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LTP of GABAergic synapses in the ventral tegmental area and beyond
Author(s) -
Nugent Fereshteh S.,
Kauer Julie A.
Publication year - 2008
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.2007.148098
Subject(s) - neuroscience , long term potentiation , gabaergic , ventral tegmental area , excitatory postsynaptic potential , metaplasticity , synaptic plasticity , inhibitory postsynaptic potential , synapse , neuronal memory allocation , synaptic fatigue , silent synapse , context (archaeology) , long term depression , biology , chemistry , ampa receptor , glutamate receptor , dopamine , receptor , paleontology , biochemistry , dopaminergic
One of the mechanisms by which the experience‐dependent reorganization of neural circuitry can occur is through changes in synaptic strength. Almost every excitatory synapse in the mammalian brain exhibits LTP (long‐term potentiation) or LTD (long‐term depression), two cellular mechanisms of synaptic plasticity. However, LTP and LTD have been reported much more rarely at fast inhibitory GABA A receptor synapses. Our recent study suggests that in vivo morphine initiates a long‐lasting alteration of GABAergic synapses in the ventral tegmental area (VTA) by blocking the mechanisms required for LTP of GABAergic synapses. Here we put this work into the context of other examples of synaptic plasticity at GABAergic synapses.