PMID- 17106878
OWN - NLM
STAT- MEDLINE
DCOM- 20070316
LR  - 20181201
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 55
IP  - 3
DP  - 2007 Feb
TI  - Microglial control of neuronal death and synaptic properties.
PG  - 233-8
AB  - Microglia have long been characterized by their immune function in the nervous 
      system and are still mainly considered in a beneficial versus detrimental 
      dialectic. However a review of literature enables to shed novel lights on 
      microglial function under physiological conditions. It is now relevant to 
      position these cells as full time partners of neuronal function and more 
      specifically of synaptogenesis and developmental apoptosis. Indeed, microglia can 
      actively control neuronal death. It has actually been shown in retina that 
      microglial nerve growth factor (NGF) is necessary for the developmental apoptosis 
      to occur. Similarly, in cerebellum, microglia induces developmental Purkinje 
      cells death through respiratory burst. Furthermore, in spinal cord, microglial 
      TNFalpha commits motoneurons to a neurotrophic dependent developmental apoptosis. 
      Microglia can also control synaptogenesis. This is suggested by the fact that a 
      mutation in KARAP/DAP12, a key protein of microglial activation impacts synaptic 
      functions in hippocampus, and synapses protein content. In addition it has been 
      now demonstrated that microglial brain-derived neurotrophin factor (BDNF) 
      directly regulates synaptic properties in spinal cord. In conclusion, microglia 
      can control neuronal function under physiological conditions and it is known that 
      neuronal activity reciprocally controls microglial activation. We will discuss 
      the importance of this cross-talk which allows microglia to orchestrate the 
      balance between synaptogenesis and neuronal death occurring during development or 
      injuries.
CI  - Copyright 2006 Wiley-Liss, Inc.
FAU - Bessis, Alain
AU  - Bessis A
AD  - Biologie Cellulaire de la Synapse, Inserm U789, Ecole Normale Superieure, 46 rue 
      d'Ulm 75005 Paris, France. alain.bessis@ens.fr
FAU - Bechade, Catherine
AU  - Bechade C
FAU - Bernard, Delphine
AU  - Bernard D
FAU - Roumier, Anne
AU  - Roumier A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Cell Communication/physiology
MH  - Cell Differentiation/physiology
MH  - Humans
MH  - Microglia/*metabolism
MH  - Nerve Growth Factors/metabolism
MH  - Neuronal Plasticity/*physiology
MH  - Neurons/*physiology
MH  - Signal Transduction/*physiology
MH  - Synapses/*physiology
RF  - 82
EDAT- 2006/11/16 09:00
MHDA- 2007/03/17 09:00
CRDT- 2006/11/16 09:00
PHST- 2006/11/16 09:00 [pubmed]
PHST- 2007/03/17 09:00 [medline]
PHST- 2006/11/16 09:00 [entrez]
AID - 10.1002/glia.20459 [doi]
PST - ppublish
SO  - Glia. 2007 Feb;55(3):233-8. doi: 10.1002/glia.20459.