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CATEGORIES:Cambridge Fly Meetings
SUMMARY:Reactive Oxygen Species Regulate Activity-Dependen
 t Neuronal Structural Plasticity - Matthew Oswald 
 (Landgraf lab\, Department of Zoology)
DTSTART;TZID=Europe/London:20160921T173000
DTEND;TZID=Europe/London:20160921T193000
UID:TALK66910AThttp://talks.cam.ac.uk
URL:http://talks.cam.ac.uk/talk/index/66910
DESCRIPTION:Neurons are inherently plastic and adjust their el
 ectrical properties but also the size of their syn
 aptic arbors in response to changes in activity. S
 uch adjustments are usually homeostatic and allow 
 cells to maintain a pre-determined activity range\
 , promoting network stability and physiologically 
 appropriate function. While homeostatic changes to
  electrical and transmitter release properties hav
 e been studied extensively\, the mechanisms that r
 egulate structural adjustment of synaptic terminal
  arbors have remained largely unexplored.  We aske
 d: How do neurons sense changes in activity\, and 
 by what mechanisms are these converted into struct
 ural changes at synaptic terminals? \nWorking with
  identified motoneurons we studied structural adju
 stment in response to elevated activity in both th
 eir postsynaptic dendritic arbors in the CNS and t
 heir presynaptic neuromuscular junctions (NMJs) in
  the periphery. We discovered that motoneurons use
  metabolic by-products\, namely Reactive Oxygen Sp
 ecies (ROS)\, a constitutive by-product of mitocho
 ndrial ATP synthesis\, as readout for neuronal act
 ivity. We find that ROS\, and hydrogen peroxide (H
 2O2) in particular\, are necessary for activity-de
 pendent synaptic terminal growth and sufficient fo
 r instigating such growth in the absence of elevat
 ed neuronal activity. We next identified a putativ
 e redox sensor\, the Parkinson’s disease-linked pr
 otein DJ-1b. DJ-1b\, in response to elevated H2O2 
 (but not O2-)\, inhibits the lipid-phosphatase PTE
 N and in doing so permits increased signalling via
  PI3K. PTEN and PI3K have been extensively linked 
 with neuronal growth and energy metabolism and are
  therefore perfectly placed to expedite homeostati
 c growth in response to elevated neuronal activity
  and ROS.\nUntil recently\, ROS were primarily con
 sidered to be a tolerated burden\, rapidly removed
  by a range of cellular ROS-buffering and scavenge
 r systems. Accumulation of ROS\, termed Oxidative 
 Stress\, results in changes in chromatin configura
 tion and gene expression\, lipid oxidation and cel
 l death\, leading to neurodegenerative pathology. 
 Our work suggests a role for ROS during normal dev
 elopment and 
LOCATION:Gurdon Institute Tea Room
CONTACT:Clara Sidor
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