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SUMMARY:Reactive Oxygen Species Regulate Activity-Dependent Neuronal Struc
 tural Plasticity - Matthew Oswald (Landgraf lab\, Department of Zoology)
DTSTART:20160921T163000Z
DTEND:20160921T183000Z
UID:TALK66910@talks.cam.ac.uk
CONTACT:Clara Sidor
DESCRIPTION:Neurons are inherently plastic and adjust their electrical pro
 perties but also the size of their synaptic arbors in response to changes 
 in activity. Such adjustments are usually homeostatic and allow cells to m
 aintain a pre-determined activity range\, promoting network stability and 
 physiologically appropriate function. While homeostatic changes to electri
 cal and transmitter release properties have been studied extensively\, the
  mechanisms that regulate structural adjustment of synaptic terminal arbor
 s have remained largely unexplored.  We asked: How do neurons sense change
 s in activity\, and by what mechanisms are these converted into structural
  changes at synaptic terminals? \nWorking with identified motoneurons we s
 tudied structural adjustment in response to elevated activity in both thei
 r postsynaptic dendritic arbors in the CNS and their presynaptic neuromusc
 ular junctions (NMJs) in the periphery. We discovered that motoneurons use
  metabolic by-products\, namely Reactive Oxygen Species (ROS)\, a constitu
 tive by-product of mitochondrial ATP synthesis\, as readout for neuronal a
 ctivity. We find that ROS\, and hydrogen peroxide (H2O2) in particular\, a
 re necessary for activity-dependent synaptic terminal growth and sufficien
 t for instigating such growth in the absence of elevated neuronal activity
 . We next identified a putative redox sensor\, the Parkinson’s disease-l
 inked protein DJ-1b. DJ-1b\, in response to elevated H2O2 (but not O2-)\, 
 inhibits the lipid-phosphatase PTEN and in doing so permits increased sign
 alling via PI3K. PTEN and PI3K have been extensively linked with neuronal 
 growth and energy metabolism and are therefore perfectly placed to expedit
 e homeostatic growth in response to elevated neuronal activity and ROS.\nU
 ntil recently\, ROS were primarily considered to be a tolerated burden\, r
 apidly removed by a range of cellular ROS-buffering and scavenger systems.
  Accumulation of ROS\, termed Oxidative Stress\, results in changes in chr
 omatin configuration and gene expression\, lipid oxidation and cell death\
 , leading to neurodegenerative pathology. Our work suggests a role for ROS
  during normal development and 
LOCATION:Gurdon Institute Tea Room
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