2014, Bonhoeffer was appointed to the Board of Governors of the UK Wellcome Trust, [4] where he served as governor until the end of 2021. In 2016, he became a scientific advisor to the Chan Zuckerberg Initiative, founded by Mark Zuckerberg and his wife Priscilla Chan. [5] In 2017, he was elected chairman of the Scientific Council of the Max Planck Society. In 2022, Bonhoeffer became the first managing director of the new Max Planck Institute for Biological Intelligence (still in foundation in 2022). [6]

Scientific focus

Bonhoeffer's work focuses on the cellular foundations of learning and memory as well as on the early postnatal development of the brain. He and his research group were the first to demonstrate the presence of "pinwheels" in the mammalian visual system, using high-resolution imaging techniques. [7] Further research dealt with nerve growth factors, in particular brain-derived neurotrophic factor (BDNF); [8] [9] the functional strengthening of synapses, which is reflected in morphological changes of neurons through the formation of new dendritic spines; [10] the targeted degradation of proteins as a mechanism for the storage of information in the nervous system; [11] and with the process by which many cell contacts that were grown during learning are inactivated but not degraded when they are not used, which should enable much faster relearning. [12]

Important discoveries

Bonhoeffer's work led to a number of important scientific discoveries. These include:

Awards and memberships

Selected scientific boards

Related Research Articles

<span class="mw-page-title-main">Chemical synapse</span> Biological junctions through which neurons signals can be sent

Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body.

<span class="mw-page-title-main">Long-term potentiation</span> Persistent strengthening of synapses based on recent patterns of activity

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

<span class="mw-page-title-main">Brain-derived neurotrophic factor</span> Protein

Brain-derived neurotrophic factor (BDNF), or abrineurin, is a protein that, in humans, is encoded by the BDNF gene. BDNF is a member of the neurotrophin family of growth factors, which are related to the canonical nerve growth factor (NGF), a family which also includes NT-3 and NT-4/NT-5. Neurotrophic factors are found in the brain and the periphery. BDNF was first isolated from a pig brain in 1982 by Yves-Alain Barde and Hans Thoenen.

Spike-timing-dependent plasticity (STDP) is a biological process that adjusts the strength of connections between neurons in the brain. The process adjusts the connection strengths based on the relative timing of a particular neuron's output and input action potentials. The STDP process partially explains the activity-dependent development of nervous systems, especially with regard to long-term potentiation and long-term depression.

Synaptogenesis is the formation of synapses between neurons in the nervous system. Although it occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development, known as exuberant synaptogenesis. Synaptogenesis is particularly important during an individual's critical period, during which there is a certain degree of synaptic pruning due to competition for neural growth factors by neurons and synapses. Processes that are not used, or inhibited during their critical period will fail to develop normally later on in life.

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus and are an integral part of memory formation and the emotional network of the Papez circuit, and of the hippocampal trisynaptic loop. It is one of the most studied synapses in the world and named after the Hungarian anatomist-neurologist Károly Schaffer.

Bursting, or burst firing, is an extremely diverse general phenomenon of the activation patterns of neurons in the central nervous system and spinal cord where periods of rapid action potential spiking are followed by quiescent periods much longer than typical inter-spike intervals. Bursting is thought to be important in the operation of robust central pattern generators, the transmission of neural codes, and some neuropathologies such as epilepsy. The study of bursting both directly and in how it takes part in other neural phenomena has been very popular since the beginnings of cellular neuroscience and is closely tied to the fields of neural synchronization, neural coding, plasticity, and attention.

<span class="mw-page-title-main">Henry Markram</span> South African-born Israeli neuroscientist

Henry John Markram is a South African-born Israeli neuroscientist, professor at the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland and director of the Blue Brain Project and founder of the Human Brain Project.

The spine apparatus (SA) is a specialized form of endoplasmic reticulum (ER) that is found in a subpopulation of dendritic spines in central neurons. It was discovered by Edward George Gray in 1959 when he applied electron microscopy to fixed cortical tissue. The SA consists of a series of stacked discs that are connected to each other and to the dendritic system of ER-tubules. The actin binding protein synaptopodin is an essential component of the SA. Mice that lack the gene for synaptopodin do not form a spine apparatus. The SA is believed to play a role in synaptic plasticity, learning and memory, but the exact function of the spine apparatus is still enigmatic.

Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules during increased neuronal activity.

<span class="mw-page-title-main">Dendritic spike</span> Action potential generated in the dendrite of a neuron

In neurophysiology, a dendritic spike refers to an action potential generated in the dendrite of a neuron. Dendrites are branched extensions of a neuron. They receive electrical signals emitted from projecting neurons and transfer these signals to the cell body, or soma. Dendritic signaling has traditionally been viewed as a passive mode of electrical signaling. Unlike its axon counterpart which can generate signals through action potentials, dendrites were believed to only have the ability to propagate electrical signals by physical means: changes in conductance, length, cross sectional area, etc. However, the existence of dendritic spikes was proposed and demonstrated by W. Alden Spencer, Eric Kandel, Rodolfo Llinás and coworkers in the 1960s and a large body of evidence now makes it clear that dendrites are active neuronal structures. Dendrites contain voltage-gated ion channels giving them the ability to generate action potentials. Dendritic spikes have been recorded in numerous types of neurons in the brain and are thought to have great implications in neuronal communication, memory, and learning. They are one of the major factors in long-term potentiation.

<span class="mw-page-title-main">Nonsynaptic plasticity</span> Form of neuroplasticity

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

Synaptic tagging, or the synaptic tagging hypothesis, was first proposed in 1997 by Uwe Frey and Richard G. Morris; it seeks to explain how neural signaling at a particular synapse creates a target for subsequent plasticity-related product (PRP) trafficking essential for sustained LTP and LTD. Although the molecular identity of the tags remains unknown, it has been established that they form as a result of high or low frequency stimulation, interact with incoming PRPs, and have a limited lifespan.

Erin Margaret Schuman, born May 15, 1963 in California, USA, is a neurobiologist who studies neuronal synapses. She is currently a Director at the Max Planck Institute for Brain Research.

Tara Keck is an American-British neuroscientist and Professor of Neuroscience and Wellcome Trust Senior Research Fellow, at University College London working in the Department of Neuroscience, Physiology, and Pharmacology. She studies experience-dependent synaptic plasticity, its effect on behaviour and how it changes during ageing and age-related diseases. She has worked in collaboration with the United Nations Population Fund on approaches for healthy ageing. Her recent work has focused on loneliness in older people, with a focus on gender. She was named a UNFPA Generations and Gender Fellow in 2022.

<span class="mw-page-title-main">Nicola Allen</span> British glial biologist

Nicola J. Allen is a British neuroscientist. Allen studies the role of astrocytes in brain development, homeostasis, and aging. Her work uncovered the critical roles these cells play in brain plasticity and disease. Allen is currently an associate professor at the Salk Institute for Biological Studies and Hearst Foundation Development Chair.

Beat H. Gähwiler, is a Swiss emeritus professor in neuroscience at the Brain Research Institute of the University of Zurich, Switzerland.

Sonja Hofer is a German neuroscientist studying the neural basis of sensory perception and sensory-guided decision-making at the Sainsbury Wellcome Centre for Neural Circuits and Behaviour. Her research focuses on how the brain processes visual information, how neural networks are shaped by experience and learning, and how they integrate visual signals with other information in order to interpret the outside world and guide behaviour. She received her undergraduate degree from the Technical University of Munich, her PhD at the Max Planck Institute of Neurobiology in Martinsried, Germany, and completed a post doctorate at the University College London. After holding an Assistant Professorship at the Biozentrum University of Basel in Switzerland for five years, she now is a group leader and Professor at the Sainsbury Wellcome Centre for Neural Circuits and Behaviour since 2018.


  1. "New Max Planck Institute for Biological Intelligence, in foundation". Retrieved 2022-04-20.
  2. I.S.T. Austria: Gehirnforscher Bonhoeffer wird erster Chef at (archived 2012-07-13)
  3. Elite-Uni: Gehirnforscher Bonhoeffer doch nicht Chef at the Wayback Machine (archived 2016-05-19)
  4. 1 2 "Professor Bryan Grenfell and Professor Tobias Bonhoeffer join the Wellcome Trust Board of Governors". Wellcome Trust. Retrieved 2022-09-01.
  5. 1 2 "So will Mark Zuckerberg alle Krankheiten besiegen" (in German). Retrieved 2022-09-01.
  6. "Structure and Organization of the Max Planck Institute for Biological Intelligence". Max Planck Institute for Biological Intelligence. Retrieved 2022-09-01.
  7. 1 2 Bonhoeffer, T; Grinvald, A (October 1991). "Iso-orientation domains in cat visual cortex are arranged in pinwheel-like patterns". Nature. 353 (6343): 429–31. Bibcode:1991Natur.353..429B. doi:10.1038/353429a0. PMID   1896085. S2CID   4342857.
  8. 1 2 Korte, M; Carroll, P; Wolf, E; Brem, G; Thoenen, H; Bonhoeffer, T (September 1995). "Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor". Proc Natl Acad Sci U S A. 92 (19): 8856–60. Bibcode:1995PNAS...92.8856K. doi: 10.1073/pnas.92.19.8856 . PMC   41066 . PMID   7568031.
  9. 1 2 Korte, M; Griesbeck, O; Gravel, C; Carroll, P; Staiger, V; Thoenen, H; Bonhoeffer, T (October 1996). "Virus-mediated gene transfer into hippocampal CA1 region restores long-term potentiation in brain-derived neurotrophic factor mutant mice". Proc Natl Acad Sci U S A. 93 (22): 12547–52. Bibcode:1996PNAS...9312547K. doi: 10.1073/pnas.93.22.12547 . PMC   38029 . PMID   8901619.
  10. 1 2 Engert, F; Bonhoeffer, T (May 1999). "Dendritic spine changes associated with hippocampal long-term synaptic plasticity". Nature. 399 (6731): 66–70. Bibcode:1999Natur.399...66E. doi:10.1038/19978. PMID   10331391. S2CID   4355911.
  11. 1 2 Fonseca, R; Vabulas, RM; Hartl, FU; Bonhoeffer, T; Nägerl, UV (October 2006). "A balance of protein synthesis and proteasome-dependent degradation determines the maintenance of LTP". Neuron. 52 (2): 239–45. doi: 10.1016/j.neuron.2006.08.015 . PMID   17046687.
  12. 1 2 Hofer, SB; Mrsic-Flogel, TD; Bonhoeffer, T; Hübener, M (January 2009). "Experience leaves a lasting structural trace in cortical circuits". Nature. 457 (7227): 313–7. Bibcode:2009Natur.457..313H. doi:10.1038/nature07487. PMC   6485433 . PMID   19005470.
  13. Nägerl, UV; Eberhorn, N; Cambridge, SB; Bonhoeffer, T (December 2004). "Bidirectional activity-dependent morphological plasticity in hippocampal neurons". Neuron. 44 (5): 759–67. doi: 10.1016/j.neuron.2004.11.016 . PMID   15572108.
  14. Reinert, S; Hübener, M; Bonhoeffer, T; Goltstein, PM (May 2021). "Mouse prefrontal cortex represents learned rules for categorization". Nature. 593 (7859): 411–417. Bibcode:2021Natur.593..411R. doi:10.1038/s41586-021-03452-z. PMC   8131197 . PMID   33883745.
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  18. "2020 newly elected members". National Academy of Sciences. Retrieved 2020-04-27.
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