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mGluRs induce a long‐term depression in the ventral tegmental area that involves a switch of the subunit composition of AMPA receptors
Author(s) -
Bellone Camilla,
Lüscher Christian
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.03979.x
Subject(s) - long term depression , neuroscience , ampa receptor , ventral tegmental area , metabotropic glutamate receptor , excitatory postsynaptic potential , long term potentiation , silent synapse , glutamatergic , glutamate receptor , chemistry , metabotropic glutamate receptor 1 , biology , dopamine , receptor , inhibitory postsynaptic potential , biochemistry , dopaminergic
Excitatory glutamatergic synapses on dopamine (DA) neurons of the ventral tegmental area (VTA) undergo long‐lasting changes during conditioning of natural rewards and in response to drug exposure. It has been suggested that the ensuing context‐dependent behavioural changes are associated with an increased efficacy of synaptic afferents determined by the balance of long‐term potentiation (LTP) and long‐term depression (LTD). However, the molecular nature of the forms of LTP/LTD involved remains elusive. Here, using acute rat brain slices, we describe a form of long‐term depression (LTD) that was engaged by synaptic activity or exogenous agonists activating group I metabotropic glutamate receptors (mGluR) and was sensitive to mGluR1 antagonists. Prior to mGluR‐LTD, AMPAR mediated excitatory postsynaptic currents (EPSCs) showed strong rectification at positive potentials and were sensitive to Joro spider toxin (JST), a selective blocker of GluR2‐lacking AMPARs. After mGluR‐LTD, AMPAR EPSCs had linear current‐voltage relations and became insensitive to JST. We conclude that activation of mGluR1s triggers a redistribution exchanging native receptors for GluR2 containing AMPARs, ultimately causing LTD that may oppose pathological neuroadaptation.