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Journal of Neuroscience, Vol 15, 2013-2020, Copyright © 1995 by Society for Neuroscience
Tetanically induced LTP involves a similar increase in the AMPA and NMDA receptor components of the excitatory postsynaptic current: investigations of the involvement of mGlu receptors
JJ O'Connor, MJ Rowan and R Anwyl
Department of Pharmacology and Therapeutics, Trinity College, Dublin, Ireland.
Whole-cell patch-clamp recordings of evoked excitatory postsynaptic
currents (EPSCs) were made from granule cells of the rat dentate gyrus in
vitro. Tetanic stimulation in control media evoked a statistically
identical long-term potentiation (LTP) of both the AMPA and NMDA
receptor-mediated components of the dual component EPSC (AM-PAR and NMDAR
EPSCs), as shown by a similar percentage increase in both components when
measured at a holding potential of -30 mV, and also by an identical time
course of the pre- and post-LTP induced EPSC at -30 mV and -70 mV.
Application of the selective metabotropic glutamate receptor (mGluR)
agonist 1S,3R-ACPD induced a transient depression followed by a rapid onset
LTP of both the AMPAR and the NMDAR components of the dual component EPSC.
The ACPD- and tetanically induced LTP of the AMPAR EPSC was NMDAR
dependent, being abolished by the NMDAR antagonist AP5. Tetanic
stimulation, and application of ACPD, also induced a relatively rapid onset
LTP of the pharmacologically isolated NMDAR EPSC. Such tetanically and
ACPD-induced LTP of the isolated NMDAR EPSC was also dependent on NMDAR
activation, being strongly inhibited by AP5. The tetanically and the
ACPD-induced LTP of the NMDAR EPSC were dependent on protein kinase C (PKC)
stimulation, being strongly inhibited by the PKC inhibitor PKCI (19-31).
The studies suggest that coactivation of the mGluR and NMDAR are required
for induction of LTP of both the AMPAR- and NMDAR-mediated synaptic
transmission. Moreover, LTP of the NMDAR-mediated synaptic transmission
appears to be dependent on coincident activation of the NMDAR and mGluR.
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