PMID- 18930747
OWN - NLM
STAT- MEDLINE
DCOM- 20090701
LR  - 20181113
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 56
IP  - 2
DP  - 2009 Feb
TI  - NMDA receptor-mediated long-term alterations in epileptiform activity in 
      experimental chronic epilepsy.
PG  - 414-21
LID - 10.1016/j.neuropharm.2008.09.009 [doi]
AB  - When epileptiform activity is acutely induced in vitro, transient partial 
      blockade of N-methyl-d-aspartic acid (NMDA) receptor-mediated calcium influx 
      leads to selective long-term depotentiation of the synapses involved in the 
      epileptic activity as well as a reduction in the probability of further 
      epileptiform activity. If such selective depotentiation occurred within foci of 
      epileptic activity in vivo, the corresponding long-term reduction in seizure 
      probability could form the basis for a novel treatment of epilepsy. Continuous 
      radiotelemetric EEG monitoring demonstrated modest acute anticonvulsant effects 
      but no long-term reductions in the probability of spontaneous seizures after 
      transient partial blockade of NMDA receptors (NMDAR) during ictal and interictal 
      activity in the kainate animal model of chronic epilepsy. In vitro, 
      depotentiation was induced when NMDAR were partially blocked during epileptiform 
      activity in hippocampal slices from control animals, but not in slices from 
      chronically epileptic rats. However in slices from epileptic animals, 
      depotentiation during epileptiform activity was induced by partial block of NMDAR 
      using NR2B- but not NR2A-selective antagonists. These results suggest that 
      chronic epileptic activity is associated with changes in NMDA receptor-mediated 
      signaling that is reflected in the pharmacology of activity- and NMDA 
      receptor-dependent depotentiation.
FAU - Hellier, Jennifer L
AU  - Hellier JL
AD  - Neuroscience Program, University of Colorado Health Sciences Center, United 
      States.
FAU - White, Andrew
AU  - White A
FAU - Williams, Philip A
AU  - Williams PA
FAU - Dudek, F Edward
AU  - Dudek FE
FAU - Staley, Kevin J
AU  - Staley KJ
LA  - eng
GR  - R01 NS034360-03/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-08/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-09/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-04/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-07/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-10/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-12/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-06/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-11/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-13/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-05S1/NS/NINDS NIH HHS/United States
GR  - R01 NS034360/NS/NINDS NIH HHS/United States
GR  - R01 NS034360-05/NS/NINDS NIH HHS/United States
PT  - Journal Article
DEP - 20081007
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Propionates)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 174575-17-8 (alpha-amino-2'-chloro-5-(phosphonomethyl)(1,1'-biphenyl)-3-propanoic 
      acid)
RN  - SIV03811UC (Kainic Acid)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Biphenyl Compounds/pharmacology
MH  - Chronic Disease
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Electric Stimulation/methods
MH  - Electroencephalography/methods
MH  - Epilepsy/chemically induced/drug therapy/*metabolism/pathology/*physiopathology
MH  - Excitatory Amino Acid Agonists
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Hippocampus/drug effects/physiopathology
MH  - In Vitro Techniques
MH  - Kainic Acid/pharmacology
MH  - Long-Term Synaptic Depression/drug effects
MH  - Male
MH  - Propionates/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Time Factors
MH  - Wakefulness
PMC - PMC2698817
MID - NIHMS98068
EDAT- 2008/10/22 09:00
MHDA- 2009/07/02 09:00
PMCR- 2010/02/01
CRDT- 2008/10/22 09:00
PHST- 2008/06/03 00:00 [received]
PHST- 2008/09/11 00:00 [revised]
PHST- 2008/09/12 00:00 [accepted]
PHST- 2008/10/22 09:00 [pubmed]
PHST- 2009/07/02 09:00 [medline]
PHST- 2008/10/22 09:00 [entrez]
PHST- 2010/02/01 00:00 [pmc-release]
AID - S0028-3908(08)00418-8 [pii]
AID - 10.1016/j.neuropharm.2008.09.009 [doi]
PST - ppublish
SO  - Neuropharmacology. 2009 Feb;56(2):414-21. doi: 10.1016/j.neuropharm.2008.09.009. 
      Epub 2008 Oct 7.