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J Neurophysiol (April 1, 2003). 10.1152/jn.00842.2002
Submitted on Submitted 23 September 2002; accepted in final form 16 December
2002
1Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, 1083 Budapest, Hungary; and 2Medical Research Council, Anatomical Neuropharmacology Unit, University Department of Pharmacology, Oxford OX1 3TH, United Kingdom
Losonczy, Attila,
Peter Somogyi, and
Zoltan Nusser.
Reduction of Excitatory Postsynaptic Responses by Persistently
Active Metabotropic Glutamate Receptors in the Hippocampus. J. Neurophysiol. 89: 1910-1919, 2003. The
release of glutamate from axon terminals is under the control of a
variety of presynaptic receptors, including several metabotropic
glutamate receptors (mGluRs). Synaptically released glutamate can
activate mGluRs within the same synapse where it was released and also
at a distance following its diffusion from the synaptic cleft. It is
unknown, however, whether the release of glutamate is under the control
of persistently active mGluRs. We tested the contribution of mGluR
activation to the excitatory postsynaptic responses recorded from
several types of GABAergic interneuron in strata oriens/alveus of the
mouse hippocampus. The application of 1 µM
(
S)--amino--[(1S,2S)-2-carboxycyclopropyl]xanthine-9-propanoic acid (LY341495), a broad-spectrum mGluR (subtypes 2/3/7/8) antagonist at this concentration, increased evoked-excitatory postsynaptic current
(eEPSC) amplitudes by 60% (n = 33). On identified cell types, LY341495 had either no effect (7 of 14 basket and 7 of 13 oriens-lacunosum moleculare, O-LM cells) or resulted in a 32 ± 30% (mean ± SD) increase in EPSC amplitudes recorded from basket cells and a seven-times greater (216 ± 102%) enhancement of
EPSCs in O-LM cells. The enhancement of the first EPSC of a
high-frequency train indicates persistent mGluR activation. During
antagonist application, the relative increase in EPSC amplitude evoked
by the second and subsequent pulses in the train was not larger than that of the first EPSC, showing no further receptor activation by the
released transmitter. The effect of mGluR subtype selective agonists
[3 µM L(+)-2-amino-4-phosphonobutyric acid (L-AP4): mGluR4/8; 600 µM L-AP4: mGluR4/7/8; 1 µM
(2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG-IU):
mGluR2/3] and an antagonist (0.2 µM LY341495: mGluR2/3/8) suggests
that persistently active mGluR2/3/8 control the excitability of
hippocampal network.
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