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SUMMARY:Special BMI LNDC SEMINAR // New advances in microglial physiology 
 and clinical relevance
DTSTART:20170202T121500
DTEND:20170202T131500
DTSTAMP:20260921T115828Z
UID:51596923b8b3a804c610bdd4289224ff2bb382dfd64f163124a9b663
CATEGORIES:Conferences - Seminars
DESCRIPTION:Renaud Jolivet\, Nuclear and Corpuscular Physics Department\, 
 University of Geneva\nMicroglia\, the brain’s immune cells\, continually
  extend and retract processes to survey the brain. This surveillance may
  be needed to prune redundant or damaged synapses during development or
  pathology\, to modulate neuronal activity and to detect pathogenic ag
 ents\, but its mechanism is obscure. To examine the signalling regulating
  microglial process movement\, we imaged and whole-cell clamped microgli
 a in situ in brain slices and in vivo. Applying ATP led to membrane h
 yperpolarization mediated by a P2Y12 receptor-linked ion channel that we
  identify as the anaesthetic-sensitive two-pore domain K+ channel THIK-1
 \, and evoked process outgrowth towards the ATP source. Blocking P2Y12 
 receptors prevented process outgrowth in response to ATP released by tis
 sue damage but did not affect the membrane potential or surveillance of 
 the brain by microglia. In contrast\, blocking tonic activity of THIK-1 
 with specific K+ channel inhibitors\, gene knockout or gaseous anaesthet
 ics\, or locally applying high [K+]o solution\, depolarised microglia wh
 ich decreased microglial ramification and inhibited surveillance of the b
 rain. Blocking THIK-1 activity also inhibited interleukin-1ß release ev
 oked by ATP/lipopolysaccharide-evoked microglial activation. Thus\, regul
 ation of the microglial membrane potential by THIK-1 channels (which are
  not expressed by the cultured microglia often used to assess brain imm
 une function) controls immune surveillance of the brain and immune effecto
 r release\, suggesting that modulation of THIK-1 channels could be used 
 to alter these functions therapeutically. The inhibitory effect of gaseou
 s anaesthetics on THIK-1 implies that brain immune function may be suppr
 essed in clinical situations using these agents.\n 
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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