PMID- 28367116
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1662-5102 (Print)
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 11
DP  - 2017
TI  - Microglial Intracellular Ca(2+) Signaling in Synaptic Development and its 
      Alterations in Neurodevelopmental Disorders.
PG  - 69
LID - 10.3389/fncel.2017.00069 [doi]
LID - 69
AB  - Autism spectrum disorders (ASDs) are neurodevelopmental disorders characterized 
      by deficits in social interaction, difficulties with language and 
      repetitive/restricted behaviors. Microglia are resident innate immune cells which 
      release many factors including proinflammatory cytokines, nitric oxide (NO) and 
      brain-derived neurotrophic factor (BDNF) when they are activated in response to 
      immunological stimuli. Recent in vivo imaging has shown that microglia sculpt and 
      refine the synaptic circuitry by removing excess and unwanted synapses and be 
      involved in the development of neural circuits or synaptic plasticity thereby 
      maintaining the brain homeostasis. BDNF, one of the neurotrophins, has various 
      important roles in cell survival, neurite outgrowth, neuronal differentiation, 
      synaptic plasticity and the maintenance of neural circuits in the CNS. 
      Intracellular Ca(2+) signaling is important for microglial functions including 
      ramification, de-ramification, migration, phagocytosis and release of cytokines, 
      NO and BDNF. BDNF induces a sustained intracellular Ca(2+) elevation through the 
      upregulation of the surface expression of canonical transient receptor potential 
      3 (TRPC3) channels in rodent microglia. BDNF might have an anti-inflammatory 
      effect through the inhibition of microglial activation and TRPC3 could play 
      important roles in not only inflammatory processes but also formation of synapse 
      through the modulation of microglial phagocytic activity in the brain. This 
      review article summarizes recent findings on emerging dual, inflammatory and 
      non-inflammatory, roles of microglia in the brain and reinforces the importance 
      of intracellular Ca(2+) signaling for microglial functions in both normal 
      neurodevelopment and their potential contributing to neurodevelopmental disorders 
      such as ASDs.
FAU - Mizoguchi, Yoshito
AU  - Mizoguchi Y
AD  - Department of Psychiatry, Faculty of Medicine, Saga University Saga, Japan.
FAU - Monji, Akira
AU  - Monji A
AD  - Department of Psychiatry, Faculty of Medicine, Saga University Saga, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170317
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC5355421
OTO - NOTNLM
OT  - BDNF
OT  - TRPC3 channels
OT  - autism spectrum disorders
OT  - calcium signaling
OT  - microglia
OT  - oxytocin
OT  - proBDNF
OT  - synapse development
EDAT- 2017/04/04 06:00
MHDA- 2017/04/04 06:01
PMCR- 2017/01/01
CRDT- 2017/04/04 06:00
PHST- 2016/11/25 00:00 [received]
PHST- 2017/02/24 00:00 [accepted]
PHST- 2017/04/04 06:00 [entrez]
PHST- 2017/04/04 06:00 [pubmed]
PHST- 2017/04/04 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2017.00069 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2017 Mar 17;11:69. doi: 10.3389/fncel.2017.00069. 
      eCollection 2017.