Dimitri Kullmann

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Dimitri Kullmann
Dimitri Kullmann Royal Society.jpg
Dimitri Kullmann at the Royal Society, London, 2018
Born
Dimitri Michael Kullmann

1958 (age 6566) [1]
London, England [1]
Education Lycée Français Charles de Gaulle [1]
Alma mater University of Oxford (BM BCh, DPhil)
Awards Baly Medal (2017) [2]
Scientific career
Fields
Institutions
Thesis Central actions of muscle receptors  (1984)
Doctoral advisor Julian Jack [4]
Website www.ucl.ac.uk/ion/research/synaptopathies/principal-investigators/dimitri-m-kullmann

Dimitri Michael Kullmann (born 1958) [1] FRS FMedSci MAE is a professor of neurology at the UCL Institute of Neurology, [2] University College London (UCL), and leads the synaptopathies initiative funded by the Wellcome Trust. [5] Kullmann is a member of the Queen Square Institute of Neurology Department of Clinical and Experimental Epilepsy [6] and a consultant neurologist at the National Hospital for Neurology and Neurosurgery. [3] [7]

Contents

Education

Kullmann was educated at the Lycée Français Charles de Gaulle [1] and studied physiology at Balliol College, Oxford [1] where he was awarded a Bachelor of Arts (BA) degree and a Doctor of Philosophy degree. [4] He studied and trained at the University of Oxford and St Thomas's Hospital Medical School at the University of London. [2] His postgraduate research was supervised by Julian Jack. [4]

Research and career

Kullmann's research [3] [7] investigates how synapses function in health and disease. [8] His laboratory helped to show how neurotransmitters activate different receptor subtypes in and around synapses, and resolved some controversies about the mechanisms of long-term changes in synaptic strength. [8] Genetic and autoimmune disorders of synaptic proteins (‘synaptopathies’) provide insights into the mechanisms of a broad range of neurological diseases including epilepsy and migraine. [8] Together with his colleagues, Kullmann has used these insights to devise gene therapy strategies that could be used to treat intractable epilepsy. [8] [3]

The Kullmann lab [3] [7] has contributed to the discovery and elucidation of silent synapses, [9] glutamate spillover, tonic inhibition, [10] long-term potentiation in interneurons, [11] neurological channelopathies [12] and Synaptopathies, gene therapy for epilepsy, [13] and mechanisms of neural oscillations. [14] Kullmann served as the editor-in-chief of the scientific journal Brain between 2014 and 2020 [15] and is on the editorial board of the journal Neuron . [16] Before working at UCL, he did postdoctoral research with Roger Nicoll at the University of California, San Francisco. [2]

Awards and honours

Kullmann was awarded the University Gold Medal in Medicine by the University of London, in 1986. [2] and the Baly Medal by the Royal College of Physicians in 2017. [2] He was elected a Guarantor of Brain in 2000, [17] elected a Fellow of the Academy of Medical Sciences (FMedSci) in 2001, [18] a Corresponding Fellow of the American Neurological Association in 2013, [19] a member of the Academia Europaea (MAE) in 2017 [20] and a Fellow of the Royal Society (FRS) in 2018. [8] He was awarded the 2023 Basic Science Research Award by the American Epilepsy Society. [21]

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<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.

<span class="mw-page-title-main">Synaptic plasticity</span> Ability of a synapse to strengthen or weaken over time according to its activity

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 neuroscience, a silent synapse is an excitatory glutamatergic synapse whose postsynaptic membrane contains NMDA-type glutamate receptors but no AMPA-type glutamate receptors. These synapses are named "silent" because normal AMPA receptor-mediated signaling is not present, rendering the synapse inactive under typical conditions. Silent synapses are typically considered to be immature glutamatergic synapses. As the brain matures, the relative number of silent synapses decreases. However, recent research on hippocampal silent synapses shows that while they may indeed be a developmental landmark in the formation of a synapse, that synapses can be "silenced" by activity, even once they have acquired AMPA receptors. Thus, silence may be a state that synapses can visit many times during their lifetimes.

In neuroscience, homeostatic plasticity refers to the capacity of neurons to regulate their own excitability relative to network activity. The term homeostatic plasticity derives from two opposing concepts: 'homeostatic' and plasticity, thus homeostatic plasticity means "staying the same through change". In the nervous system, neurons must be able to evolve with the development of their constantly changing environment while simultaneously staying the same amidst this change. This stability is important for neurons to maintain their activity and functionality to prevent neurons from carcinogenesis. At the same time, neurons need to have flexibility to adapt to changes and make connections to cope with the ever-changing environment of a developing nervous system.

Epileptogenesis is the gradual process by which a typical brain develops epilepsy. Epilepsy is a chronic condition in which seizures occur. These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure.

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<span class="mw-page-title-main">Synaptopathy</span> Medical condition

A synaptopathy is a disease of the brain, spinal cord or peripheral nervous system relating to the dysfunction of synapses. This can arise as a result of a mutation in a gene encoding a synaptic protein such as an ion channel, neurotransmitter receptor, or a protein involved in neurotransmitter release. It can also arise as a result of an autoantibody targeting a synaptic protein. Synaptopathies caused by ion channel mutations are also known as synaptic channelopathies. An example is episodic ataxia. Myasthenia gravis is an example of an autoimmune synaptopathy. Some toxins also affect synaptic function. Tetanus toxin and botulinum toxin affect neurotransmitter release. Tetanus toxin can enter the body via a wound, and botulinum toxin can be ingested or administered therapeutically to alleviate dystonia or as cosmetic treatment.

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References

  1. 1 2 3 4 5 6 Anon (2019). "Kullmann, Prof. Dimitri Michael" . Who's Who (online Oxford University Press  ed.). Oxford: A & C Black.(Subscription or UK public library membership required.)
  2. 1 2 3 4 5 6 7 "Prof Dimitri Michael Kullmann: Iris View Profile". University College London. Retrieved 2 October 2016.
  3. 1 2 3 4 5 6 7 8 Dimitri Kullmann publications indexed by Google Scholar OOjs UI icon edit-ltr-progressive.svg
  4. 1 2 3 Kullman, Dimitri Michael (1984). Central actions of muscle receptors (DPhil thesis). University of Oxford. OCLC   59330270. EThOS   uk.bl.ethos.353099. Archived from the original on 16 December 2019. Retrieved 6 June 2018.
  5. "Synaptopathies". University College London. 17 July 2014. Retrieved 2 October 2016.
  6. "DCEE". University College London. 29 May 2020. Retrieved 7 June 2021.
  7. 1 2 3 Dimitri Kullmann publications from Europe PubMed Central
  8. 1 2 3 4 5 Anon (2018). "Professor Dimitri Kullmann FMedSci FRS". royalsociety.org. London: Royal Society. Archived from the original on 24 May 2018. One or more of the preceding sentences incorporates text from the royalsociety.org website where:
    "All text published under the heading 'Biography' on Fellow profile pages is available under Creative Commons Attribution 4.0 International License." --Royal Society Terms, conditions and policies at the Wayback Machine (archived 2016-11-11)
  9. Kullmann, Dimitri M. (1994). "Amplitude fluctuations of". Neuron. 12 (5): 1111–1120. doi:10.1016/0896-6273(94)90318-2. PMID   7910467. S2CID   54357872.
  10. Semyanov, Alexey; Walker, Matthew C.; Kullmann, Dimitri M.; Silver, R.Angus (2004). "Tonically active GABAA receptors: modulating gain and maintaining the tone". Trends in Neurosciences. 27 (5): 262–269. doi:10.1016/j.tins.2004.03.005. ISSN   0166-2236. PMID   15111008. S2CID   2660172.
  11. Lamsa, Karri P.; Heeroma, Joost H.; Somogyi, Peter; Rusakov, Dmitri A.; Kullmann, Dimitri M. (2007). "Anti-Hebbian long-term potentiation in the hippocampal feedback inhibitory circuit". Science. 315 (5816): 1262–1266. Bibcode:2007Sci...315.1262L. doi:10.1126/science.1137450. ISSN   1095-9203. PMC   3369266 . PMID   17332410.
  12. Kullmann, Dimitri M. (2010). "Neurological channelopathies". Annual Review of Neuroscience. 33: 151–172. doi:10.1146/annurev-neuro-060909-153122. ISSN   1545-4126. PMID   20331364.
  13. Wykes, Robert C.; Heeroma, Joost H.; Mantoan, Laura; Zheng, Kaiyu; MacDonald, Douglas C.; Deisseroth, Karl; Hashemi, Kevan S.; Walker, Matthew C.; Schorge, Stephanie (2012). "Optogenetic and potassium channel gene therapy in a rodent model of focal neocortical epilepsy". Science Translational Medicine. 4 (161): 161ra152. doi:10.1126/scitranslmed.3004190. ISSN   1946-6242. PMC   3605784 . PMID   23147003.
  14. Akam, Thomas; Oren, Iris; Mantoan, Laura; Ferenczi, Emily; Kullmann, Dimitri M. (2012). "Oscillatory dynamics in the hippocampus support dentate gyrus–CA3 coupling". Nature Neuroscience . 15 (5): 763–768. doi:10.1038/nn.3081. ISSN   1546-1726. PMC   3378654 . PMID   22466505.
  15. "Editorial board | Brain". Brain.oxfordjournals.org. 26 September 2016. Archived from the original on 11 October 2014. Retrieved 2 October 2016.
  16. "Editorial Board: Neuron". cell.com.
  17. "Guarantors of Brain". Guarantors of Brain. Retrieved 11 August 2016.
  18. "Professor Dimitri Kullmann FMedSci". acmedsci.ac.uk. Retrieved 2 October 2016.
  19. "American Neurological Association (ANA)". Myana.org. Retrieved 1 November 2016.
  20. Hoffmann, Ilire Hasani, Robert. "Academy of Europe: Kullmann Dimitri". ae-info.org.{{cite web}}: CS1 maint: multiple names: authors list (link)
  21. "Dimitri M. Kullmann, D.Phil., FRS, FMedSci, MAE, Receives the 2023 Basic Science Research Award".

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