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The Journal of Neuroscience, May 1, 2002, 22(9):3434-3444
Long-Term Depression Induced by Postsynaptic Group II
Metabotropic Glutamate Receptors Linked to Phospholipase C and
Intracellular Calcium Rises in Rat Prefrontal Cortex
S.
Otani1,
H.
Daniel1,
M.
Takita2, and
F.
Crépel1
1 Neurobiologie des Processus Adaptatifs,
Université de Paris VI, 75005 Paris, France, and
2 Neurobionics Group, National Institute of Applied
Industrial Science and Technology, Tsukuba 305, Japan
We have previously shown (Otani et al., 1999b) that bath
application of
(2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG IV), the agonist of group II metabotropic glutamate
receptors (mGluRs), induces postsynaptic
Ca2+-dependent long-term depression (LTD) of layer
I-II to layer V pyramidal neuron glutamatergic synapses of rat medial
prefrontal cortex. In the present study, we examined detailed
mechanisms of this DCG IV-induced LTD. First, the group II mGluR
antagonist (RS)- -methylserine-O-phosphate
monophenyl ester blocked DCG IV-induced LTD, and another group
II agonist
(2S,3S,4S)-CCG/(2S,1'S,2'S)-2-(carboxycyclopropyl)glycine-induced LTD, suggesting that LTD is indeed mediated by the activation of group
II mGluRs. Second, DCG IV-induced LTD was blocked by the NMDA receptor
antagonist AP-5, whereas DCG IV did not potentiate NMDA
receptor-mediated synaptic responses. Interruption of single test
stimuli during DCG IV application blocked DCG IV-induced LTD. These
results suggest that small NMDA receptor-mediated responses evoked by
single synaptic stimuli contribute to DCG IV-induced LTD. Third, DCG
IV-induced LTD was blocked or reduced by the following drugs:
phospholipase C inhibitor U-73122 (bath-applied or
postsynaptically injected), postsynaptically injected IP3
receptor blocker heparin, phospholipase D-linked mGluR blocker PCCG-13,
PKC inhibitor RO318220, postsynaptically injected PKC inhibitor
PKC(19-36), and PKA inhibitor KT-5720. Fourth, fluorescent
Ca2+ analysis techniques revealed that DCG IV
increases Ca2+ concentration in prefrontal
layer V pyramidal neurons. These Ca2+ rises and the
LTD were both blocked by postsynaptic heparin in the same cells. Taken
together, these results suggest that postsynaptic group II mGluRs,
linked to phospholipase C and probably also phospholipase D, induce LTD
through postsynaptic PKC activation and IP3
receptor-mediated postsynaptic increases of Ca2+ concentration.
Key words:
long-term depression; synaptic plasticity; prefrontal
cortex; group II metabotropic glutamate receptors; IP3
receptors; calcium release; phospholipase C; phospholipase D; protein
kinase C; protein kinase A
Copyright © 2002 Society for Neuroscience 0270-6474/02/2293434-11$05.00/0
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