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SUMMARY:Phosphatidylserine signaling in developmental synaptic pruning - U
 rte Neniskyte\,  EMBL &amp\; Vilnius University
DTSTART:20160909T110000Z
DTEND:20160909T120000Z
UID:TALK67342@talks.cam.ac.uk
CONTACT:47293
DESCRIPTION:The development of a complex nervous system is accompanied by 
 a generation of superfluous neuronal connections that are removed when neu
 ral circuits mature. Why are so many synapses lost\, what determines which
  synapses are eliminated\, what are the molecular mechanisms involved\, an
 d what are the consequences of not getting it right? Synaptic pruning appe
 ars to be highly selective process that ensures selective elimination of s
 ome synapses and the maintenance of others. Structural and functional refi
 nement of synaptic network is tightly related to the presence of brain imm
 une cells microglia that actively contact and engulf unnecessary synapses.
  Aberrant or impaired microglial function leads to abnormal synaptic densi
 ties and dysfunctional connectivity that causes morphological\, functional
  and behavioral deficits. For example\, brain imaging and post-mortem stud
 ies suggest the role of deficient synaptic pruning in neurodevelopmental d
 isorders\, such as autism and schizophrenia. The reduction of brain volume
  and reduced density of dendritic spines in schizophrenia is suggestive of
  over-pruning\, whereas increased brain volume and dendritic spine densiti
 es may indicate under-pruning in autism. Microglial phagocytic function ha
 s been implicated to have a central role in synaptic pruning\; however\, n
 euronal “eat-me” signal that discriminates weak and strong synapses re
 mains to be identified. Using organotypic hippocampal slice cultures and i
 n vivo mouse models we investigate the role of phosphatidylserine as a neu
 ronal surface signal that labels synapses for elimination thus ensuring pr
 oper brain development and circuit maturation.
LOCATION:Seminar Room 1\, Hopkins Building\, Biochemistry Department\, Cam
 bridge
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