PMID- 25896886
OWN - NLM
STAT- MEDLINE
DCOM- 20160126
LR  - 20150504
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 114
DP  - 2015 May
TI  - NMDA receptor NR2B subunits contribute to PTZ-kindling-induced hippocampal 
      astrocytosis and oxidative stress.
PG  - 70-8
LID - S0361-9230(15)00063-5 [pii]
LID - 10.1016/j.brainresbull.2015.04.002 [doi]
AB  - The N-methyl-d-aspartate (NMDA) receptor plays an important role in the 
      pathophysiology of several neurological diseases, including epilepsy. The present 
      study investigated the effect of NMDA receptor NR2B subunits on 
      pentylenetetrazole (PTZ)-kindling-induced pathological and biochemical events in 
      mice. Our results showed that PTZ-kindling up-regulates the expression of NMDA 
      receptor NR2B subunits in the hippocampus and that kindled mice were 
      characterized by significant astrocytosis and neuron loss in the hippocampus. 
      Oxidative stress, including excessive malondialdehyde (MDA) production and 
      decreased enzymatic activities of superoxide dismutase (SOD) and glutathione 
      peroxidase (GSH-PX), were detected in the hippocampus after the mice were fully 
      kindled. Additionally, expression of brain-derived neurotrophic factor (BDNF) in 
      the hippocampus was found to be up-regulated in PTZ-kindled mice. However, 
      selectively blocking NMDA receptor NR2B subunits by ifenprodil significantly 
      suppressed PTZ-kindling-induced hippocampal astrocytosis, oxidative stress and 
      neuron loss. Furthermore, blocking NMDA receptor NR2B subunits also abolished 
      PTZ-kindling-induced BDNF expression. These results indicate that NMDA receptor 
      NR2B subunits contribute to epilepsy-associated pathological and biochemical 
      events, including hippocampal astrocytosis, oxidative stress and neuron loss, and 
      these events might be correlated with up-regulation of BDNF expression.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Zhu, Xinjian
AU  - Zhu X
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China. Electronic address: xinjianzhu@seu.edu.cn.
FAU - Dong, Jingde
AU  - Dong J
AD  - Department of Neurology, Nanjing Brain Hospital, Nanjing, China.
FAU - Shen, Kai
AU  - Shen K
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China.
FAU - Bai, Ying
AU  - Bai Y
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China.
FAU - Zhang, Yuan
AU  - Zhang Y
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China.
FAU - Lv, Xuan
AU  - Lv X
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China.
FAU - Chao, Jie
AU  - Chao J
AD  - Department of Physiology, Medical School of Southeast University, Nanjing, China.
FAU - Yao, Honghong
AU  - Yao H
AD  - Department of Pharmacology, Medical School of Southeast University, Nanjing, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150417
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Piperidines)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - R8OE3P6O5S (ifenprodil)
RN  - WM5Z385K7T (Pentylenetetrazole)
SB  - IM
MH  - Animals
MH  - Astrocytes/drug effects/pathology/*physiology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cell Death/drug effects/physiology
MH  - Epilepsy/metabolism
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Gliosis/drug therapy/pathology/*physiopathology
MH  - Glutathione Peroxidase/metabolism
MH  - Hippocampus/drug effects/pathology/*physiopathology
MH  - Kindling, Neurologic/drug effects/pathology/*physiology
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Mice, Inbred C57BL
MH  - Neurons/drug effects/pathology/physiology
MH  - Oxidative Stress/drug effects/*physiology
MH  - Pentylenetetrazole
MH  - Piperidines/pharmacology
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*metabolism
MH  - Superoxide Dismutase/metabolism
OTO - NOTNLM
OT  - Astrocytosis
OT  - BDNF
OT  - Epilepsy
OT  - Kindling
OT  - NMDA receptor
EDAT- 2015/04/22 06:00
MHDA- 2016/01/27 06:00
CRDT- 2015/04/22 06:00
PHST- 2014/11/28 00:00 [received]
PHST- 2015/03/30 00:00 [revised]
PHST- 2015/04/06 00:00 [accepted]
PHST- 2015/04/22 06:00 [entrez]
PHST- 2015/04/22 06:00 [pubmed]
PHST- 2016/01/27 06:00 [medline]
AID - S0361-9230(15)00063-5 [pii]
AID - 10.1016/j.brainresbull.2015.04.002 [doi]
PST - ppublish
SO  - Brain Res Bull. 2015 May;114:70-8. doi: 10.1016/j.brainresbull.2015.04.002. Epub 
      2015 Apr 17.