NDLI: Extrasynaptic NR2B and NR2D subunits of NMDA receptors shape ‘superslow’ afterburst EPSC in rat hippocampus

Content Provider	PubMed Central
Author	Lozovaya, Natasha A. Grebenyuk, Sergei E. Tsintsadze, Timur Sh Feng, Bihua Monaghan, Daniel T. Krishtal, Oleg A.
Copyright Year	2004
Abstract	In conditions of facilitated synaptic release, CA3/CA1 synapses generate anomalously slow NMDA receptor-mediated EPSCs (EPSCNMDA). Such a time course has been attributed to the cooperation of synapses through glutamate spillover. Imitating a natural pattern of activity, we have applied short bursts (2–7 stimuli) of high-frequency stimulation and observed a spike-to-spike slow-down of the EPSCNMDA kinetics, which accompanied synaptic facilitation. It was found that the early component of the EPSCNMDA and the burst-induced late component of the EPSCNMDA have distinct pharmacological properties. The competitive NMDA antagonist R-(—)-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (D-CPP), which has higher affinity to NR2A than to NR2B subunits and lowest affinity at NR2D subunits, significantly slowed down the decay rate of the afterburst EPSC while leaving the kinetics of the control current unaffected. In contrast, ifenprodil, a highly selective NR2B antagonist, and [±]-cis-1-[phenanthren-2yl-carbonyl]piperazine-2,3-dicarboxylic acid (PPDA), a competitive antagonist that is moderately selective for NR2D subunits, more strongly inhibited the late component of the afterburst EPSCNMDA. The receptors formed by NR2B and (especially) NR2D subunits are known to have higher agonist sensitivity and much slower deactivation kinetics than NR2A-containing receptors. Furthermore, NR2B is preferentially and NR2D is exclusively located on extrasynaptic membranes. As the density of active synapses increases, the confluence of released glutamate makes EPSC decay much longer by activating more extrasynaptic NR2B- and NR2D-subunit-containing receptors. Long-term potentiation (LTP) induced by successive rounds of burst stimulation is accompanied by a long-term increase in the contribution of extrasynaptic receptors in the afterburst EPSCNMDA.
Related Links	http://dx.doi.org/10.1113/jphysiol.2004.063792
Ending Page	463
Page Count	13
Starting Page	451
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 2
Volume Number	558
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2004-07-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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