Dr Ragnhildur Thóra Káradóttir
Neurotransmitter signalling to central nervous system progenitor cells
Cambridge Stem Cell Institute, Gleeson Building
Ragnhildur Thóra Káradóttir graduated with a degree in Biochemistry from the University of Iceland in 2000. She then completed a four-year Wellcome Trust PhD in Neuroscience at UCL under the supervision of Prof. David Attwell. She continued working with Prof. Attwell as a postdoctoral researcher, before being awarded a Royal Society Dorothy Hodgkin Research Fellowship which she used to work with Prof. Charles ffrench-Constant at the University of Cambridge. In 2008 she established her own independent research group in Cambridge and in 2011 she was awarded the Wellcome Trust Research Career Development fellowship.
She is currently an editor for the journal Brain Plasticity and a guest editor for Neuroscience and for Neuropharmacology.
- 2006 Doctor of Philosophy (PhD) in Neuroscience from University of London.
Thesis title: Neurotransmitter signalling to oligodendrocytes
- 2001 Admission to the 4 year PhD Programme in Neuroscience at University College London
- 2000 BSc in Biochemistry from the University of Iceland, 1st Class.
Research project: Role of melatonin in Seasonal Affective Disorder
- 2011 Wellcome Trust Career Development Research Fellow
- 2007 Dorothy Hodgkin Research Fellow of the Royal Society held in Dept. of Veterinary Medicine University of Cambridge
- 2006 Postdoctoral research fellow with Prof. David Attwell, Dept. Physiology University College London
- 2001- Wellcome Trust PhD student on 4 year PhD in Neuroscience, Department of Physiology 2005 University College London
CurePSP, Paul G Allen Family Foundation, Lister Institute, MNI McGill-Cambridge collaboration, Wellcome Trust
The lab’s research interests are neurotransmitter signalling to oligodendrocyte progenitor cells (OPC; a type of CNS stem cell), in both health and disease.
For our brain to work properly, enabling us to feel, move, talk, see, think and learn, fast electrical communication between nerve cells is essential. This is achieved by insulating the nerves with a fatty substance called myelin. In diseases like multiple sclerosis, spinal cord injury and stroke, myelin is lost, while in cerebral palsy myelin fails to develop. Lack of myelin causes physical and mental disability.
Myelin is provided by cells called oligodendrocytes, which develop from oligodendrocyte precursor cells (OPCs). OPCs are 5% of all cells in the adult brain and can turn into most cell types in the brain. Most importantly, OPCs can repair myelin, but this repair often fails.
We have discovered that OPCs express a protein previously only thought to be expressed in neurons, as it is known for being essential for learning. But in OPCs it enables them to sense activity in the neurons. Furthermore, we found that OPCs enter into a dialogue with neurons and this dialogue and neuronal activity, acting on the protein we found, directs OPCs to become myelin-making oligodendrocytes in both health and disease.
We are now investigating how signals in the cells’ environment interact with OPCs to instruct them to move to regions where myelin is needed, and to generate myelin-making oligodendrocytes, with special focus on the neuron to OPCs dialogue.
The long-term aim of this work is to understand how OPCs become myelinating cells, and how we can influence them to repair myelin in disease.
Mariann Kovacs (Visitor)
For our brain to work, fast electrical communication between nerve cells is essential. This is achieved by insulating the nerves with a fatty substance called myelin. In diseases like multiple sclerosis, spinal cord injury and stroke, myelin is lost, while in cerebral palsy myelin fails to develop. Lack of myelin causes physical and mental disability. Myelin is provided by cells called oligodendrocytes, which develop from oligodendrocyte precursor cells (OPCs). In the adult, OPCs can repair myelin, but this repair often fails for reasons currently unknown. OPCs can also develop into other types of brain cell, including nerve cells, but it is not known what controls this choice of cell identity. We study how OPCs generate myelin during development and in disease. By investigateing how signals in the cells’ environment interact with the properties of the OPCs to instruct them to migrate, generate myelin-making oligodendrocytes, or develop into other brain cells. The aim of this work is to understand how OPCs decide to become myelinating cells, how we can influence them to repair myelin in disease.
- Gautier HO, Evans K, Lundgaard I, James F, Lao-Peregrin C, Franklin RJM, Káradóttir R (2015). Neuronal activity regulates remyelination via glutamate signaling to oligodendrocyte progenitors. Nature Communications 6: 8518. PMCID:PMC4600759
- Lundgaard I, Luzhynskaya A, Stockley JH, Wang Z, Evans KA, Swire M, Volbracht K, Gautier HO, Franklin RJM, ffrench-Constant C, Attwell D, Káradóttir R (2013). Neuregulin and BDNF induce a switch to NMDA receptor dependent myelination by oligodendrocytes. PLoS Biol. 11(12): e1001743. PMCID:PMC3876980
- Káradóttir R, Hamilton N, Bakiri Y & Attwell D (2008). Spiking and nonspiking classes of oligodendrocyte precursor glia in CNS white matter. Nature Neuroscience 11(4): 450-456. PMCID:PMC2615224
- Káradóttir R, Attwell D (2006). Combining patch-clamping of cells in brain slices with immunocytochemical labelling to define cell type and developmental stage. Nature Protocols 1(4): 1977-1985. PMCID:PMC2682777
- Káradóttir R, Cavalier P, Bergersen LH, Attwell D (2005). NMDA receptors are expressed in oligodendrocytes and activated in ischaemia. Nature 438: 1162-1166. PMCID:PMC1416283