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SUMMARY:Glutamate\, Spikes\, and White Matter Disease - Dr. Ragnhildur Ká
 radóttir\, Department of Veterinary Medicine.
DTSTART:20090319T150000Z
DTEND:20090319T153000Z
UID:TALK16494@talks.cam.ac.uk
CONTACT:Hannah Critchlow
DESCRIPTION:For the brain to work properly fast information transmission n
 eeds to take place\, which is achieved by insulating neuronal axons with m
 yelin.  Myelin is made by cells called oligodendrocytes. In multiple scler
 osis\, cerebral palsy\, stroke and spinal injury myelin is damaged\, leadi
 ng to mental and physical disability. Myelin damage can be repaired by so-
 called oligodendrocyte precursor cells\, that can differentiate into new o
 ligodendrocytes and remyelinate the axons\, but this process often fails. 
  Recently we have made two discoveries that may contribute significantly t
 o our understanding of both myelination and remyelination. First\, both ol
 igodendrocytes and their precursors respond to the neurotransmitter glutam
 ate via AMPA and NMDA receptors and this signalling may regulate myelinati
 on. Secondly\, there are actually two types of oligodendrocyte precursor c
 ell present both in the developing and the mature brain: one type can fire
  action potentials and senses its environment by receiving synaptic input\
 , whereas the other type lacks action potentials and synaptic input.  Furt
 hermore\, simulating the diseases mentioned above leads to a rise of extra
 cellular glutamate concentration generating an inward current in oligodend
 rocytes and OPCs\, in part via NMDA receptors. These results make NMDA rec
 eptors on oligodendrocyte lineage cells a therapeutic target in white matt
 er disease.
LOCATION:William Harvey Lecture Theatre\, School of Clinical Medicine\, Ad
 denbrooke's Hospital.
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