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A dendrite or dendron is a branched cytoplasmic process that extends from a nerve cell that propagates the electrochemical stimulation received from other neural cells to the cell body, or soma, of the neuron from which the dendrites project. Electrical stimulation is transmitted onto dendrites by upstream neurons via synapses which are located at various points throughout the dendritic tree.
A dendritic spine is a small membrane protrusion from a neuron's dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron's cell body. Most spines have a bulbous head, and a thin neck that connects the head of the spine to the shaft of the dendrite. The dendrites of a single neuron can contain hundreds to thousands of spines. In addition to spines providing an anatomical substrate for memory storage and synaptic transmission, they may also serve to increase the number of possible contacts between neurons. It has also been suggested that changes in the activity of neurons have a positive effect on spine morphology.
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.
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.
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.
Kalirin, also known as Huntingtin-associated protein-interacting protein (HAPIP), protein duo (DUO), or serine/threonine-protein kinase with Dbl- and pleckstrin homology domain, is a protein that in humans is encoded by the KALRN gene. Kalirin was first identified in 1997 as a protein interacting with huntingtin-associated protein 1. Is also known to play an important role in nerve growth and axonal development.
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.
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.
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, has been proposed 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.
The name granule cell has been used for a number of different types of neurons whose only common feature is that they all have very small cell bodies. Granule cells are found within the granular layer of the cerebellum, the dentate gyrus of the hippocampus, the superficial layer of the dorsal cochlear nucleus, the olfactory bulb, and the cerebral cortex.
Memory allocation is a process that determines which specific synapses and neurons in a neural network will store a given memory. Although multiple neurons can receive a stimulus, only a subset of the neurons will induce the necessary plasticity for memory encoding. The selection of this subset of neurons is termed neuronal allocation. Similarly, multiple synapses can be activated by a given set of inputs, but specific mechanisms determine which synapses actually go on to encode the memory, and this process is referred to as synaptic allocation. Memory allocation was first discovered in the lateral amygdala by Sheena Josselyn and colleagues in Alcino J. Silva's laboratory.
Addiction is a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences. The process of developing an addiction occurs through instrumental learning, which is otherwise known as operant conditioning.
Synaptic stabilization is crucial in the developing and adult nervous systems and is considered a result of the late phase of long-term potentiation (LTP). The mechanism involves strengthening and maintaining active synapses through increased expression of cytoskeletal and extracellular matrix elements and postsynaptic scaffold proteins, while pruning less active ones. For example, cell adhesion molecules (CAMs) play a large role in synaptic maintenance and stabilization. Gerald Edelman discovered CAMs and studied their function during development, which showed CAMs are required for cell migration and the formation of the entire nervous system. In the adult nervous system, CAMs play an integral role in synaptic plasticity relating to learning and memory.
Erin Margaret Schuman, born May 15, 1963, in California, US, 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 is the Vice-Dean International for the Faculty of Life Sciences. 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.
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.
References
- ↑ "New Max Planck Institute for Biological Intelligence, in foundation". idw-online.de. Retrieved 2022-04-20.
- ↑ ORF.at: I.S.T. Austria: Gehirnforscher Bonhoeffer wird erster Chef at archive.today (archived 2012-07-13)
- ↑ ORF.at: Elite-Uni: Gehirnforscher Bonhoeffer doch nicht Chef at the Wayback Machine (archived 2016-05-19)
- 1 2 "Professor Bryan Grenfell and Professor Tobias Bonhoeffer join the Wellcome Trust Board of Governors". Wellcome Trust. 7 July 2014. Retrieved 2022-09-01.
- 1 2 "So will Mark Zuckerberg alle Krankheiten besiegen" (in German). Welt.de. 10 November 2016. Retrieved 2022-09-01.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- ↑ 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.
- ↑ 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.
- ↑ "Mitgliederverzeichnis: Tobias Bonhoeffer". Academia Europaea. Retrieved 2017-06-20.
- ↑ "EMBO membership entry for Tobias Bonhoeffer". European Molecular Biology Organization. Retrieved 2023-03-15.
- ↑ "List of Members: Tobias Bonhoeffer". German National Academy of Sciences Leopoldina. Retrieved 2022-09-01.
- ↑ "2020 newly elected members". National Academy of Sciences. Retrieved 2020-04-27.
- ↑ "Die IU Hochschulleitung" (in German). IU Internationale Hochschule. Retrieved 2022-09-01.
