PMID- 17439491
OWN - NLM
STAT- MEDLINE
DCOM- 20070621
LR  - 20161124
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 25
IP  - 7
DP  - 2007 Apr
TI  - High pressure modulation of NMDA receptor dependent excitability.
PG  - 2045-52
AB  - Pressure above 1.1 MPa induces in mammals and humans the high pressure 
      neurological syndrome (HPNS). HPNS is characterized by cognitive and motor 
      decrements associated with sleep disorders, EEG changes, tremor, and convulsions 
      that ultimately may lead to death. Previous theories proposed that augmented 
      response of the glutamatergic N-methyl-D-aspartate receptor (NMDAR) or reduced 
      GABAergic inhibition may be involved. Recently, we have reported that isolated 
      NMDAR response was augmented at high pressure. We now test whether this 
      augmentation induces neuronal hyperexcitability. We studied high pressure effects 
      on pharmacologically isolated NMDAR field excitatory postsynaptic potentials 
      (fEPSPs) and on their efficacy in generating population spikes (PSs). 
      Sprague-Dawley male rats were used. Hippocampal coronal brain slices were 
      prepared, constantly superfused with physiological solutions, gas-saturated at 
      normobaric pressure, and compressed up to 10.1 MPa with helium. fEPSPs and PSs 
      were recorded from the dendritic and the somatic layers of CA1 pyramidal neurons 
      in response to Schaefer collaterals stimulation with trains of five stimuli at 25 
      Hz. Pressure caused PSs to appear earlier in the train. However, PS delay, rise 
      time and decay time were increased and PS amplitude, frequency, and number were 
      decreased in the last responses in the train. The decrease in late fEPSPs was 
      associated with a reduction of the total number of PSs in the train, apparently 
      without a change in the synaptic efficacy. These results may partially explain 
      the neuronal hyperexcitability observed at pressure. Therefore, it is postulated 
      that significant hyperexcitability is attained at pressure only when the normal 
      fast fEPSP is intact.
FAU - Mor, Amir
AU  - Mor A
AD  - Department of Physiology, Faculty of Health Sciences and Zlotowski Center for 
      Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel. 
      morami12@gmail.com
FAU - Grossman, Yoram
AU  - Grossman Y
LA  - eng
PT  - Journal Article
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Quinoxalines)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 62T278S1MX (FG 9041)
SB  - IM
MH  - Animals
MH  - *Atmospheric Pressure
MH  - Excitatory Amino Acid Antagonists/metabolism
MH  - Excitatory Postsynaptic Potentials/physiology
MH  - High Pressure Neurological Syndrome/etiology/*metabolism
MH  - Hippocampus/cytology/metabolism
MH  - Humans
MH  - Male
MH  - Quinoxalines/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Synaptic Transmission/physiology
EDAT- 2007/04/19 09:00
MHDA- 2007/06/22 09:00
CRDT- 2007/04/19 09:00
PHST- 2007/04/19 09:00 [pubmed]
PHST- 2007/06/22 09:00 [medline]
PHST- 2007/04/19 09:00 [entrez]
AID - EJN5479 [pii]
AID - 10.1111/j.1460-9568.2007.05479.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 2007 Apr;25(7):2045-52. doi: 10.1111/j.1460-9568.2007.05479.x.