PMID- 15749335
OWN - NLM
STAT- MEDLINE
DCOM- 20050512
LR  - 20131121
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 131
IP  - 4
DP  - 2005
TI  - N-methyl-D-aspartic acid-induced and Ca-dependent neuronal swelling and its 
      retardation by brain-derived neurotrophic factor in the epileptic hippocampus.
PG  - 801-12
AB  - Dentate granule cell (DGC) swelling was studied by imaging changes in light 
      transmittance from hippocampal slices in the rat pilocarpine model of epilepsy 
      and human epileptic specimens. Brief bath-application of N-methyl-D-aspartic acid 
      (NMDA) induced swelling in the control rat DGC (physiological swelling). 
      Physiological swelling was short-lasting, and rapidly recovered upon removal of 
      NMDA. In contrast, the swelling induced in the pilocarpine-treated rat 
      hippocampus and human epileptic hippocampus (epileptic swelling) was 
      long-lasting, and often recovered slowly over an hour. Both types of swelling 
      were blocked by the NMDA receptor (NMDAR) antagonist, D-APV, suggesting that they 
      shared the same induction mechanism. However, the swellings differed in their 
      sensitivity to a calcium chelator, 
      1.2-bis(2-aminophenoxy)ethane-N,N,N,N-tetra-acetate (BAPTA), and an endoplasmic 
      reticulum (ER) Ca2+-ATPase inhibitor, thapsigargin (TG). BAPTA and TG affected 
      only epileptic swelling, and physiological swelling was spared. This suggested 
      that the NMDAR-induced epileptic swelling might involve an additional mechanism 
      for its maintenance, likely recruiting ER Ca2+ stores. Brain-derived neurotrophic 
      factor (BDNF) slightly attenuated physiological swelling, and blocked epileptic 
      swelling. The present study suggests a functional link between the activation of 
      NMDAR and a release of Ca2+ from internal stores during the induction of 
      epileptic swelling, and a neuroprotective role of BDNF on the NMDAR-induced 
      swelling in the epileptic hippocampus.
FAU - Isokawa, M
AU  - Isokawa M
AD  - Department of Physiology and Program in Neuroscience University of Maryland, 655 
      West Baltimore Street, Baltimore, MD 21201, USA. misok001@umaryland.edu
LA  - eng
GR  - NS 31180/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Chelating Agents)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Neuroprotective Agents)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - 67526-95-8 (Thapsigargin)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
RN  - K22DDW77C0 (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphatases/antagonists & inhibitors
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Calcium/metabolism/*physiology
MH  - Cell Size
MH  - Chelating Agents/pharmacology
MH  - Cytosol/metabolism/ultrastructure
MH  - Dentate Gyrus/cytology/pathology
MH  - Egtazic Acid/*analogs & derivatives/pharmacology
MH  - Epilepsy/*pathology
MH  - Excitatory Amino Acid Agonists/*pharmacology
MH  - Hippocampus/*pathology
MH  - Light
MH  - Male
MH  - N-Methylaspartate/*pharmacology
MH  - Neurons/*drug effects/ultrastructure
MH  - Neuroprotective Agents/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Thapsigargin/pharmacology
EDAT- 2005/03/08 09:00
MHDA- 2005/05/13 09:00
CRDT- 2005/03/08 09:00
PHST- 2004/12/08 00:00 [accepted]
PHST- 2005/03/08 09:00 [pubmed]
PHST- 2005/05/13 09:00 [medline]
PHST- 2005/03/08 09:00 [entrez]
AID - S0306-4522(05)00028-X [pii]
AID - 10.1016/j.neuroscience.2004.12.008 [doi]
PST - ppublish
SO  - Neuroscience. 2005;131(4):801-12. doi: 10.1016/j.neuroscience.2004.12.008.