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Activation of mGlu receptors induces LTD without affecting postsynaptic sensitivity of CA1 neurons in rat hippocampal slices
Author(s) -
Rammes Gerhard,
Palmer Mary,
Eder Matthias,
Dodt HansUlrich,
Zieglgänsberger Walter,
Collingridge Graham L.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.033514
Subject(s) - long term depression , ampa receptor , metabotropic glutamate receptor , postsynaptic potential , neuroscience , glutamate receptor , metabotropic receptor , nmda receptor , excitatory postsynaptic potential , neurotransmission , receptor , silent synapse , agonist , chemistry , biology , inhibitory postsynaptic potential , biochemistry
Two forms of long‐term depression (LTD) of excitatory synaptic transmission have been identified in the mammalian CNS, which are induced by the synaptic activation of N ‐methyl‐ d ‐aspartate (NMDA) and metabotropic glutamate (mGlu) receptors, respectively. The mGlu receptor‐dependent form of LTD can be activated by application of 3,5‐dihydroxyphenylglycine (DHPG), a group I selective mGlu receptor agonist. DHPG‐induced LTD is increasingly being used to investigate the mechanisms of mGlu receptor‐dependent LTD. However, recent experiments have argued for both a pre‐ and postsynaptic locus of expression of DHPG‐induced LTD. In the present study we report that DHPG‐induced LTD is not associated with changes in the sensitivity of CA1 neurons to bath applied AMPA. Furthermore, in contrast to homosynaptic LTD, DHPG‐induced LTD is also not associated with changes in sensitivity to focally uncaged l ‐glutamate. These data do not support the notion that DHPG‐induced LTD requires a modification of AMPA receptors, such as their internalisation, but are compatible with a presynaptic mechanism of expression.