PMID- 23298414
OWN - NLM
STAT- MEDLINE
DCOM- 20130826
LR  - 20220311
IS  - 1878-108X (Electronic)
IS  - 0166-2236 (Linking)
VI  - 36
IP  - 3
DP  - 2013 Mar
TI  - Glia and epilepsy: excitability and inflammation.
PG  - 174-84
LID - S0166-2236(12)00205-6 [pii]
LID - 10.1016/j.tins.2012.11.008 [doi]
AB  - Epilepsy is characterized by recurrent spontaneous seizures due to 
      hyperexcitability and hypersynchrony of brain neurons. Current theories of 
      pathophysiology stress neuronal dysfunction and damage, and aberrant connections 
      as relevant factors. Most antiepileptic drugs target neuronal mechanisms. 
      However, nearly one-third of patients have seizures that are refractory to 
      available medications; a deeper understanding of mechanisms may be required to 
      conceive more effective therapies. Recent studies point to a significant 
      contribution by non-neuronal cells, the glia--especially astrocytes and 
      microglia--in the pathophysiology of epilepsy. This review critically evaluates 
      the role of glia-induced hyperexcitability and inflammation in epilepsy.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Devinsky, Orrin
AU  - Devinsky O
AD  - Epilepsy Center, Department of Neurology, NYU School of Medicine, New York, NY 
      10016, USA. od4@nyu.edu
FAU - Vezzani, Annamaria
AU  - Vezzani A
FAU - Najjar, Souhel
AU  - Najjar S
FAU - De Lanerolle, Nihal C
AU  - De Lanerolle NC
FAU - Rogawski, Michael A
AU  - Rogawski MA
LA  - eng
GR  - NS072094/NS/NINDS NIH HHS/United States
GR  - NS077582/NS/NINDS NIH HHS/United States
GR  - NS079202/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20130105
PL  - England
TA  - Trends Neurosci
JT  - Trends in neurosciences
JID - 7808616
RN  - 0 (Anticonvulsants)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Ion Channels)
RN  - 0 (Nerve Tissue Proteins)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - Anticonvulsants/pharmacology/therapeutic use
MH  - Blood-Brain Barrier
MH  - Body Water/metabolism
MH  - Calcium Signaling
MH  - Cytokines/metabolism
MH  - Drug Resistance
MH  - Encephalitis/complications/*physiopathology
MH  - Epilepsy/drug therapy/etiology/immunology/pathology/*physiopathology
MH  - Extracellular Space/metabolism
MH  - Gliosis/pathology/physiopathology
MH  - Glutamic Acid/metabolism
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Ion Channels/physiology
MH  - Microcirculation
MH  - Models, Neurological
MH  - Nerve Tissue Proteins/physiology
MH  - Neuroglia/*physiology
MH  - Neurons/metabolism
MH  - Potassium/metabolism
EDAT- 2013/01/10 06:00
MHDA- 2013/08/27 06:00
CRDT- 2013/01/10 06:00
PHST- 2012/07/07 00:00 [received]
PHST- 2012/11/15 00:00 [revised]
PHST- 2012/11/29 00:00 [accepted]
PHST- 2013/01/10 06:00 [entrez]
PHST- 2013/01/10 06:00 [pubmed]
PHST- 2013/08/27 06:00 [medline]
AID - S0166-2236(12)00205-6 [pii]
AID - 10.1016/j.tins.2012.11.008 [doi]
PST - ppublish
SO  - Trends Neurosci. 2013 Mar;36(3):174-84. doi: 10.1016/j.tins.2012.11.008. Epub 
      2013 Jan 5.