PMID- 10580501
OWN - NLM
STAT- MEDLINE
DCOM- 19991210
LR  - 20141120
IS  - 0028-0836 (Print)
IS  - 0028-0836 (Linking)
VI  - 402
IP  - 6759
DP  - 1999 Nov 18
TI  - Kainate receptors are involved in synaptic plasticity.
PG  - 297-301
AB  - The ability of synapses to modify their synaptic strength in response to activity
      is a fundamental property of the nervous system and may be an essential component
      of learning and memory. There are three classes of ionotropic glutamate receptor,
      namely NMDA (N-methyl-D-aspartate), AMPA
      (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid) and kainate
      receptors; critical roles in synaptic plasticity have been identified for two of 
      these. Thus, at many synapses in the brain, transient activation of NMDA
      receptors leads to a persistent modification in the strength of synaptic
      transmission mediated by AMPA receptors. Here, to determine whether kainate
      receptors are involved in synaptic plasticity, we have used a new antagonist,
      LY382884 ((3S, 4aR, 6S,
      8aR)-6-((4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydro
      isoquinoline-3-carboxylic acid), which antagonizes kainate receptors at
      concentrations that do not affect AMPA or NMDA receptors. We find that LY382884
      is a selective antagonist at neuronal kainate receptors containing the GluR5
      subunit. It has no effect on long-term potentiation (LTP) that is dependent on
      NMDA receptors but prevents the induction of mossy fibre LTP, which is
      independent of NMDA receptors. Thus, kainate receptors can act as the induction
      trigger for long-term changes in synaptic transmission.
FAU - Bortolotto, Z A
AU  - Bortolotto ZA
AD  - MRC Centre for Synaptic Plasticity, Department of Anatomy, Medical School,
      University of Bristol, UK.
FAU - Clarke, V R
AU  - Clarke VR
FAU - Delany, C M
AU  - Delany CM
FAU - Parry, M C
AU  - Parry MC
FAU - Smolders, I
AU  - Smolders I
FAU - Vignes, M
AU  - Vignes M
FAU - Ho, K H
AU  - Ho KH
FAU - Miu, P
AU  - Miu P
FAU - Brinton, B T
AU  - Brinton BT
FAU - Fantaske, R
AU  - Fantaske R
FAU - Ogden, A
AU  - Ogden A
FAU - Gates, M
AU  - Gates M
FAU - Ornstein, P L
AU  - Ornstein PL
FAU - Lodge, D
AU  - Lodge D
FAU - Bleakman, D
AU  - Bleakman D
FAU - Collingridge, G L
AU  - Collingridge GL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Nature
JT  - Nature
JID - 0410462
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Isoquinolines)
RN  - 0 (LY382884)
RN  - 0 (Receptors, AMPA)
RN  - 0 (Receptors, Kainic Acid)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - H030S2S85J (Kynurenic Acid)
SB  - IM
CIN - Nature. 2000 Aug 31;406(6799):957. PMID: 10984042
MH  - Animals
MH  - Cell Line
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Excitatory Postsynaptic Potentials
MH  - Hippocampus/physiology
MH  - Humans
MH  - In Vitro Techniques
MH  - Isoquinolines/pharmacology
MH  - Kynurenic Acid/pharmacology
MH  - Long-Term Potentiation/drug effects/*physiology
MH  - Mossy Fibers, Hippocampal/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, AMPA/drug effects/metabolism
MH  - Receptors, Kainic Acid/antagonists & inhibitors/*physiology
MH  - Receptors, N-Methyl-D-Aspartate/drug effects/metabolism
MH  - Synapses/*physiology
MH  - Synaptic Membranes/metabolism
MH  - Synaptic Transmission
EDAT- 1999/12/02 09:00
MHDA- 2001/03/23 10:01
CRDT- 1999/12/02 09:00
PHST- 1999/12/02 09:00 [pubmed]
PHST- 2001/03/23 10:01 [medline]
PHST- 1999/12/02 09:00 [entrez]
AID - 10.1038/46290 [doi]
PST - ppublish
SO  - Nature. 1999 Nov 18;402(6759):297-301. doi: 10.1038/46290.