PMID- 30430968
OWN - NLM
STAT- MEDLINE
DCOM- 20190718
LR  - 20190718
IS  - 0317-1671 (Print)
IS  - 0317-1671 (Linking)
VI  - 45
IP  - 6
DP  - 2018 Nov
TI  - Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting 
      N-Methyl-d-Aspartic Acid Receptors.
PG  - 675-681
LID - 10.1017/cjn.2018.331 [doi]
AB  - BACKGROUND: We have previously shown that low-intensity ultrasound (LIUS), a 
      noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen 
      and glucose deprivation (OGD) or treatment with glutamate, a mediator of 
      OGD-induced edema, in acute rat hippocampal slice model in vitro. METHODS: In 
      this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid 
      (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these 
      different glutamate receptor agonists induce edema. The hippocampal slices were 
      then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor 
      (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on 
      edema formation. RESULTS: We observed that treatment with NMDA, an agonist of 
      ionotropic glutamate receptors, induced brain edema at similar degrees compared 
      with that induced by OGD. However, treatment with DHPG, an agonist of 
      metabotropic glutamate receptors, did not significantly induce brain edema. 
      Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented 
      brain edema formation by both OGD and NMDA in a concentration-dependent manner. 
      N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an 
      intensity-dependent manner when ultrasound was administered at 30, 50, or 100 
      mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS 
      reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. CONCLUSION: 
      These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation 
      by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema 
      formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need 
      further investigation.
FAU - Hada, Binika
AU  - Hada B
AD  - 1Department of Biomedical Sciences,Inha University College of 
      Medicine,Incheon,Korea.
FAU - Karmacharya, Mrigendra Bir
AU  - Karmacharya MB
AD  - 2Department of Physiology and Biophysics,Inha University College of 
      Medicine,Incheon,Korea.
FAU - Park, So R
AU  - Park SR
AD  - 2Department of Physiology and Biophysics,Inha University College of 
      Medicine,Incheon,Korea.
FAU - Choi, Byung H
AU  - Choi BH
AD  - 1Department of Biomedical Sciences,Inha University College of 
      Medicine,Incheon,Korea.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Can J Neurol Sci
JT  - The Canadian journal of neurological sciences. Le journal canadien des sciences 
      neurologiques
JID - 0415227
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, Amino Acid)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (aspartic acid receptor)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 6384-92-5 (N-Methylaspartate)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Excitatory Amino Acid Antagonists/*pharmacology
MH  - Glucose/metabolism
MH  - Glutamic Acid/metabolism
MH  - Hippocampus/metabolism/physiopathology
MH  - Male
MH  - N-Methylaspartate/*pharmacology
MH  - Rats, Sprague-Dawley
MH  - Receptors, Amino Acid/drug effects/metabolism
MH  - Receptors, N-Methyl-D-Aspartate/drug effects/*metabolism
MH  - *Ultrasonography/adverse effects
OTO - NOTNLM
OT  - N-Methyl-d-aspartate receptor
OT  - Brain edema
OT  - Ischemia
OT  - Low-intensity ultrasound
OT  - Oxygen and glucose deprivation
EDAT- 2018/11/16 06:00
MHDA- 2019/07/19 06:00
CRDT- 2018/11/16 06:00
PHST- 2018/11/16 06:00 [entrez]
PHST- 2018/11/16 06:00 [pubmed]
PHST- 2019/07/19 06:00 [medline]
AID - S0317167118003311 [pii]
AID - 10.1017/cjn.2018.331 [doi]
PST - ppublish
SO  - Can J Neurol Sci. 2018 Nov;45(6):675-681. doi: 10.1017/cjn.2018.331.